Manuela Malsy, Veronika Hofer, Stephan Schmidbauer, Bernhard Graf, Anika Bundscherer
Introduction: Pancreatic ductal adenocarcinoma is one of the most aggressive malignancies in humans. The main reason for its unfavourable prognosis is the combination of rapid tumour growth, early-onset metastasis and currently still inadequate diagnostic and therapeutic options. Thus, only very few patients are eligible for radical resection of the primary tumour as the only curative treatment option available so far. In the perioperative period, tumour progression and metastasis are facilitated by the activation of key signalling pathways and the altered regulation of transcription factors. Various tumour entities have shown increased expression of the integrin-3 receptor subunit, which correlates with more rapid tumour progression and metastasis through advanced migration, invasion and proliferation. The influence of perioperative medication and postoperative pain management remains unclear. To investigate the effects of ketamine, s-ketamine and MK 801 on integrin beta-3-mediated cell migration in pancreatic cancer cells in vitro.
Methods: The effects of ketamine, s-ketamine and MK 801 on integrin beta-3 expression were investigated with immunoblot. Cell migratory potentials were analysed using a Cell Migration Assay Kit with a Boyden chamber, in which cells migrate through a semipermeable membrane under different stimuli.
Results: Stimulation with ketamine and MK 801 significantly promoted migration in pancreatic cancer cells, increasing the expression of integrin beta-3.
Conclusion: Novel therapeutic approaches target the effective modulation of specific signalling and transcription pathways. The prerequisite for such 'target therapies' is comprehensive knowledge about the respective carcinogenesis. Further studies are required to identify the underlying disease mechanisms of pancreatic carcinoma.
{"title":"Effects of Ketamine, S-Ketamine and MK 801 on Integrin Beta-3-mediated Cell Migration in Pancreatic Carcinoma.","authors":"Manuela Malsy, Veronika Hofer, Stephan Schmidbauer, Bernhard Graf, Anika Bundscherer","doi":"10.26502/jcsct.5079183","DOIUrl":"https://doi.org/10.26502/jcsct.5079183","url":null,"abstract":"<p><strong>Introduction: </strong>Pancreatic ductal adenocarcinoma is one of the most aggressive malignancies in humans. The main reason for its unfavourable prognosis is the combination of rapid tumour growth, early-onset metastasis and currently still inadequate diagnostic and therapeutic options. Thus, only very few patients are eligible for radical resection of the primary tumour as the only curative treatment option available so far. In the perioperative period, tumour progression and metastasis are facilitated by the activation of key signalling pathways and the altered regulation of transcription factors. Various tumour entities have shown increased expression of the integrin-3 receptor subunit, which correlates with more rapid tumour progression and metastasis through advanced migration, invasion and proliferation. The influence of perioperative medication and postoperative pain management remains unclear. To investigate the effects of ketamine, s-ketamine and MK 801 on integrin beta-3-mediated cell migration in pancreatic cancer cells <i>in vitro</i>.</p><p><strong>Methods: </strong>The effects of ketamine, s-ketamine and MK 801 on integrin beta-3 expression were investigated with immunoblot. Cell migratory potentials were analysed using a Cell Migration Assay Kit with a Boyden chamber, in which cells migrate through a semipermeable membrane under different stimuli.</p><p><strong>Results: </strong>Stimulation with ketamine and MK 801 significantly promoted migration in pancreatic cancer cells, increasing the expression of integrin beta-3.</p><p><strong>Conclusion: </strong>Novel therapeutic approaches target the effective modulation of specific signalling and transcription pathways. The prerequisite for such 'target therapies' is comprehensive knowledge about the respective carcinogenesis. Further studies are required to identify the underlying disease mechanisms of pancreatic carcinoma.</p>","PeriodicalId":73634,"journal":{"name":"Journal of cancer science and clinical therapeutics","volume":"6 4","pages":"446-451"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9910313/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10707593","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Tyrus Omondi Swaya, D. Opondo, David O. Atandi, Benard Guyah, Ng’wena Gideon Magak
