tag:blogger.com,1999:blog-24123772678903199442024-03-05T11:27:19.139-08:00Lupine Publishers Cancer JournalLupine Publishers Cancer Journalhttp://www.blogger.com/profile/09600300951943945390noreply@blogger.comBlogger85125tag:blogger.com,1999:blog-2412377267890319944.post-43895222416134218372021-11-25T02:44:00.006-08:002021-11-25T02:44:44.197-08:00Lupine Publishers | Open Access Journal of Oncology and Medicine (OAJOM)<p><br /> </p><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/a/AVvXsEgxIcnqo62--5nWI9Uo0XXKXYweK0zEkCJtWEiUlzCqEaMxpZdT3V-wkjhCvbBq7m1oiJz_r3OhbNwnBRAvU-UiCLnVTTecvOoOCcpDfhTDn1tdO1gSsytUz_-sBAjukHC6BxUiNcp9HZjHPD39DMtx5pxSlJx9vMKqCfLB0UEyNR_cqcmwwjyGYcWS=s311" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="162" data-original-width="311" height="162" src="https://blogger.googleusercontent.com/img/a/AVvXsEgxIcnqo62--5nWI9Uo0XXKXYweK0zEkCJtWEiUlzCqEaMxpZdT3V-wkjhCvbBq7m1oiJz_r3OhbNwnBRAvU-UiCLnVTTecvOoOCcpDfhTDn1tdO1gSsytUz_-sBAjukHC6BxUiNcp9HZjHPD39DMtx5pxSlJx9vMKqCfLB0UEyNR_cqcmwwjyGYcWS=w379-h162" width="379" /> </a></div><div class="separator" style="clear: both; text-align: center;"> </div><div class="separator" style="clear: both; text-align: justify;"><span style="font-family: times;"><b style="-webkit-text-stroke-width: 0px; background-color: white; color: #202122; font-size: 14px; font-style: normal; font-variant-caps: normal; font-variant-ligatures: normal; letter-spacing: normal; text-align: start; text-decoration-color: initial; text-decoration-style: initial; text-decoration-thickness: initial; text-indent: 0px; text-transform: none; white-space: normal; word-spacing: 0px;">Thanksgiving</b><span style="-webkit-text-stroke-width: 0px; background-color: white; color: #202122; display: inline !important; float: none; font-size: 14px; font-style: normal; font-variant-caps: normal; font-variant-ligatures: normal; font-weight: 400; letter-spacing: normal; text-align: start; text-decoration-color: initial; text-decoration-style: initial; text-decoration-thickness: initial; text-indent: 0px; text-transform: none; white-space: normal; word-spacing: 0px;"><span> </span>is a national<span> </span></span>holiday<span style="-webkit-text-stroke-width: 0px; background-color: white; color: #202122; display: inline !important; float: none; font-size: 14px; font-style: normal; font-variant-caps: normal; font-variant-ligatures: normal; font-weight: 400; letter-spacing: normal; text-align: start; text-decoration-color: initial; text-decoration-style: initial; text-decoration-thickness: initial; text-indent: 0px; text-transform: none; white-space: normal; word-spacing: 0px;"><span> </span>celebrated on various dates in the United States, Canada, Grenada, Saint Lucia, and Liberia. It began as a day of giving thanks and sacrifice for the blessing of the<span> </span></span>harvest<span style="-webkit-text-stroke-width: 0px; background-color: white; color: #202122; display: inline !important; float: none; font-size: 14px; font-style: normal; font-variant-caps: normal; font-variant-ligatures: normal; font-weight: 400; letter-spacing: normal; text-align: start; text-decoration-color: initial; text-decoration-style: initial; text-decoration-thickness: initial; text-indent: 0px; text-transform: none; white-space: normal; word-spacing: 0px;"><span> </span>and of the preceding year. Similarly named festival holidays occur in Germany and Japan. Thanksgiving is celebrated on the<span> </span></span>second Monday of October<span style="-webkit-text-stroke-width: 0px; background-color: white; color: #202122; display: inline !important; float: none; font-size: 14px; font-style: normal; font-variant-caps: normal; font-variant-ligatures: normal; font-weight: 400; letter-spacing: normal; text-align: start; text-decoration-color: initial; text-decoration-style: initial; text-decoration-thickness: initial; text-indent: 0px; text-transform: none; white-space: normal; word-spacing: 0px;"><span> </span>in Canada and on the<span> </span></span>fourth Thursday of November<span style="-webkit-text-stroke-width: 0px; background-color: white; color: #202122; display: inline !important; float: none; font-size: 14px; font-style: normal; font-variant-caps: normal; font-variant-ligatures: normal; font-weight: 400; letter-spacing: normal; text-align: start; text-decoration-color: initial; text-decoration-style: initial; text-decoration-thickness: initial; text-indent: 0px; text-transform: none; white-space: normal; word-spacing: 0px;"><span> </span>in the United States and around the same part of the year in other places. Although Thanksgiving has historical roots in religious and cultural traditions, it has long been celebrated as a<span> </span></span>secular<span style="-webkit-text-stroke-width: 0px; background-color: white; color: #202122; display: inline !important; float: none; font-size: 14px; font-style: normal; font-variant-caps: normal; font-variant-ligatures: normal; font-weight: 400; letter-spacing: normal; text-align: start; text-decoration-color: initial; text-decoration-style: initial; text-decoration-thickness: initial; text-indent: 0px; text-transform: none; white-space: normal; word-spacing: 0px;"><span> </span>holiday as well.</span></span> <br /></div><p></p>Lupine Publishers Cancer Journalhttp://www.blogger.com/profile/09600300951943945390noreply@blogger.com0tag:blogger.com,1999:blog-2412377267890319944.post-43688167573713025242021-08-09T05:06:00.005-07:002021-08-09T05:06:32.876-07:00Lupine Publishers | Advances in Treating Relapsed Diffuse Large B Cell Lymphoma Treatment<p style="text-align: center;"> Lupine Publishers | Open Access Journal of Oncology and Medicine</p><p style="text-align: center;"> <br /></p><p style="text-align: center;"></p><div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjYaelAf9PKRlpVxlm4MBkyWmqg3qiMU76KncIqidm2bJetCTGs73metrj7Z7rtWWH00ie-0fYBwZfE9fKKBAe8tfIhPCFzxjr_mb7Eh6NtVkdd1_NFl_QyBirZsFDv4hwAP7Kpb37ZFXw/s1052/openaccessjournals-cancer-Oncology-OAJOM.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" data-original-height="1052" data-original-width="744" height="320" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjYaelAf9PKRlpVxlm4MBkyWmqg3qiMU76KncIqidm2bJetCTGs73metrj7Z7rtWWH00ie-0fYBwZfE9fKKBAe8tfIhPCFzxjr_mb7Eh6NtVkdd1_NFl_QyBirZsFDv4hwAP7Kpb37ZFXw/s320/openaccessjournals-cancer-Oncology-OAJOM.jpg" width="226" /></a></div><br /> <a id="Abstract">
<h2 style="margin-top: -90px; padding-top: 90px;">Abstract</h2></a>
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<p>Diffuse large B cell lymphoma (DLBCL) is the most common type of
non-Hodgkin lymphoma (NHL), comprising about 25% of all
mature NHL. First-line therapy cures about 40-60% of patients. High dose
chemotherapy followed by autologous stem cell transplant
can cure about 50% of patients at relapse. Transplant-ineligible
patients have shorter survival with every line of subsequent
therapies with a median overall survival (OS) of 10 months at second
line and 4.7 months at fourth lines of therapy. There is unmet
need to treat patients with relapsed DLBCL. Chimeric antigen receptor
T-Cells (CAR-T), with now three FDA- approved products to
treat relapsed DLBCL, provide a cure in about 40% of patients. Other
recently approved agents include antibody-drug conjugate
targeting CD79b (Polatuzumab Vedotin), Anti-CD19 antibodies
(Tafasitamab-cxix), and nuclear export inhibitor XPO1 (Selinexor)
have provided a hope to patients with relapsed DLBCL. We will discuss
these new approvals with comparison of response rate and
side effect profiles.</p>
<p><b>Keywords:</b> Diffuse Large B Cell Lymphoma; CAR-T Cell Therapy; Tafasitamab; Relapsed Refractory Lymphoma; Polatuzumab</p>
<a id="Introduction">
<h2 style="margin-top: -90px; padding-top: 90px;">Introduction</h2><h2 style="margin-top: -90px; padding-top: 90px;"> </h2></a><p>Non-Hodgkin lymphoma (NHL) is the eighth cause of cancer
death. With an estimated 81,560 new cases and 20,720 deaths in
2021 [1] DLBCL is the most common type of NHL comprising about
25% of all NHL cases [2].</p>
<p>The prognosis depends on different factors at diagnosis
including histological subtypes (Germinal center (GC) type versus
non-GC subtypes) [3], genetic subtypes (double HIT) [4], patient
age, stage of the disease, extra nodal involvement, and elevated LDH
(IPI scoring) 5. Other important prognostic factors can be assessed
after starting therapy, includes response at interim PET scan
(PET scan after 2-4 cycles of therapy)6. Initial therapy for DLBCL
remained the same for all different prognostic factors and different
risk group which is the famous combination of chemotherapy
R-CHOP (rituximab, cyclophosphamide, doxorubicin hydrochloride,
vincristine, and prednisolone) despite multiple attempts to try to
find a better alternative [7-9]. Except for high grade DLBCL with
c-Myc and BCL2 and/or BCL6 gene rearrangement which most
centers comfortable with using R-EPOCH chemotherapy regimen
[10]. With the stander of care R-CHOP, about 30% of diffuse large
B cell lymphoma patients relapse within the first 5 years [11]. Poor
response to initial therapy and, or very early relapse (within the
first six months), or what is called refractory disease is one of the
worse predictors of poor survival based on data from scholar-1
study [12].</p>
<p>Current stander of care at relapse including high dose
chemotherapy followed by autologous stem cell transplant [13]. In
patient with very high-risk relapse (relapse within 1 year of therapy
or refractory patients) there is a suggestion that early therapy with
CAR-T cell may improve outcome. this question will be answered
once we receive data from the now completed ZUMA7, and BELINDA
and TRANSFORM trials comparing different CAR-T cell products
(axicabtagene, Tisagenlecleucel, Lisocabtagene respectively) to the
current stander of care i.e., high dose chemotherapy followed by
autologous stem cell transplant in this very high-risk population.