Background: Prostein is a newly reported prostate cancer biomarker. Nonetheless, no reports on African population are available. The current study aimed to determine the prostein expression in archived prostatic core biopsies in Western Kenya. Methods: This was a retrospective study conducted on malignant and benign prostatic tissue core biopsies of 106 patients from Jaramogi Oginga Odinga Teaching and Referral Hospital and division of urology at Synergy Clinics, Kisumu between January 2018 to May 2021. Manual Immunohistochemical technique was performed on each of the 106 samples and on the following non-prostatic male control biopsies; Testis, Penis, Liver and Esophagus. Cellular location of prostein staining was evaluated microscopically and classified as cytoplasmic or nucleocytoplasmic. Intensity of prostein expression was assessed and graded according the immunohistochemistry composite score. Results: The mean (SE) age was 72.00 ± 0.93 years. 97.2% of malignant and all the benign prostate tissue stained positive for prostein whereas the four non-prostatic male tissues were negative. Staining intensities were weak (24.5%), Moderate (17.0%), strong (55.7%) and non-stained (2.8%). The staining was highly immunolocalized within the cytoplasm (95.1% cases) as compared to nucleocytoplasmic (2.0% cases). The mean immunoreactivity composite score was 1.91 ± 0.96 (0.0-3.14). Strongly stained sections of both acinar and intraductal adenocarcinoma had a staining pattern clustered within the cytoplasm in a perinuclear location whereas the weakly stained sections had less coarse brown cytoplasmic granular appearing. Conclusion: Prostein is expressed in both acinar and intraductal adenocarcinoma and can be routinely used in differential diagnosis of prostate cancer even in remote settings.
{"title":"Immunohistochemical Analysis of Prostein in Needle Core Biopsies of Acinar and Intraductal Prostatic Adenocarcinoma in Western Kenya Population","authors":"Tyrus Omondi Swaya, D. Opondo, David O. Atandi, Benard Guyah, Ng’wena Gideon Magak","doi":"10.26502/jcsct.5079164","DOIUrl":"https://doi.org/10.26502/jcsct.5079164","url":null,"abstract":"Background: Prostein is a newly reported prostate cancer biomarker. Nonetheless, no reports on African population are available. The current study aimed to determine the prostein expression in archived prostatic core biopsies in Western Kenya. Methods: This was a retrospective study conducted on malignant and benign prostatic tissue core biopsies of 106 patients from Jaramogi Oginga Odinga Teaching and Referral Hospital and division of urology at Synergy Clinics, Kisumu between January 2018 to May 2021. Manual Immunohistochemical technique was performed on each of the 106 samples and on the following non-prostatic male control biopsies; Testis, Penis, Liver and Esophagus. Cellular location of prostein staining was evaluated microscopically and classified as cytoplasmic or nucleocytoplasmic. Intensity of prostein expression was assessed and graded according the immunohistochemistry composite score. Results: The mean (SE) age was 72.00 ± 0.93 years. 97.2% of malignant and all the benign prostate tissue stained positive for prostein whereas the four non-prostatic male tissues were negative. Staining intensities were weak (24.5%), Moderate (17.0%), strong (55.7%) and non-stained (2.8%). The staining was highly immunolocalized within the cytoplasm (95.1% cases) as compared to nucleocytoplasmic (2.0% cases). The mean immunoreactivity composite score was 1.91 ± 0.96 (0.0-3.14). Strongly stained sections of both acinar and intraductal adenocarcinoma had a staining pattern clustered within the cytoplasm in a perinuclear location whereas the weakly stained sections had less coarse brown cytoplasmic granular appearing. Conclusion: Prostein is expressed in both acinar and intraductal adenocarcinoma and can be routinely used in differential diagnosis of prostate cancer even in remote settings.","PeriodicalId":73634,"journal":{"name":"Journal of cancer science and clinical therapeutics","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69347874","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Clinical Characteristics and Prognostic Values of PIK3CA Mutation in Colorectal Patients. Clinical Therapeutics (2022): Abstract Objective: This study aimed to investigate the role of PIK3CA mutation in the prognosis of Colorectal Cancer (CRC). Methods: The clinical data of 386 CRC patients who underwent next-generation sequencing (NGS) test in the First Affiliated Hospital of Zhengzhou University from January 2017 to December 2020 were retrospectively reviewed. The associations between PIK3CA mutation and clinicopathologic characteristics of CRC patients were analyzed by chi-square test and Fisher’s exact test. Kaplan-Meier curves and Cox models were conducted to assess possible prognostic values of PIK3CA mutation. Results: PIK3CA mutation was found in 88 (22.8%) of the 386 CRC patients. The percentage of MSI-H in PIK3CA mutated patients were higher than that in PIK3CA wild-type patients (P < 0.0001). The Median Overall Survival (mOS) of patients with PIK3CA mutation was significantly higher than that of wild-type patients (P = 0.0112). The progression free survival (PFS) of the mutated patients was also significantly prolonged compared with that of the wild type (P = 0.0132). Results of multivariate analysis showed that PIK3CA wild-type was independent risk factor for the survival of CRC patients. Conclusion: PIK3CA mutation had an important impact on the clinic pathologic features and the prognosis for CRC patients. The survival of PIK3CA mutated patients was significantly prolonged, which needs further studies of large sample size, and long follow-up period to provide robust evidence.
{"title":"Clinical Characteristics and Prognostic Values of PIK3CA Mutation in Colorectal Cancer Patients","authors":"Jinming Han, Jianxiang Shi, Miao Jiang, Ruowen Zhang, Shuiling Jin, Yongliang Jia, H. Zong","doi":"10.26502/jcsct.5079149","DOIUrl":"https://doi.org/10.26502/jcsct.5079149","url":null,"abstract":"Clinical Characteristics and Prognostic Values of PIK3CA Mutation in Colorectal Patients. Clinical Therapeutics (2022): Abstract Objective: This study aimed to investigate the role of PIK3CA mutation in the prognosis of Colorectal Cancer (CRC). Methods: The clinical data of 386 CRC patients who underwent next-generation sequencing (NGS) test in the First Affiliated Hospital of Zhengzhou University from January 2017 to December 2020 were retrospectively reviewed. The associations between PIK3CA mutation and clinicopathologic characteristics of CRC patients were analyzed by chi-square test and Fisher’s exact test. Kaplan-Meier curves and Cox models were conducted to assess possible prognostic values of PIK3CA mutation. Results: PIK3CA mutation was found in 88 (22.8%) of the 386 CRC patients. The percentage of MSI-H in PIK3CA mutated patients were higher than that in PIK3CA wild-type patients (P < 0.0001). The Median Overall Survival (mOS) of patients with PIK3CA mutation was significantly higher than that of wild-type patients (P = 0.0112). The progression free survival (PFS) of the mutated patients was also significantly prolonged compared with that of the wild type (P = 0.0132). Results of multivariate analysis showed that PIK3CA wild-type was independent risk factor for the survival of CRC patients. Conclusion: PIK3CA mutation had an important impact on the clinic pathologic features and the prognosis for CRC patients. The survival of PIK3CA mutated patients was significantly prolonged, which needs further studies of large sample size, and long follow-up period to provide robust evidence.","PeriodicalId":73634,"journal":{"name":"Journal of cancer science and clinical therapeutics","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69348268","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Manami Tanaka, Tomoo Tanaka, Xiaolong Zhu, Fei Teng, Hong Lin, Zhu-Quan Luo, Ying Pan, S. Sadahiro, Toshiyuki Suzuki, Y. Maeda, Ding Wei, Zheng Lu
Manami Tanaka ( tubu0125@gmail.com ) Bradeion Institute of Medical Sciences, Co., Ltd. Tomoo Tanaka Bradeion Institute of Medical Sciences, Co., Ltd. Xiaolong Zhu Beijing Genomics Institute Teng Fei Hong Lin BGI-Shenzhen Zhu Luo BGI-Japan Ying Pan BGI-Shenzhen Sotaro Sadahiro Tokai University School of Medicine Toshiyuki Suzuki Oiso Hospital attached to Tokai University School of Medicine Yuji Maeda Kanagawa National Hospital Ding Wei Japan Kampo NewMedicine, Co., Ltd. Zhengxin Lu QiDong Gaitianli Medicines Co. Ltd.