Treatment after relapse from second line of therapy inpatient who
continue to maintain reasonable performance status is CAR-T cell
therapy. Different CAR-T cell products are currently FDA approved
to treat relapsed DLBCL after failure of at least two lines of therapy
including Axicabtagene ciloleucel (Axi-Cel), Tisagenlecleucel and
Lisocabtagene maraleucel(liso-cel). CAR-T provide about 40-55%
complete response rate (CR). Most worrisome Toxicity including
cytokine release syndrome (CRS) and neurological toxicity [14-16].
See Table 1 for comparing of different CAR-T cell products. Of note
patient with DHL and DEL benefited from CAR-T cell therapy at
relapse with Best overall response (ORR) was 56% (10/18) for DEL
patients, 50% (5/10) for DHL patients which was not different from
non-DHL/DEL in a retrospective data evaluation4. In patient who
are intolerable to transplant or are ineligible for CAR-T therapy or
had a relapse after CAR-T cell therapy there is no stander approach.
Recent advances in newer agent gave some hope in managing these
patients with improving survival.</p><p><b>Polatuzumab Vedotin</b></p>
<p>Polatuzumab Vedotin (Pola) is an antibody-drug conjugated
that bind to CD79b which is present in all B-lymphocytes including
mature malignant B-Cells delivering the microtubule inhibitor
(MMAE) causing direct cytotoxicity. Polatuzumab alone or in
combination with anti-CD20 antibody had a modest response with
CR ranging from 0-13% [17-18]. The combination of Polatuzumab,
Bendamustine and Rituximab was approved by FDA for patients
with relapsed DLBCL after failure of at least 2 lines of therapy. In
phase II randomized study comparing Pola BR to BR alone. The
median age of patient on Pola BR arm was 67, 25% had prior stem
cell transplant and 75% were refractory to prior line of therapy. ORR
was 63% (25 of 40 patients) with CR rate of 40%. 48% of patients
remained in CR at 1 year. Common side effects included fatigue,
infusion reaction, neuropathy, and pancytopenia and increase risk
of infection [19].</p>
<p><b>Tafasitamab</b></p>
<p>Tafasitamab (Tafa) is a Fc-enhanced, humanized, anti-CD19
monoclonal antibody. its FC portion is enhanced by modulating
two amino acids that leads to increase affinity to Fcy receptors. As
single agent Tafa has a response in DLBCL of 26% with responses
lasting >12 months [20]. Phase II L-MIND study studied the
combination of Tafa with lenalidomide as previous in vitro studies
showed synergetic activity [21]. The study showed impressive
CR rate of 43% with median duration of response of about 34
months. To compare the data from Pola-BR and Tafa-Lenalidomide
combinations refer to (Table 2).</p><p><b>Selinexor</b></p>
<p>Selinexor is an XPO1(exportin 1) inhibitor. XPO1 is responsible
for removal of multiple tumor suppressor genes out of the nucleus
like P53, P73 and IkBk outside nucleus and inhabiting their
function. The FDA had approved Selinexor as a single agent for
the treatment of relapsed or refractory DLBCL after at least 2 lines
of therapy. The approval was based on SADAL study, which was a
Phase II study that included 134 patients, 45% were 70 years or
older, 4% with DHL,41% had more than 3 lines of previous therapy
with 72% refractory to the last line, 13% had elevated LDH. Single
agent Selinexor resulted in ORR of 29%(95%CI:22,38) with CR rate
of 13% with response duration of 6 months. Most common adverse
reaction was fatigue, gastrointestinal side effects and pancytopenia
[22]. Preclinical data suggest that the inhibition of XPO1 can
provide a therapeutic target for DHL [23-24].</p>
<p><b>Bispecific T cell engager</b></p>
<p>Bispecific T-Cell engager (BiTe) therapy provide a promising
off the shelve immune therapy for multiple cancers including
NHL. In the contrary to CAR-T cell therapy, BiTe does not require
manufacturing time or pre-infusion conditioning chemotherapy.
Side effect can be similar but potentially less severe than CAR-T
including CRS and neurological toxicity [25]. At this time BiTE
therapy is not FDA approved to treat NHL but multiple trials across
the world are testing different BiTe as single agent or with different
combination including combining BiTe with Polatuzumab, with
lenalidomide or other combinations. Recently published phase I/
II trial with Glofitamab, Bivalent CD20-target T-cell engaging BiTe.
The study included 171 patients, 90% refectory to prior lines of
therapy with median of 3 previous lines of therapy, 74% had DLBCL.
ORR was in the phase II dose was 65.7% with CR of 57.1%. 84%
of Cr patients had a maximum of 27.4 duration of response. Grade
¾ CRS was seen in 3.4% and grade 3 CNS toxicity in 1.2% [26].
Other promising BiTes including Blinatumomab, Epicoritamab,
Monsunetuzumab and others [27-30].</p>
<p><b>Immune-Checkpoint Inhibitors in lymphoma</b></p>
<p>Immune check point inhibitors including programmed cell
death /ligand inhibitors PD1 and PD-L1 inhibitors and CTL4
inhibitors have so far limited role in the therapy of DLBCL in the
absence of biomarker targeted therapy. Future use may include
pretesting for PD1 expression or the use of checkpoint inhibitors
with combination [31].</p>
<p><b>CD47 Inhibitors</b></p>
<p>CD47 is present in virtually all cancer cells and it over
expression is associated with poor prognosis. It is an inhibitory
signal to macrophages (Do not Eat me signal) and inhabitation of
CD47 lead to potentially increasing macrophage activation and
tumor destruction. In addition, macrophages will present more
tumor antigen and increase T-cell mediated cytotoxicity [32]. In
Phase I/II trial combining CD47 inhibitor 5F9 with rituximab, the
study included 22 patients (15 had DLBCL). Among patients with
DLBCL, objective response rate was 40% with CR rate of 33%. Most
common side effects were anemia and infusion reaction [33].</p>
<a id="Conclusion and opinion">
<h2 style="margin-top: -90px; padding-top: 90px;">Conclusion and opinion</h2></a>
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The treatment of relapsed DLBCL remains a challenge. With
the approval of now three CAR-T cell therapy product we do have
a chance of curing at least a third of those patients. Other may
not benefit or may not have access to CAR-T cell therapy. Recently
approved regimens that provide a good promise are the Tafa and
lenalidomide combination and polatuzumab with Rituximab and
Bendamustine combination. Although we have some patients with
prolonged responses these combination does not provide a cure
as of now. And most patients eventually succumb to their disease.