{"title":"Hair Growth and Restoration by Transcriptional Control of Tissue Regeneration in Cancer Recovery Process by Huaier","authors":"Manami Tanaka, Tomoo Tanaka, Xiaolong Zhu, Fei Teng, Hong Lin, Zhu-Quan Luo, Ying Pan, S. Sadahiro, Toshiyuki Suzuki, Y. Maeda, Ding Wei, Zheng Lu","doi":"10.26502/jcsct.5079167","DOIUrl":"https://doi.org/10.26502/jcsct.5079167","url":null,"abstract":"Manami Tanaka ( tubu0125@gmail.com ) Bradeion Institute of Medical Sciences, Co., Ltd. Tomoo Tanaka Bradeion Institute of Medical Sciences, Co., Ltd. Xiaolong Zhu Beijing Genomics Institute Teng Fei Hong Lin BGI-Shenzhen Zhu Luo BGI-Japan Ying Pan BGI-Shenzhen Sotaro Sadahiro Tokai University School of Medicine Toshiyuki Suzuki Oiso Hospital attached to Tokai University School of Medicine Yuji Maeda Kanagawa National Hospital Ding Wei Japan Kampo NewMedicine, Co., Ltd. Zhengxin Lu QiDong Gaitianli Medicines Co. Ltd.","PeriodicalId":73634,"journal":{"name":"Journal of cancer science and clinical therapeutics","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69348719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M. Giani, K. Tavella, Irene Renda, Enrico Tartarotti, J. Nori, E. Vanzi, S. Bianchi, T. Susini
Purpose : We evaluated the efficacy of neoadjuvant chemotherapy in reducing locally advanced and early breast cancers size, improving breast-conserving surgery rates and its long-term outcomes. Our first aim was to test whether patients achieving a partial pathological response of good quality after neoadjuvant chemotherapy (tumor shrinkage >50% from the original clinical-instrumental size to the size evaluated by the pathologist on the surgical specimen) had better disease-free and overall survival rates than those with a tumor size reduction <50%. Patients and Methods : We analyzed 64 patients initially candidate to mastectomy, treated with neoadjuvant chemotherapy and subsequent surgery at our institution. Results : We observed tumor size reduction in 95% of the cases resulting in downstaging in 67.2% of the patients. Women with tumor size reduction >50% after NACT had better 10-years disease-free survival and overall survival rates than women with reduction <50% (p=0.002 and p<0.05, respectively). In a multivariate analysis, tumor size reduction >50% (HR=4.29, p=0.004) was an independent predictor of disease-free survival, whereas significance was not reached concerning overall survival. Treatment with neoadjuvant chemotherapy allowed to half the rate of mastectomy, as breast-conserving surgery was used in 50% of the cases. Overall, we had recurrences in 37.5% patients. We found no significant increase in local or distant recurrences after breast conserving surgery, as compared with mastectomy. Conclusions : Our data suggest that a tumor size reduction >50% after neoadjuvant chemotherapy may represent a prognostic factor for low risk of recurrence. The use of breast-conserving surgery was not associated with significantly higher risk of local relapse.