With sequencing different combination and possibly prolonged
maintenance therapy as, possible with the use of BiTE or other
targeted agents we may see in the future an improved survival of
relapsed refractory lymphoma.</p><p>Read More Lupine Publishers Oncology and medicine Articles :
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<b>Lupine Publishers | Open Access Journal of Oncology and Medicine</b><br />
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<a href="https://www.blogger.com/u/1/null" id="Introduction" style="background: 0px 0px rgb(255, 255, 255); border: 0px; box-sizing: border-box; color: #0a71b5; font-family: "Open Sans", sans-serif; font-size: 14px; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;"></a><br />
<h2 style="background: 0px 0px; border: 0px; box-sizing: border-box; color: #185fa1; font-family: Raleway, sans-serif; font-size: 20px !important; font-weight: 600; line-height: 20px; margin: -90px 0px 10px; outline: 0px; padding: 90px 0px 0px; vertical-align: baseline; width: 558.156px;">
Introduction</h2>
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<span style="background-color: white; font-family: "Open Sans", sans-serif; font-size: 15px; text-align: justify;">Adenoid cystic carcinoma (ACC) is also called cylindroma, which is considered as a kind of low-grade malignant tumor and often occurs in head and neck salivary gland tissue. Most of them happened in submandibular gland and minor salivary glands while rarely happened in thymus. There are only 7 cases had already reported before all around the world. Our case is diagnosed as thymic carcinoma with adenoid cystic carcinomalike features by pathology after surgery; it is different with other cases because he had accepted a surgery six years ago because of the mediastinal mass and pleural effusion. Because of the symptom of chest tightness, he came to see doctor again and finally find there was a mediastinal mass and accepted the treatment of surgery. The medical history of our case maybe provides some inspiration of the pathogenic of thymic carcinoma with adenoid cystic carcinoma like features.</span></div>
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<b style="background: 0px 0px; border: 0px; box-sizing: border-box; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">Information and history</b></h3>
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A 60 years old male came to our hospital because of chest tightness in 2009/10. The enhanced chest CT showed “A large mass measuring 9.2*10.1cm² in the right side of the mediastinal which the average CT value is 9 Hu. The border with the superior vena cava and the right atrial and mediastinum is less clear. The right side of the chest is hydropneumothorax, Hydropericardium. The ultrasonic showed there is a mass of mixed echo in the right chest which had strong echo light and liquid visible mass dark space inside it. The test of pleural effusion by pleural puncture showed that was hematodes exudates without cancer cells. He accepted a surgery to resection of the mass by posterolateral thoracotomy, the pathology showed “Mostly considered as hematoma with organization according to clinical”. After the surgery ,he recovered and discharged from our hospital.</div>
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It is said by himself that there was found a mediastinal mass in his chest by CT in the year of 2010(the imaging data has been lost), and he taking chinese traditional medicein(herbal medicine) for tow month. After that he reexamination a chest CT showed the mediastinal mass was disappeared so he didn’t have the follow-up according to the doctor’s advice. 2014/10/13, he had a chest CT examination showed there is a 15*13cm² cystic with solid abnormal density shadow in the right front mediastium; Mediastinal lymph node is enlarged; Density of soft tissue in chest wall which is considered as metastatic. He reexamined a chest CT in 2015/1/4 but did not show significant change. Finally, he came to hospital again because of the intermittent chest pain. Complete the checks after hospitalization, lung function show” FEV1 : 3.94L, FEV1/FVC : 79%”, the enhanced chest CT showed “there is a 15.2*11.6cm² cystic with solid abnormal density shadow in the right front mediastium, the border is smooth and the density inside is uniform, the CT value is 18Hu; Right pulmonary atelectasis, the chest wall and diagram pars maybe have already metastasis tumor”.</div>
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<b style="background: 0px 0px; border: 0px; box-sizing: border-box; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">a. Anamnesis:</b> The patient with high blood pressure for more than 20 years, he use reserpin and Chinese traditional medicine to ctrl his high blood press by himself, but the effect is poor. His blood pressure was stabled for able 108/90mmHg for all years. Smoking 20 years and quit it for 23 years. We asked his medical history repeatedly, he denied the history of trauma and hemorrhagic disease.</div>
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<b style="background: 0px 0px; border: 0px; box-sizing: border-box; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">b. Preoperative diagnosis:</b> anterior mediastinum space occupying lesion, malignant tumor is the most possible. The chest wall maybe already metastasized. We suggested him to accept PET/CT to make the tumor’s metabolic strength clear and conform the primary focal; Or accept thoracentesis by fine needle to definite the pathological diagnosis. The patient and his family refused it and screamed for an operation.</div>
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So the surgery was planned. The patient was placed in the supine position under general anesthesia. Via median sternotomy. We saw the tumor was located in right anterior mediastinum, 12*12*10cm³, it was dense adhesion with mediastinal pleura, pericardium, diaphragm and right lung. The tumor is invading and partly wrapped around superior vena cava. Cut out part of the tumor tissue and sent to the examination of fast frozen section and the result was benign tumor. Then we completed removal of the tumor and cut one right rib and the tumor on the chest wall, the fast frozen section also report “benign tumor”. The tumor was solid and multicystic hemorrhagic with many sediment sample material. The diagnosis of the frozen section considered that most possible is encapsulated empyema. So we use polyninylpyrrolidone and normal saline to rinse the chest repeatedly and the closed thoracic conventionally.</div>
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The result of postoperative pathological: thymic carcinoma with adenoid cystic carcinomalike features with chest wall invasion, the tissue of cystiform is hyperplasia of fibrous tissue and stale hemorrhage. The result of immunohistochemical : CK(+), EMA(-), CK(L)(+), E-Ca(++), ER(+), PR(-), Ki67(10%), CK8/18(+), CD56 Focal(+), NSE(-), Syn(-), CgA(-).After the surgery, we checked the patient’s oral cavity, head and neck region but not found and obvious abnormal. 6 month pasted and we have not found any indication of tumor recurrence. He is still in follow up now.</div>
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<a href="https://www.blogger.com/u/1/null" id="Discussion" style="background: 0px 0px rgb(255, 255, 255); border: 0px; box-sizing: border-box; color: #de8d23; font-family: "Open Sans", sans-serif; font-size: 14px; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;"><h2 style="background: 0px 0px; border: 0px; box-sizing: border-box; color: #185fa1; font-family: Raleway, sans-serif; font-size: 20px !important; line-height: 20px; margin: -90px 0px 10px; outline: 0px; padding: 90px 0px 0px; vertical-align: baseline; width: 558.156px;">
Discussion</h2>
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Adenoid cystic carcinoma is salivary gland tumor, but can still be reported in breast [1], lung [2], esophageal [3], postate [4]. Thymic carcinoma with adenoid cystic carcinoma like features is very rare. Only 7 cases have already be reported all around the world before while all cases is not in China.</div>
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Thymic carcinomas are defined as thymic epithelial neoplasmas, which are classified into 10 different histological types according to the 2015 update of the WHO classification, i.e.[5]</div>
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a. squamous-cell carcinoma</div>
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b. basal cell carcinoma</div>
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c. mucoepidermoid carcinoma</div>
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d. lymphoepithelioma-like carcinoma</div>
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e. sarcomatoid carcimoa</div>
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f. clear cell carcinoma</div>
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g. adenocarcinoma</div>
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h. NUT carcinoma</div>
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i. unclassified carcinoma</div>
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j. other rare thymic carcinoma.</div>
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Within the group of adenocarcinoma, four histologic subtypes are known: papillary adenocarcinoma; thymic carcinoma with adenoid cystic carcinomalikefeatures; mucinous adenocarcinoma; adenocarcinoma, non specifically. Compared with the 2004 update of the WHO classification, the name of adenoid cystic carcinoma is changed to thymic carcinoma with adenoid cystic carcinomalike features. It lack the real features of adenoid cystic carcinoma in the character of immunohistochemical because it is generate from the thymus (Table 1) [6-8].</div>
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<b style="background: 0px 0px; border: 0px; box-sizing: border-box; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">Table 1: </b>The character of the cases of thymic carcinoma with adenoid cystic carcinomalike features which are reported so far.</div>
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<a href="https://lupinepublishers.com/cancer-journal/table/Lupinepublishers-openaccess-cancer-Oncology.ID.000117.T001.png" style="background: 0px 0px; border: 0px; box-sizing: border-box; color: #0a71b5; margin: 0px; outline: 0px; padding: 0px; text-decoration-line: none; vertical-align: baseline;" target="_blank"><img alt="Lupinepublishers-openaccess-cancer-Oncology" src="https://lupinepublishers.com/cancer-journal/table/Lupinepublishers-openaccess-cancer-Oncology.ID.000117.T001.png" style="background: 0px 0px; border: 0px; box-sizing: border-box; display: block; margin: 13px auto; outline: 0px; padding: 0px; vertical-align: baseline;" title="Click here to view Large Scheme 1" width="100%" /></a></center>
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<b style="background: 0px 0px; border: 0px; box-sizing: border-box; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">The Character of Clinical</b></h3>
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All of the clinical character of the cases which have already been reported is summarized above (chart-1). Thymic carcinoma with adenoid cystic carcinoma like features is very rare, most of them are occurred in elderly and few distant metastases. But it can show the character of aggressive growth and directly invasive chest wall; pericardium and other adjacent tissue. The initial symptoms of the patients are fever; cough; dyspnea; chest pain; the sense of suppression in the chest and the loss of weight [9]. thymic carcinoma with adenoid cystic carcinoma like features is generated in the tissue of thymus which located in the mediastinum, and the size of the most tumor is large. The severity of the clinical symptoms is uncorrelated with the size of the tumor.</div>
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Although the size of the tumor is large, the symptoms of patients is not severely even cannot let them go to see doctor. The clinical symptoms is formed because of the oppress by the tumor, there is no obviously symptoms in early stage, with the growth of tumor , the patient will appear the atypical symptoms such as cough; fever; dyspnea; chest pain and so on. Because thymic carcinoma with adenoid cystic carcinomalike features is a low grade malignancy, all cases had the features of gradual onset and grow progress. So only one case that had already metastases to rib was reported that is different whit the character of adenoid cystic carcinoma in salivary. According to the Masaoka stage of thymus tumor, our case is in stage β.</div>
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<b style="background: 0px 0px; border: 0px; box-sizing: border-box; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">The Character of Pathology</b></h3>
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The macroscopic view of the tumor: Most of them are consist of huge gritty and firm cystic solid mass with smooth border. Some of them have complete capsule. The cross-section showed multicystic, necrotic tissue mixed with fibrotic, yellow tissue nodules. Some of them can be observed the papillary hyperplasia and plenty of hemorrhagic effusion.</div>
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<b style="background: 0px 0px; border: 0px; box-sizing: border-box; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">a. The microscopic view of the tumor:</b> The character of our case is similar as salivary adenoid cystic carcinoma. The cystic and cribriform texture neoplastic nest is consist of basoloid cell carcinoma ,and bloody fluid or granular basophilic myxoid stroma full of the cyst. The microscopic view of the thymic carcinoma with adenoid cystic carcinomalike features can be classified as three types. If the tumor cell is undifferentiated, it will show the solid structure with irregular funicular or dense array by basaloid cells(solid type). If the tumor cell is differentiation to the glandular epithelium, it will show the gland tubular structure consist of the inner layer of columnar epithelium and the outside of the myoepithelial cells with homogeneous eosinophilic mucin full of the cavity of the tubule(tubular type). If the tumor cell is differentiation to the myoepithelial cell, it will show the cribriform structure with homogeneous basophilic cell matrix(cribriform type)[10]. The classify of thymic carcinoma with ACC like features is closely connected with the prognosis, so we infer that the prognosis of solid type is the worst while the prognosis of tubular type and the cribriform type is more better.</div>
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<b style="background: 0px 0px; border: 0px; box-sizing: border-box; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">b. Immuno histochemistry:</b> CK and CKL all showed positive in our case, they were marked at the epithelium which consist of cribriform structure. E-Ca(++) prompted the tumor has a certain invasive in accordance with the invasion of chest wall. Ki67(10%) prompted the active proliferation. CD56(focal +) is the new character that has not be reported before ER(+) prompted this case may be sensitive to endocrine therapy, but there isn’t any evidence of evidence-based medicine support it so the clinical significance needs to be confirmed.</div>
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Summarize other documents , we can get the following conclusion:</div>
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i. These marks is contribute to the diagnosis of thymic carcinoma with adenoid cystic carcinomalike features if they are positive: CollagenIV, laminin, P63, CK34betaE12, Ki67(1- 10%)</div>
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ii. These marks is contribute to the diagnosis of thymic carcinoma with adenoid cystic carcinomalike features if they are negative: Syn, NSE, CD117, CgA.</div>
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The molecular marks research of this disease has not yet been carried out. There are reports that suggested MYB-NFIB fusion gene, NF-κB, MMP-2, survivin is related to adenoid cystic carcinoma [11], and it is helpful to the molecular marks research of thymic carcinoma with adenoid cystic carcinomalike features.</div>
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<b style="background: 0px 0px; border: 0px; box-sizing: border-box; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">The Differential Diagnosis</b></h3>
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PET/CT has great significance to this disease in differential diagnosis, it can estimate whether the mass is primary tumor or metastases. The report suggested the tumor of this disease show high value of SUV max in PET/CT while its metastases can also show unusually high value of SUV max [9]. The retrospective analysis show that have a examination of PET /CT before surgery is correct and meaningful. In the primary thymic carcinoma, this disease should be distinguished with basaloma. In morphology, most of the tumor cell of basaloma is cubic cells with small and deep dyeing nucleus which array form lobulated or funicular [12,13]. The results of Immuno histochemistry can confirm that our case can be diagnosed as thymic carcinoma with adenoid cystic carcinoma like features.</div>
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<b style="background: 0px 0px; border: 0px; box-sizing: border-box; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">The treatment and prognosis</b></h3>
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Surgery is given priority to this disease at present and radiation therapy can according to the situation. The effect of chemotherapy for this disease is poor and if take chemotherapy as a routine treatment is still controversial. Some professional insist of that adenoid cyst carcinoma cannot get enough benefit from chemotherapy, so we should treat chemotherapy as the last treatment [14]. We believe that A case report and review of thymic carcinoma with adenoid cystic carcinoma like features is a low level malignant tumor so the it should have better prognosis after standardized treatment. But we still should be carefully evaluated before surgery and if we suspect the diagnosis as thymic tumor with ACC like carcinoma or huge mediastinal mass, PET/CT will be suggested to confirm the quality of the mass and whether there is metastases or not.</div>
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Locally metastasis and the chest wall invasion should not be the absolute contraindications of surgery because as a low level malignant tumor, if we resection the tumor and metastases completely and take some radiation therapy appropriately, nice quality of life will get. In our case a recurrence is appear after the surgery in 2009, but he said itself that the mediastinal mass was once disappeared after the treatment of Chinese traditional medicine. So we guess that Chinese traditional medicine may effective for this disease.</div>
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<b style="background: 0px 0px; border: 0px; box-sizing: border-box; margin: 0px; outline: 0px; padding: 0px; vertical-align: baseline;">The discussion of pathogenesis</b></h3>
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A case report and review of thymic carcinoma with adenoid cystic Carcinoma like features is a kind of thymic carcinoma, it is generated from thymic epithelial cells. If the tumor cell is differentiation to the myoepithelial cell, it will show the cribriform structure with homogeneous basophilic cell matrix. The medical history of our case is so specially that he found the mediastinal mass six years ago and experienced the surgery. The pathological report at the time of 2009 showed “hematoma with organization”. Organization means the absorption process by new granulation tissue if necrotic tissue, thrombus, .com or foreign body cannot be dissolved or absorbed or separated or discharged. The granulation tissue contains abundant myocyte and some of them will differentiate to myofibroblast after the stimulate of cytokines.</div>
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And these cytokines that can induce differentiation may induce the differentiate thymic epithelial cell to myoepithelium and finally generate to the type of cribriform of thymic carcinoma with adenoid cystic carcinomalike features is a kind of thymic carcinoma. This maybe one of the triggers of this disease although still need to establish by experiments. According to the inference above, we consider coagulate hemothorax and mediastinal hematoram may result thymic carcinoma with adenoid cystic carcinoma like features. In order to avoid the remained thymus tissue be stimulated to differentiate to thymic carcinoma, in the surgery of mediastinal hematoma, thymectomy completely is necessary and fat tissue of mediastinal should be resection completely too.<br /><br />Read More Lupine Publishers Oncology and medicine Articles : </div>
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Lupine Publishers Cancer Journalhttp://www.blogger.com/profile/09600300951943945390noreply@blogger.com0tag:blogger.com,1999:blog-2412377267890319944.post-41910143438058202712020-05-13T05:19:00.000-07:002020-05-13T05:19:07.488-07:00Lupine Publishers | Promising Role of Fractional Calculus in Biomedicine and Biophysics<div dir="ltr" style="text-align: left;" trbidi="on">
<b>Lupine Publishers | Open Access Journal of Oncology and Medicine</b><br />
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<b><br /></b>
<br />
<div class="MsoNormal" style="line-height: 12.0pt; margin-bottom: 6.0pt; mso-outline-level: 2; vertical-align: baseline;">
<b><span style="color: #185fa1; font-family: "Cambria","serif"; mso-ascii-theme-font: major-latin; mso-bidi-font-family: Arial; mso-fareast-font-family: "Times New Roman"; mso-hansi-theme-font: major-latin;">Introduction<o:p></o:p></span></b></div>
<div class="MsoNormal" style="background: white; line-height: 15.6pt; margin-bottom: .0001pt; margin-bottom: 0in; margin-left: 0in; margin-right: 0in; margin-top: .1in; text-align: justify; vertical-align: baseline;">
<span style="font-family: "Cambria","serif"; font-size: 9.0pt; mso-ascii-theme-font: major-latin; mso-bidi-font-family: Arial; mso-fareast-font-family: "Times New Roman"; mso-hansi-theme-font: major-latin;">The
study of complex systems and investigation of their structural and dynamical
properties have attracted considerable interests among scientists in general
and physicists, biologists and medical researchers in particular. Complex
systems can be found almost everywhere however the highest level of
complexities is related to living and biological organisms and systems. Due to
the lack of a reliable and effective tool to investigate such systems, we have
not reached to the complete understanding and comprehensive pictures of the
phenomena and processes which occur in these systems. Of course a comprehensive
knowledge of biological and biomedical complex phenomena will be achieved when
we employ simultaneously different field of science and engineering including:
biology, chemistry, physics, mathematics, mechanical engineering and so on.<o:p></o:p></span></div>
<div class="MsoNormal" style="background: white; line-height: 15.6pt; margin-bottom: .0001pt; margin-bottom: 0in; margin-left: 0in; margin-right: 0in; margin-top: .1in; text-align: justify; vertical-align: baseline;">
<span style="font-family: "Cambria","serif"; font-size: 9.0pt; mso-ascii-theme-font: major-latin; mso-bidi-font-family: Arial; mso-fareast-font-family: "Times New Roman"; mso-hansi-theme-font: major-latin;">Fortunately
in recent year's powerful tool of fractional calculus has been proposed for
study of complex and nonlinear phenomena. It is in fact very useful tool for
describing the behavior of nonlinear systems which are characterized by:
special kind of non-locality, long-term memory and fractal properties. There
exist many biological objects and systems with memory, nonlocal effects and
nonlinear behaviors and such these non-localities and memory effects in
biological objects and systems mean that the next state of the organism or
system relies not only on its present state but also upon all of its previous
states. As a result, the concept of fractional dynamics and in fact adopting
fractional calculus can play an important role in the study of dynamical
biological systems. Up to now few number of important issues such as: protein
folding phenomena and mechanics of cancer cells (for more details see the
references which have investigated physics of protein and physics of cancer in
detail) have been investigated using the framework of fractional dynamics [1].<o:p></o:p></span></div>
<div class="MsoNormal" style="background: white; line-height: 15.6pt; margin-bottom: .0001pt; margin-bottom: 0in; margin-left: 0in; margin-right: 0in; margin-top: .1in; text-align: justify; vertical-align: baseline;">