{"title":"Prognostic Role of Tumor Size Reduction >50% after Neoadjuvant Chemotherapy for Breast Cancer","authors":"M. Giani, K. Tavella, Irene Renda, Enrico Tartarotti, J. Nori, E. Vanzi, S. Bianchi, T. Susini","doi":"10.26502/jcsct.5079174","DOIUrl":"https://doi.org/10.26502/jcsct.5079174","url":null,"abstract":"Purpose : We evaluated the efficacy of neoadjuvant chemotherapy in reducing locally advanced and early breast cancers size, improving breast-conserving surgery rates and its long-term outcomes. Our first aim was to test whether patients achieving a partial pathological response of good quality after neoadjuvant chemotherapy (tumor shrinkage >50% from the original clinical-instrumental size to the size evaluated by the pathologist on the surgical specimen) had better disease-free and overall survival rates than those with a tumor size reduction <50%. Patients and Methods : We analyzed 64 patients initially candidate to mastectomy, treated with neoadjuvant chemotherapy and subsequent surgery at our institution. Results : We observed tumor size reduction in 95% of the cases resulting in downstaging in 67.2% of the patients. Women with tumor size reduction >50% after NACT had better 10-years disease-free survival and overall survival rates than women with reduction <50% (p=0.002 and p<0.05, respectively). In a multivariate analysis, tumor size reduction >50% (HR=4.29, p=0.004) was an independent predictor of disease-free survival, whereas significance was not reached concerning overall survival. Treatment with neoadjuvant chemotherapy allowed to half the rate of mastectomy, as breast-conserving surgery was used in 50% of the cases. Overall, we had recurrences in 37.5% patients. We found no significant increase in local or distant recurrences after breast conserving surgery, as compared with mastectomy. Conclusions : Our data suggest that a tumor size reduction >50% after neoadjuvant chemotherapy may represent a prognostic factor for low risk of recurrence. The use of breast-conserving surgery was not associated with significantly higher risk of local relapse.","PeriodicalId":73634,"journal":{"name":"Journal of cancer science and clinical therapeutics","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69348790","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mixed-phenotype acute leukemia (MPAL) is rare subtype of leukemia characterized by blasts with both acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML) markers. MPAL is a high-risk disease which represents only 2%–3% of acute leukemias and involves a genetically and immunophenotypically diverse group of patients with poor clinical outcomes. The limited incidence and lack of prospective data on therapeutic outcomes poses uncertainty about the best approach for patients with MPAL. The modest evidence on therapeutic decisions is based on uncontrolled studies and retrospective data suggesting higher remission rates with an ALL-like induction approach than with an AML-like regimen followed by allogeneic stem cell transplant during the complete remission. Advances in understanding the genetic landscape of MPAL demonstrates that most cases are associated with somatic mutations in tumor suppressors, transcription factors, and epigenetic regulators. Recent studies showed that MPALs derive from multipotent primitive cells with considerable genetic diversity, which may promote treatment with targeted therapy. Prospective studies should be prioritized to provide answers about this innately heterogeneous disease.