<span style="font-family: "Cambria","serif"; font-size: 9.0pt; mso-ascii-theme-font: major-latin; mso-bidi-font-family: Arial; mso-fareast-font-family: "Times New Roman"; mso-hansi-theme-font: major-latin;">However
many other important issues still remain as open issues, such as: modeling of
interactions between light (laser) and biological tissue and modeling of
intracellular (and intercellular) interactions in the framework of fractional
dynamics. As a physicist or biologists and even medical researchers, we always
are able to model natural phenomena for instance modeling of tumor growth using
systems of differential equations and nowadays it is well know that the
fractional-order ones are more comprehensive and also incorporate memory effect
and the concept of non-locality in the model.<o:p></o:p></span></div>
<div class="MsoNormal" style="background: white; line-height: 15.6pt; margin-bottom: .0001pt; margin-bottom: 0in; margin-left: 0in; margin-right: 0in; margin-top: .1in; text-align: justify; vertical-align: baseline;">
<span style="font-size: 9pt;"><span style="font-family: Cambria, serif;">Mathematically
the idea is in fact, to rewrite the ordinary governing differential equations
in the fractional form by replacing the standard derivative with a fractional
derivative of arbitrary order which is defined in the Caputo sense as follows:</span></span><span style="font-size: 9pt;"><span style="font-family: Cambria, serif;"><br />where
Γ denotes the Gamma function and , . And its Laplace transform can be given by:</span></span></div>
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<span style="font-family: "Cambria","serif"; font-size: 9.0pt; mso-ascii-theme-font: major-latin; mso-bidi-font-family: Arial; mso-fareast-font-family: "Times New Roman"; mso-hansi-theme-font: major-latin;"><br /></span></div>
<div class="MsoNormal" style="background: white; line-height: 15.6pt; margin-bottom: .0001pt; margin-bottom: 0in; text-align: justify; vertical-align: baseline;">
<span style="font-size: 9pt;"><span style="font-family: Cambria, serif;">Where, </span><i style="font-family: Cambria, serif;"><span style="border: none windowtext 1.0pt; mso-border-alt: none windowtext 0in; padding: 0in;">F(s)</span></i><span style="font-family: Cambria, serif;"> is the
Laplace transform of </span><i style="font-family: Cambria, serif;"><span style="border: none windowtext 1.0pt; mso-border-alt: none windowtext 0in; padding: 0in;">f (t</span></i><span style="font-family: Cambria, serif;">). Solutions of
fractional differential equations generally will be expressed using a
generalized special function named as Mittag-Leffler function. This function
can be considered as a generalized exponential function and has several
different forms. For instance the one-parameter Mittag-Leffler function is
defined by the series expansion as:</span></span><span style="font-size: 9pt;"><span style="font-family: Cambria, serif;"><br />Where </span><i style="font-family: Cambria, serif;"><span style="border: none windowtext 1.0pt; mso-border-alt: none windowtext 0in; padding: 0in;">C</span></i><span style="font-family: Cambria, serif;"> is the set of
complex numbers? It is worth mentioning that the exponential function is just a
special case of </span><b style="font-family: Cambria, serif;"><i><span style="border: none windowtext 1.0pt; mso-border-alt: none windowtext 0in; padding: 0in;">α</span></i></b><span style="font-family: Cambria, serif;"> = </span><b style="font-family: Cambria, serif;"><i><span style="border: none windowtext 1.0pt; mso-border-alt: none windowtext 0in; padding: 0in;">l</span></i></b><span style="font-family: Cambria, serif;"> Mittag-Leffler function, for example for the
special case of , the Mittag-Leffler function Eq. (3) reduces to the
exponential function </span><i style="font-family: Cambria, serif;"><span style="border: none windowtext 1.0pt; mso-border-alt: none windowtext 0in; padding: 0in;">E</span></i></span><i><sub><span style="border: none windowtext 1.0pt; font-family: "Cambria","serif"; font-size: 6.0pt; mso-ascii-theme-font: major-latin; mso-bidi-font-family: Arial; mso-border-alt: none windowtext 0in; mso-fareast-font-family: "Times New Roman"; mso-hansi-theme-font: major-latin; padding: 0in;">1</span></sub></i><i><span style="border: none windowtext 1.0pt; font-family: "Cambria","serif"; font-size: 9.0pt; mso-ascii-theme-font: major-latin; mso-bidi-font-family: Arial; mso-border-alt: none windowtext 0in; mso-fareast-font-family: "Times New Roman"; mso-hansi-theme-font: major-latin; padding: 0in;">(z)
= e</span></i><i><sup><span style="border: none windowtext 1.0pt; font-family: "Cambria","serif"; font-size: 7.0pt; mso-ascii-theme-font: major-latin; mso-bidi-font-family: Arial; mso-border-alt: none windowtext 0in; mso-fareast-font-family: "Times New Roman"; mso-hansi-theme-font: major-latin; padding: 0in;">z</span></sup></i><span style="font-family: Cambria, serif; font-size: 9pt;"> . This point is very important because of
that the natural exponential function has been considered as a fundamental
function of natural science and in particular biology up to now, so that many
phenomena could be described using it and now scientist are able to think that
with such this new framework (i.e. fractional differential equations and their
solutions in terms of Mittag-Leffler functions) they can find many new results
and information about biological and biomedical phenomena [2,3].</span></div>
<div class="MsoNormal" style="background: white; line-height: 15.6pt; margin-bottom: .0001pt; margin-bottom: 0in; margin-left: 0in; margin-right: 0in; margin-top: .1in; text-align: justify; vertical-align: baseline;">
<span style="font-family: "Cambria","serif"; font-size: 9.0pt; mso-ascii-theme-font: major-latin; mso-bidi-font-family: Arial; mso-fareast-font-family: "Times New Roman"; mso-hansi-theme-font: major-latin;">Finally,
based on all above mentioned reasons, as a conclusion we should say that we
believe that the powerful tool of fractional calculus and in fact the frame
work of fractional dynamics can give.com new insights in understanding and
modeling of nonlinear complex phenomena in various living cellular structures
and their interactions and we invite all biologist and medical researchers to
consider this new powerful approach for their future studies.<br style="mso-special-character: line-break;" />
<!--[if !supportLineBreakNewLine]--><br style="mso-special-character: line-break;" />
<!--[endif]--></span><span style="font-family: "Cambria","serif"; font-size: 10.0pt; mso-ascii-theme-font: major-latin; mso-bidi-font-family: Arial; mso-fareast-font-family: "Times New Roman"; mso-hansi-theme-font: major-latin;"><o:p></o:p></span></div>
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Lupine Publishers Cancer Journalhttp://www.blogger.com/profile/09600300951943945390noreply@blogger.com0tag:blogger.com,1999:blog-2412377267890319944.post-74280180027244113882020-03-12T05:27:00.001-07:002020-03-12T05:27:16.781-07:00Lupine Publishers: Lupine Publishers | Principles of the Military Con...<a href="https://lupinepublishers.blogspot.com/2020/03/lupine-publishers-principles-of.html?spref=bl">Lupine Publishers: Lupine Publishers | Principles of the Military Con...</a>: Lupine Publishers- Anthropological and Archaeological Sciences Journal Impact Factor Introduction A way from the regular th...Lupine Publishers Cancer Journalhttp://www.blogger.com/profile/09600300951943945390noreply@blogger.com0tag:blogger.com,1999:blog-2412377267890319944.post-19788058883029265882020-03-12T05:24:00.003-07:002020-03-12T05:24:59.573-07:00Lupine Publishers | Acute Erythroblastic Leukemia Revealed by Dermatological Manifestations<div dir="ltr" style="text-align: left;" trbidi="on">
<b>Lupine Publishers | Open Access Journal of Oncology and Medicine</b><br />
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<a href="https://www.blogger.com/null" id="Abstract">
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Abstract</h2>
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Acute erythroblastic leukemia is characterized by the proliferation
of a predominant erythrocyte population on other lineages. Cutaneous
manifestations remain rare and misleading, making the diagnosis of
difficult to suspect as first-line. Here, we report an unusual and rare
case of acute leukemia in a 24 year old male with gingival hypertrophy
and dermatological manifestations. This case emphasizes that dentist and
dermatologist should be well acquainted with these manifestations of
systemic diseases.<br />
<a href="https://www.blogger.com/null" id="Case Report">
<h2 style="margin-top: -90px; padding-top: 90px;">
Case Report</h2>
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We report the case of 24 years old patient, with no significant
pathological history, who had a rash for 10 days in a context of fever
and very bad general condition. At admission the patient was febrile,
tachycardic and dyspneic. Physical examination revealed
erythemato-purplished papulo-nodules on the face, trunk, limbs and a
gingival hyperplasia. The oral state was deplorable. Bilateral cervical
lymphadenopathy was also found without the patosplenomegaly (Figures
1-3). The biological assessment showed a CRP of 150 and a pancytopenia
with a Hbat 7.5g / dl, normal VGM and CCMH, a deep thrombocytopeniaat
85000 / l, leukocytesat 1500 / l. The blood smear showed 35% of
circulating blasts and 22% of erythroblasts (Figure 4).<br />
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<b>Figure 1:</b> Clinical Manifestations of AML.<br />
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<img src="https://lupinepublishers.com/cancer-journal/images/Lupinepublishers-openaccess-cancer-Oncology.ID.000106.G001.png" width="60%" /></div>
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<b>Figure 2:</b> Clinical Manifestations of AML.<br />
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<b>Figure 3:</b> Clinical Manifestations of AML.<br />
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<img src="https://lupinepublishers.com/cancer-journal/images/Lupinepublishers-openaccess-cancer-Oncology.ID.000106.G003.png" width="60%" /></div>
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<b>Figure 4:</b> Blood smear showing 35% of circulating blasts.<br />
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<img src="https://lupinepublishers.com/cancer-journal/images/Lupinepublishers-openaccess-cancer-Oncology.ID.000106.G004.png" width="60%" /></div>
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The medullo gram showed a hyper-cellular marrow with a rate of
myeloblasts greater than 45% compared to all non-erythroblastic elements
and erythroblastic hyperplasia estimated at more than 65%; with signs
of dyserythropoiesis suggestive of the diagnosis of erythroleukemia
(Figure 5). Blood immune phenol typing was positive for CD13, CD33, MPO
and Glycophotin A. The evolution was unfavourable; the patient died due
to massive alveolarhemorrhage.<br />
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<b>Figure 5:</b> Hyper cellular marrow infiltrated by a blastic contingent estimated at 45%.<br />
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<img src="https://lupinepublishers.com/cancer-journal/images/Lupinepublishers-openaccess-cancer-Oncology.ID.000106.G005.png" width="60%" /></div>
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Acute erythroblastic leukemia is characterized by the proliferation
of a pre dominantery throcyte population on other lineages. There are
two types: Erythroleukemia: defined by the presence in the bone marrow
of more than 50% of the erythroid precursors of all the medullary cells,
and more than 20% of myeloblasts of the whole non-erythrocytemedullary
cells - Pure erythroid leukemia: it presents a neoplastic proliferation
made of more than 80% of erythrocyte cells without obvious presence of
the myeloblastic contingent [1]. It is usually manifested by signs of
bone marrow failure and cytopenia [2,3], skin involvement remains rare,
varied and disorienting the diagnosis; they are found mainly in Acute
myelovlastic leukemia [4,5]. Cutaneous manifestations during leukemia
are infrequent and varied. They designate all the cutaneouslesions
related to the haematological malignancy directly or indirectly
following their treatment; we essentially distinguish.<br />
The specific dermatological lesions which can reveal hematological
diseases [4], are mainly represented by leukaemides (leukaemia cutis),
which are red brown to purple dermal papules, plaques or nodules.