{"title":"Inside the Biology of Acute Leukemias of Ambiguous Lineage: Diagnostic Work-Up, Genomic and Clinical Characterization","authors":"Binsah S George, Anneliese Gonzalez, A. Rios","doi":"10.26502/jcsct.5079165","DOIUrl":"https://doi.org/10.26502/jcsct.5079165","url":null,"abstract":"Mixed-phenotype acute leukemia (MPAL) is rare subtype of leukemia characterized by blasts with both acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML) markers. MPAL is a high-risk disease which represents only 2%–3% of acute leukemias and involves a genetically and immunophenotypically diverse group of patients with poor clinical outcomes. The limited incidence and lack of prospective data on therapeutic outcomes poses uncertainty about the best approach for patients with MPAL. The modest evidence on therapeutic decisions is based on uncontrolled studies and retrospective data suggesting higher remission rates with an ALL-like induction approach than with an AML-like regimen followed by allogeneic stem cell transplant during the complete remission. Advances in understanding the genetic landscape of MPAL demonstrates that most cases are associated with somatic mutations in tumor suppressors, transcription factors, and epigenetic regulators. Recent studies showed that MPALs derive from multipotent primitive cells with considerable genetic diversity, which may promote treatment with targeted therapy. Prospective studies should be prioritized to provide answers about this innately heterogeneous disease.","PeriodicalId":73634,"journal":{"name":"Journal of cancer science and clinical therapeutics","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69348655","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Angiosarcoma is a rare form of sarcoma that is rarely associated with paraneoplastic syndromes. Its association with increased Erythropoietin (EPO) secretion has only been reported in one case. We report the case of a 73-year-old female patient presenting with a mass on the parotid gland, which was identified to be an angiosarcoma, demonstrated through biopsy and Positron Emission Tomography (PET) scan. The laboratory studies demonstrated elevated hemoglobin and hematocrit levels, with a markedly increased serum erythropoietin level. The workup for primary polycythemia was negative. The patient was treated with immediate phlebotomy on 3 occasions and then started paclitaxel, initially alone and then erythropoietin levels normalized. The repeat PET scan after the third cycle of paclitaxel showed a mixed response with improved size of the mass but increased intensity probably a reflection of the inflammatory response from chemotherapy. These findings suggest that the patient's polycythemia was secondary to increased erythropoietin secretion from her angiosarcoma
{"title":"Erythrocytosis As A Paraneoplastic Syndrome in A Case of Angiosarcoma","authors":"Caroline Hana, G. Hanna, A. Hussein","doi":"10.26502/jcsct.5079160","DOIUrl":"https://doi.org/10.26502/jcsct.5079160","url":null,"abstract":"Angiosarcoma is a rare form of sarcoma that is rarely associated with paraneoplastic syndromes. Its association with increased Erythropoietin (EPO) secretion has only been reported in one case. We report the case of a 73-year-old female patient presenting with a mass on the parotid gland, which was identified to be an angiosarcoma, demonstrated through biopsy and Positron Emission Tomography (PET) scan. The laboratory studies demonstrated elevated hemoglobin and hematocrit levels, with a markedly increased serum erythropoietin level. The workup for primary polycythemia was negative. The patient was treated with immediate phlebotomy on 3 occasions and then started paclitaxel, initially alone and then erythropoietin levels normalized. The repeat PET scan after the third cycle of paclitaxel showed a mixed response with improved size of the mass but increased intensity probably a reflection of the inflammatory response from chemotherapy. These findings suggest that the patient's polycythemia was secondary to increased erythropoietin secretion from her angiosarcoma","PeriodicalId":73634,"journal":{"name":"Journal of cancer science and clinical therapeutics","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69348323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ludovic Plaisance, Céline Chapelle, Silvy Laporte, Benjamin Planquette, Laurent Bertoletti, Nicolas Falvo, Francis Couturaud, Lionel Falchero, Isild Mahé, Hélène Helfer, Sadji Dennaoui, Guy Meyer, Isabelle Mahé
Background and objectives: Few data are available about anticoagulation management beyond 6 months in patients with cancer associated thrombosis (CAT). Our objective was to describe anticoagulant treatment modalities up to 12 months.
Methods: The management of the anticoagulant treatment beyond 6 months was described in this initially retrospective non-interventional French multicenter study in patients treated with low-molecular-weight heparins (LMWH) still alive at the end of an initial 6-month treatment period. Clinical outcomes, including venous thromboembolism, recurrence, bleeding and deaths have been published previously.
Results: Among the 432 patients (mean age 66.5±12.7 years) included in the study, 332 were followed up to 12 months while 96 patients deceased before study end and 4 patients were lost-to-follow-up. At 6 months, anticoagulant therapy was stopped in 74 patients, 56 were switched to vitamin K antagonists (VKA) (16.1% [95%CI, 12.4%-20.4]), 30 to direct oral anticoagulants (DOAC) (8.6% [95%CI, 5.9%-12.1]). LMWHs were maintained in 256 patients (73.6% [95%CI, 68.6-78.1]). During the follow-up, LMWHs were definitively discontinued in 86 patients (33.7%), the main reason being a favorable course of the cancer (16 patients, 18.6%), or the thromboembolic disease (11 patients, 12.8%), whereas concern about bleeding risk was low (2 patients, 2.3%).