Granulocyticsarcom as an extra-medullary tumour masses, ulcerated
plaques and gingival hypertrophy [5]. The infectious dermatoses
secondary to the biological disturbances accompanying the malignan
themopathy and their treatments. The occurrence of specific
cutaneouslesions in leukemia is synonymous with a major aggravation of
the prognosis (with for example a survival twice as short if there is a
specific cutaneous involvement); this seriousness make some authors
propose different treatments with a medium-long stay
hospitalization[6-8].<br />
In our case, acute myelonlastic leukemia 6 (AML 6 ) was revealed by
diffuse leukemias resulting from the infiltration and proliferation of
malignantha ematological cells (blasts) in the skin and by gingival
hyperplasia secondary to mucosal infiltration [5]. The clinical
presentation of acute leukemia including AML6 in the form of ulcer
ativenecroticgingivitis in the foreground, is a rare form to be
remembered, mentioned in all courses of medicine and dentistry,
stipulating that Gingival involvement is a classic feature of leukemia
[6] The frequent association of skin cancers with haematological
malignancies is also highlighted in several publications [5].<br />
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The cutaneous localizations are among the rarest extreme dullary
lesions of acute myeloid leukaemia’s (AML) not exceeding 1%. They are
generally considered as factors of worse prognosis. Their cytogenetic or
mutational specificities remain un established to date.<br />
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Lupine Publishers Cancer Journalhttp://www.blogger.com/profile/09600300951943945390noreply@blogger.com0tag:blogger.com,1999:blog-2412377267890319944.post-78067882552987453892020-02-27T03:59:00.000-08:002020-02-27T03:59:45.677-08:00Lupine Publishers | Subjection between Breast Cancer and Body Mass Index, the Role of L-Carnitine in Prediction and Outcomes of the Disease<div dir="ltr" style="text-align: left;" trbidi="on">
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Increasing the effectiveness of antitumor therapy in breast cancer
patients who take L-carnitine during preoperative systemic antitumor
therapy compared with patients receiving standard neoadjuvant systemic
antitumor therapy served as a prerequisite for studying possible
antitumor mechanisms of L-carnitine. The positive effect of L-carnitine
is due to the transfer of palm-n-LC through the inner membrane into the
mitochondrial matrix, which promotes the formation of a significant
number of ATP molecules. It has also been shown that L-carnitine can
have a double protective effect, enhancing the energy dynamics of the
cell and inhibiting the hyperexcitability of the cell membrane, that
making it an ideal nutrient for the prevention and treatment of cancer.
This article summarizes the results of epidemiological and clinical
studies of the use of L-carnitine in the treatment of breast cancer<br />
<b class="key-color">Keywords:</b> Body mass index (BMI); Breast cancer (BC); Obesity; Overall survival; L carnitine<br />
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<br />Introduction</h2>
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The incidence of breast cancer in the world in general and in Ukraine
in particular is growing. In 2017, in Ukraine the incidence reached 16
percent of female population, for which, the breast cancer ranked first
in structure of oncological incidence among women. In analyzing the data
of the National Cancer Registry of Ukraine, it should be noted, that in
comparison with 2014 year, the prevalence rate of breast cancer in
2016has increased by 5,1%, that indicates importance of improvement
diagnostic procedures and methods of treatment it [1]. Studying the
scientific literature on this subject, we noticed that there is a strong
biological relationship between obesity and a poor outcome of breast
cancer. And having analysed the date of Ministry of Health in Ukraine it
can be concluded, that about 26% of women in 2017 year had overweight
or obesity.<br />
Obesity has a chronic metabolic character, which is the result of the
interaction of the endogenous factors, environmental conditions and
lifestyle. Endogenous factors could be considered a violation of the
genetic and hormonal balance. The external conditions and type of
lifestyle include irregular rhythm nutrition, use of substandard
products and sedentary lifestyle. Obesity is the first risk factor for
metabolic syndrome, diabetes type II, cardiovascular disease and some
forms of cancer, including breast cancer. Since overweight is a risk
factor for breast cancer, there is reason to believe that among patients
with breast cancer the percentage of obese women is higher than in the
population. The risk of breast cancer in postmenopausal women by 30%, it
is more than in premenopausal, women with obesity-50%. Furthermore it
was proven that obesity is associated with poor prognosis in patients
with breast cancer, regardless of menopausal status, and effectiveness
of systemic medication breast cancer in patients that have over weight
is lower than in patients with normal BMI.<br />
Although obesity is associated with a poor outcome in women with
breast cancer, it is unclear how weight loss after diagnosis will change
its course and results. Recently, complementary and alternative
medicine (CAM) is widely accepted among patients with breast cancer,
which may provide several beneficial effects including reduction of
therapy-associated toxicity, improvement of cancer-related symptoms,
fostering of the immune system, and even direct anticancer effects [2].
L-carnitine is a metabolite of C<sub>4</sub> oil LC, which is involved
in the transfer of palm-n-LC through the inner membrane into the
mitochondrial matrix and is a substrate for the formation of ATP
molecules. Carnitine is a trim ethylated amino acid naturally
synthesized in the liver, brain and kidneys from protein lysine and
methionine. Several factors, such as sex hormones and glucagon, can
influence the distribution and level of carnitine in tissues [3,4].<br />
In the absence of L-carnitine, the inner membrane of the mitochondria
becomes impermeable to fatty acids, which entails a chain of various
metabolic disorders in the human body. Carnitine has a modulating effect
on the function of acetylcholine excitatory neurotransmitter, glutamate
excitatory amino acid, insulin growth factor-1 (IGF-1) and nitric oxide
(NO)[3]. Also proved, that L-carnitine may have a dual protective
effect by enhancing the energy dynamics of the cell and inhibiting cell
membrane hyper excitability, which make it an ideal nutrient for cancer
prevention and treatment [5]. In view of the foregoing, the study of the
influence of the body mass index on the effectiveness of systemic
treatment of breast cancer is an urgent scientific problem and a
promising field of research. This article presents the information of
epidemiological and clinical studies of the influence of the body mass
index on the effectiveness of breast cancer treatment by individualizing
therapeutic measures taking into account the characteristics of
patient's metabolism.<br />
<b>Studies on the Effects of BMI on The Course and Outcome of Breast Cancer and the Role of L-Carnitine in the Treatment of Cancer:</b>
The effectiveness of the prescribing of L-carnitine for breast cancers'
treatment, as well as the effect of BMI on the outcome of the disease
is proven in epidemiological and clinical studies.<br />
<h3>
<b>Epidemiological and Clinical Studies</b></h3>
DSM Chan and co-authors [6] reported that women who have BMI> 30
course and outcomes of breast cancer are significantly worse than women
with BMI <30. They proved, that women with BMI> 30 have the
overall relative risk of total mortality 1.41, women with BMI of 25>
30 - 1.07. At the same time, for every 5 kg / m<sup>2</sup> of the
increase BMI, the risk of both total mortality and mortality from breast
cancer increased, namely by 18% and 14%, respectively M. Protani and
co-authors [7] have shown that women with breast cancer, who are
suffering in obesity, have lower survival rate than women with breast
cancer without obesity. Recently published data of randomized clinical
researches by ML Neuhouser and coauthors [8] demonstrated, that for
women> 50 years old, with 2 and 3 stages of obesity (BMI> 35) is
typically the development of GR+ breast cancer.<br />
Similarly, B. Pajares et al. [9] who found significantly worse
results for patients with BMI >35 compared with patients with BMI
<25, stated that the magnitude of the effect depended on the cancer
subtype (estrogen receptor (ER) / progesterone (PR) positive and HER2
negative, HER2 positive, triple negative). An analysis of the pooled
data of the three adjuvant studies of the Eastern Cooperative Cancer
Group showed significantly worse results for patients with obesity (BMI
> 30) than for patients with normal BMI with a hormonal
receptor-positive disease. And it was noted absence of negative effect
of obesity on survival in patients with other breast cancer subtypes. C
Fontanella et al. [10] studied the effect of BMI on different molecular
subtypes of breast cancer and concluded that in women with ER /
PR-positive and HER2-negative breast cancer, as well as with TNBC, the
risk of death is significantly higher than in other subtypes of cancer.<br />
It is proved that even the highest BMI figures are not a risk factor
for death for patients with luminal A-like subtype of breast cancer. The
reason for this is that fatty tissue produces an excessive amount of
estrogen, a high level of which is associated with an increased risk of
developing breast, endometrial, ovarian and some other cancers. It has
also been proven that the level of adipokine, that promotes cell
proliferation, increases in the blood with increasing of level of fat in
organism. And adiponectin, which people with obesity have less than
people with normal BMI, can have anti proliferative effects. Such data
can serve as evidence of the effect of BMI on the course and outcome of
breast cancer. Yet another proof of influence developing metabolic
syndrome on the course and outcome of breast cancer was proposed by R.
Bhandari et al. [11]. They proved that that the presence of metabolic
disorders (that is, the metabolic syndrome) is associated with an
increased risk of breast cancer in adult women.<br />
The above data led to the need to investigate medicines that
contribute to fat burning, such as L-carnitine. Based on the data
provided by Rania M. Khalil and co-authors [12], we can prove the
positive effect of this medicine on the course and outcome of breast
cancer. The study showed that patients who received Tamoxifen with
L-carnitine had significant decrease of Her-2 / neu and IGF-1 level (P
<0.05) in the serum compared with patients who received only
Tamoxifen. Using of L-carnitine led to significant decrease Her- 2 / neu
level in the serum (P <0.05) compared to each of the control
patients, namely, 59.5%. The effect of tamoxifen on IGF-1 (P <0.05)
-decrease its level by 5.4% [13].However, it has been proved that using
of L-carnitine in the treatment of ER+ breast cancer does not
significantly reduce the level of estradiol, but leads to decrease both
tumor markers CEA and CA15.3 (P <0.05,% decrease by 80.9% and 67, 8%,
respectively) [13].<br />
Using of L-carnitine in patients with breast cancer and obesity
improves the metabolism of fatty acids in mitochondria, restores normal
mitochondrial function and, thus, improves the general condition and
quality of patients’ life [14]. Carnitine may alsomimic some of the
biological activities of glucocorticoids, particularly immunomodulation,
via suppressing TNF-a and IL-12 release from monocytes (5). L-carnitine
as adjuvant therapy in cisplatin-treated cancer patients proved a
beneficial effect in reducing the cisplatin- induced organ toxicity
[15]. It is possible that, the extremely lipophilic nature of carnitine
may be responsible for the decrease in EGFbinding [16]. Carnitine may
insert in the cell membrane and/or interact with one of the many
cellular enzymes having lipid substrates or cofactors. In addition,
carnitine may interact directly with the EGFR [17].<br />
Experimental evidence is available showing that ROS may induce the
light and independent phosphorylation of the EGFR activating Her-2/neu.
Moreover, the expression of the receptor is induced in conditions of
oxidative stress [18]. L-carnitine, via its free radical scavenging and
antioxidant properties, may inhibit ROS-mediated EGFR phosphorylation.
It has been found that palmitoyl-carnitine can inhibit the activity of
heart and brain protein kinase C in a competitive manner and subsequent
phosphorylation of the EGFR [19]. Although the tumor markers and IGF-1
showed no significant difference in TAM-treated patients before and
after administration of L-CAR, there was a tendency to decline after
L-CAR supplementation [13]. The results of the above studies became a
prerequisite for conducting clinical studies aimed at establishing the
role of L-carnitine in the treatment of breast cancer.<br />
To date, the search in the online clinical research registration
system ClinicalTrials.gov using key words L-carnitine + breast cancer
has revealed several studies evaluating the efficacy and safety of
L-carnitine in the treatment of breast cancer patients. Analyzing the
obtained results, we can conclude that L-carnitine was the drug of
choice for neuropathies, as a consequence of chemotherapy, in patients
with breast cancer.
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<br />Conclusion</h2>
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L-carnitine is widely used in clinical practice. However, recently
this medicine causes growing interest among oncologists. In a number of
studies, L-carnitine has proven itself as a medicine that capable,
during the preoperative systemic antitumor therapy, to increase its
effectiveness compared with standard neoadjuvant systemic antitumor
therapy. And also, taking L-carnitine with neoadjuvant systemic
antitumor therapy helps to increase the number of cases of complete
morphological regression (V degree of therapeutic pathomorphosis). To
date, there are several clinical studies that are researching using
L-carnitine in various malignant tumors, the results of which are the
basis for further in-depth study of the effect of the medicine in the
treatment of malignant neoplasms.<br />
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Lupine Publishers Cancer Journalhttp://www.blogger.com/profile/09600300951943945390noreply@blogger.com0tag:blogger.com,1999:blog-2412377267890319944.post-9963643435689915292020-02-06T05:15:00.000-08:002020-02-06T05:15:13.608-08:00Lupine Publishers | Somatic Mutations in Cancer-Free Individuals: A Liquid Biopsy Connection <div dir="ltr" style="text-align: left;" trbidi="on">
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<b>Lupine Publishers | Open Access Journal of Oncology and Medicine</b></div>
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<h2 style="text-align: left;">
Abstract</h2>
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Somatic mutations have been perceived as the causal event in the
origin of the vast majority of cancers. Advanced massively parallel,
highthroughput
DNA sequencing have enabled the comprehensive characterization of
somatic mutations in a large number of tumor samples for
precision and personalized therapy. Understanding how these observed
genetic alterations give rise to specific cancer phenotypes represents
an ultimate goal of cancer genomics. However, somatic mutations are also
commonly found in healthy individuals, which interfere with the
effectiveness for cancer diagnostics.<br />
<b>Keywords:</b> Somatic mutation; Germline; Cell-free DNA; Liquid biopsy; Next-generation sequencing<br />
<b>Abbreviations:</b> NGS: Next-Generation Sequencing ; cfDNA: Cell-free DNA; MAF: Mutant Allele Frequency</div>
<h2 style="text-align: left;">
Introduction</h2>
<div style="text-align: left;">
<b>Mutations in healthy individuals are not all germline</b><br />
Over the course of our lifetime, there are many millions of cell
divisions in the body. By chance alone, mutations will definitely
occur. Indeed, spontaneous somatic mutations constantly occur
in individual cells. These background mutations arise either from
replication errors or from DNA damage that is repaired incorrectly
or left unrepaired, and have been detected in healthy tissues,
including blood, skin, liver, colon, and small intestine [1-3]. Deepsequencing
studies in normal tissues also surprisingly identified
cancer-driving mutations, e.g., in blood, driver mutations can be
detected in ~10%of individuals older than 65 years of age and
resemble patterns seen in leukemia patients. Individuals carrying
these driver mutations have an elevated future risk of blood
cancers [4-6], suggesting that these are genuine precancerous
clones. Further, a detailed analysis of 31,717 cancer cases and
26,136 cancer-free controls from 13 genome-wide association
studies revealed that the majority, if not all, of aberrations that
were observed in the cancer-associated cohort were also seen in
cancer-free subjects, albeit at lower frequency [7,8].<br />
Somatic mutations in healthy individuals are very prevalent,
with an average mutation number of around 2–6 mutations/1 M
bases [9,10]. The baseline somatic mutation spectrum in healthy
population not only can help fill the gaps for the establishing early
cancer diagnosis strategies, but also argues against the idea of using
normal cells as germline control to make somatic mutation calls in
sequencing tests. Moreover, the same driver mutation could exist
in both tumor and normal cells yet with distinct biological effects,
we should not simply define the threshold of mutation detection by
removing the background mutations found in a healthy population.
Taken together, we need to incorporate and carefully calibrate the
background somatic mutations in healthy individuals; the fact is
they are not all germline mutations.<br />
<b>Somatic driver mutations found in healthy population
by liquid biopsy</b><br />
With the dramatically decreased cost of next-generation
sequencing (NGS) in recent years, it is now practical to screen a
large number of individuals at ultra-deep sequencing depths to
identify cancer-related mutations. Cell-free DNA (cfDNA) in the
blood circulation of cancer patients (as liquid biopsy) have emerged
as key biomarkers for cancer monitoring and treatment decisionmaking
[11]. Both academic research groups and industry players
are chasing the pan-cancer screening by a simple blood draw.
However, the reliable and accurate application of cfDNA detection
requires better understanding of background somatic information
in healthy individuals.<br />
We performed ultra-deep target sequencing on 50 cancerassociated
genes for plasma cfDNA from a cohort of 129 apparently healthy cancer-free subjects. To increase the confidence of the
called mutations, we here defined the mutation as the variant allele
frequency greater than 1% and the average depth more than 5,000 xs
for demonstration. Our data revealed an age-independent mutation
spectrum with average 3.12 somatic mutations per subject (Figure
1). The most frequently mutated genes are TP53 (42%), KIT (6%),
KDR (5.5%), PIK3CA (5.5%), EGFR (5%) and PTEN (3.7%). These
results highlighted the prevalence of some cancer-associated driver
mutations in healthy individuals as background mutations. We also
demonstrated the concordance between our results and a recent
study for revealing the real somatic mutation in healthy population.<br />
<b>Figure 1:</b> Distribution plots of somatic mutation detected in a cohort of 129 healthy subjects.<br />
The study by Xia et al. [12] examined the background somatic
mutations in white blood cells and cfDNA in healthy controls based
on sequencing data from 821 non-cancer individuals with the aim of
understanding the baseline profile of somatic mutations detected in
cfDNA. The data comparison was summarized in Figure 2. Although
there are differences in study cohort composition, sample volume,
extraction methodology and analytical platform, the end results are
remarkably similar, i.e., average 3 mutations per subject with an
almost identical list of frequently mutated genes. Although varying
mutation spectra in cancers have often been attributed to cancerspecific
processes, our data suggest that at least a subset of these
mutations actually reflect normal tissue-specific processes. This
concept is consistent with the idea that a substantial fraction of the
mutations found in cancers occur in normal stem cells [13,14].<br />
<b>Figure 2:</b> Comparison of somatic mutation detection in healthy population from two studies.<br />
<b>Normal tissue as a germline control not justified</b><br />
There is evidence for the presence of tumor-derived cfDNA in
early cancers [15]. However, the real fraction of cfDNA that shed by
tumor rather than the background somatic mutations is not well
illustrated. For clinical application, the low level of tumor mutation
as well as the heterogeneity of background mutation present in
the circulation needs to be clearly addressed and differentiated
to achieve accuracy. Unfortunately, this goal can’t be achieved by
pushing detection limit of current advanced technology to below
0.01% mutant allele frequency (MAF). Contrarily, the higher
sensitivity will guarantee higher chance to pick up background somatic
mutations. Also, the clinical relevance of those lowpercentage
tumor mutations is still debatable in terms of treatment
decision or regimen change. Each human individual is unique.
Every cancer patient is different. No two tumors are the same
even resides within the same patient; to distinguish the definitive
cancer-specific mutations from background signals observable
in plasma is extremely daunting. Evaluation of specificity in
plasma cfDNA profiles from large numbers of healthy individuals
as representative controls for the cancer population seems farfetched
with uncertainty, especially when standardized protocol
and optimized technology are still lacking.<br />
Unlike tissue genomic DNA, circulating cfDNA is so diluted
and dynamic with a relatively short half-life, making single-point
measurement not suitable for clinical application. We reason that
cfDNA in circulation is truly under a continuous selection pressure
to select for highly aggressive/proliferative clones, as disease
progressing the low-abundant tumor clones will either evolve and
dominate or vanish by the immune clean-up processes, therefore
longitudinal clinical follow-up should be performed to identify
the best time and target for precision therapy, meanwhile to filter
out contaminating background mutations. To achieve high clinical
specificity, a cfDNA-based test must be capable of distinguishing
between the background signals originating from non-cancer or
pre-cancerous processes and the invasive malignancy of clinical
interest. It is still possible that mutational signatures in cfDNA
could distinguish basic biological processes from malignant and
pathological processes.<br />
<b>Figure 3:</b> A representative mutational trending curve after filtering out background mutations.<br />
Here we propose a combined approach based on the tumor
evolutional principle of “survival and domination of the fittest”
in circulation that is to perform multiple time-point monitoring,
filter out potential background mutations (e.g., <1% MAF), reduce
sample input volume and interrogate multiple databases. A
representative mutational trending curve following our approaches
was shown (Figure 3). Our findings underscore the importance of
an assessment of the landscape of somatic mutations in cancerfree
population, and associated mutation signatures. Somatic
mutations and mosaicism in healthy individuals have implications
not only for early detection, diagnosis and treatment of cancer
using liquid biopsy but also emerging technologies in healthcare.
We recommend caution while extending the mutation conclusions
to cancer patients by employing matched normal tissue as germline
control. To increase sample input and push liquid biopsy sensitivity
toward <1% may not serve the interest of detecting low-frequency
mutant allele, but only to increase the chance of background
mutation contamination. Application of artificial intelligence,
machine-learning on big database to create an algorithm for highrisk
population screening of cancer is a good idea for preventive
medicine, yet the outcome is uncertain given the uniqueness of
every patient, each tumor - one size can’t fit all.<br />
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Read More Lupine Publishers Oncology and medicine Articles : <a href="https://lupine-publishers-cancer-journal.blogspot.com/">https://lupine-publishers-cancer-journal.blogspot.com/</a><br />
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Lupine Publishers Cancer Journalhttp://www.blogger.com/profile/09600300951943945390noreply@blogger.com0tag:blogger.com,1999:blog-2412377267890319944.post-51036425047964746422020-01-23T05:34:00.003-08:002020-01-23T05:34:48.532-08:00Lupine Publishers| Immunotherapy in Some Types of Tumors<div dir="ltr" style="text-align: left;" trbidi="on">
<b>Lupine Publishers| Open Access Journal of Oncology and Medicine</b><br />
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<h2 style="margin-top: -90px; padding-top: 90px;">
<a href="https://www.blogger.com/null" id="Charasteristics">Charasteristics</a></h2>
<br />
a) Immunotherapy exerts its antitumor action by stimulating
the response immune response of patients to cancer, unlike
classic treatments, which directly attack the tumor<br />
b) Previously immunotherapy was limited to patients in
whom the conventional treatment, usually with chemotherapy,
but currently in patients with some types of tumors, such as
melanoma or some lung cancers, is already considered the
treatment of first choice<br />
c) Immunotherapy is able to control some types of malignant
tumors prognosis very long, even for several years<br />
d) Immunotherapy exerts its antitumor action by stimulating
the immune response of patients against cancer, unlike classic
treatments, which attack directly to the tumor. This implies a
series of advantages and characteristics of this novelty strategy.<br />
e) Its main advantage is its ability to control the tumor for very
long periods of time in a certain percentage of patients, which
varies according to the type of cancer. In some patients with
tumors that were previously considered incurable, at this time
they are getting very long survivals, even years.<br />
f) Currently, immunotherapy with antibodies that block PD-1
receptors or action on these PD-L1 protein receptors has
shown efficacy against a large number of tumors, including
among others melanoma, cancers of the lung, kidney, bladder,
these treatments are usually administered intravenously and
their toxicity is usually lower than conventional treatments,
such as chemotherapy<br />
g) However, between a 5-15% of patients can develop
relevant toxicities, which are usually due to the activation of
the immune system against the patient’s own organism. The
organs most frequently affected by these reactions are: the
lung (“pneumonitis”), which manifests in the form of cough and
shortness of breath; and the digestive tract (“colitis”), which
presents as diarrhea. When they are used as unique drugs,<br />
which is the most usual Now a days, toxicity is not usually a
major problem. However, when they use in combination,
their frequency and severity is greater. New immunotherapy
strategies Despite these results, there is still a long way to go,
given that today Only 40-60% of melanoma patients benefit
from these treatments between 10 and 30% of patients with
other types of tumors.<br />
Some of the main ones Developing strategies to improve the
effectiveness of immunotherapy are:<br />
<br />
<b>a) Combination Immunotherapy:</b> During the development
of a tumor it is they can alter several phases of the immune
response. Therefore, the use simultaneous treatment of two
or more immunotherapy treatments is one of the strategies
more used to increase antitumor efficacy. The combinations of
immunotherapy have shown significant activity in patients with
melanoma and renal cancer. The main mechanisms of action
of drugs which are used for these combinations are: directly
activate the answer immunological; unlock the inhibition of
the immune response produced by many tumors; or provide
fundamental elements to trigger the immune response, as
antigens or cells of the immune system New vaccines: antitumor
vaccines consist of administering patient tumor antigens
(small fragments of it, usually proteins), for the immune
system to recognize them and thus put in place the antitumor
immune response. Modern molecular biology techniques
have allowed to advance a lot in the processes of selection of
antigens with greater possibilities of triggering these responses
and, therefore, this is one of the most hopeful ways for the
development of new treatments of immunotherapy. Currently
there is an anti-cancer vaccine against cancer prostate whose
use in patients is approved in the USA. (Sipuleucel). In addition,
some vaccines against infectious diseases can confer a high
degree of protection against tumors associated with them
(for example: human papilloma virus, associated with cervical
cancer, or hepatitis B virus, associated with hepatocarcinoma).Vaccination against these viral infections dramatically reduces
the incidence of associated tumors.<br />
<br />
<b>b) CAR-T Cells (Chimeric Antigen Receptor, or Antigenic
Receptor Chimeric):</b> It consists of extracting the patient’s
immune cells; process them in the laboratory to express an
antigen that specifically recognizes to tumor cells; and readminister
them to the patient, to attack the tumor. This
strategy is having considerable efficacy in patients with some
types of leukemia, although its use in patients with solid tumors
It seems more complicated. In addition, it is associated with
relevant toxicities, although the Most can be controlled with
specialized medical care. As we have already seen, the small
advances, taken together, are relevant. From here our motto
from SEOM: In Oncology, each advance is written in capital
letters. These small advances, considered each of them in
isolation, could have have been considered of little relevance,
but accumulated among themselves have led to change in many
cases in a remarkable way the prognosis and the quality of life
of many patients. In oncology, each advance is written with
capital letters (madrid, february 19, 2018).<br />
<br />
<b>c) CAR-T cells (Chimeric Antigen Receptor, or Antigen
Receptorchimeric):</b> it consists of extracting the patient’s
immune cells; process them in the laboratory to express an
antigen that specifically recognizes to tumor cells; and readminister
them to the patient, to attack the tumor. This
strategy is having considerable efficacy in patients with some
types of leukemia, although its use in patients with solid
tumors. It seems more complicated.<br />
<br />
Read More <a href="https://lupine-publishers-cancer-journal.blogspot.com/">Lupine Publishers Oncology and medicine</a> Articles : <a href="https://lupine-publishers-cancer-journal.blogspot.com/">https://lupine-publishers-cancer-journal.blogspot.com/</a><br />
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