Conclusion: Anticoagulation beyond 6 months and up to 12 months was in accordance with clinical practice guidelines suggesting that treatment should be continued as long cancer is active or in the absence of bleeding risk. Anticoagulant treatment discontinuation beyond 6 months was influenced by the favorable courses of both malignancy and thromboembolic disease, as well as patient's preference.
{"title":"Reasons Influencing Long-Term Anticoagulant Treatment Beyond 6 Months for Cancer-Associated Thrombosis in USCAT, A 432-Patient Retrospective Non-Interventional Study.","authors":"Ludovic Plaisance, Céline Chapelle, Silvy Laporte, Benjamin Planquette, Laurent Bertoletti, Nicolas Falvo, Francis Couturaud, Lionel Falchero, Isild Mahé, Hélène Helfer, Sadji Dennaoui, Guy Meyer, Isabelle Mahé","doi":"10.26502/jcsct.5079122","DOIUrl":"https://doi.org/10.26502/jcsct.5079122","url":null,"abstract":"<p><strong>Background and objectives: </strong>Few data are available about anticoagulation management beyond 6 months in patients with cancer associated thrombosis (CAT). Our objective was to describe anticoagulant treatment modalities up to 12 months.</p><p><strong>Methods: </strong>The management of the anticoagulant treatment beyond 6 months was described in this initially retrospective non-interventional French multicenter study in patients treated with low-molecular-weight heparins (LMWH) still alive at the end of an initial 6-month treatment period. Clinical outcomes, including venous thromboembolism, recurrence, bleeding and deaths have been published previously.</p><p><strong>Results: </strong>Among the 432 patients (mean age 66.5±12.7 years) included in the study, 332 were followed up to 12 months while 96 patients deceased before study end and 4 patients were lost-to-follow-up. At 6 months, anticoagulant therapy was stopped in 74 patients, 56 were switched to vitamin K antagonists (VKA) (16.1% [95%CI, 12.4%-20.4]), 30 to direct oral anticoagulants (DOAC) (8.6% [95%CI, 5.9%-12.1]). LMWHs were maintained in 256 patients (73.6% [95%CI, 68.6-78.1]). During the follow-up, LMWHs were definitively discontinued in 86 patients (33.7%), the main reason being a favorable course of the cancer (16 patients, 18.6%), or the thromboembolic disease (11 patients, 12.8%), whereas concern about bleeding risk was low (2 patients, 2.3%).</p><p><strong>Conclusion: </strong>Anticoagulation beyond 6 months and up to 12 months was in accordance with clinical practice guidelines suggesting that treatment should be continued as long cancer is active or in the absence of bleeding risk. Anticoagulant treatment discontinuation beyond 6 months was influenced by the favorable courses of both malignancy and thromboembolic disease, as well as patient's preference.</p>","PeriodicalId":73634,"journal":{"name":"Journal of cancer science and clinical therapeutics","volume":"5 3","pages":"347-362"},"PeriodicalIF":0.0,"publicationDate":"2021-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10167753/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9466590","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-05-27DOI: 10.21203/RS.3.RS-536721/V1
A. Noguchi, T. Nishida, Hideki Hatta, Kohji Takagi, Toshiko Kakiuchi, Shinichi Tanaka, Takashi Minamisaka, T. Nakajima, J. Imura
Background: Cetuximab is a powerful anti-neoplastic agent that can inhibit cell growth in oral squamous cell carcinomas (OSCCs). Unfortunately, there are cases with unfavorable outcomes. Because few studies have focused on the combined effects of cetuximab and histone deacetylase (HDAC) inhibitors, we aimed to evaluate the antitumor effect of cetuximab in combination with HDAC inhibitors in human OSCC cell lines, and investigate the mechanism of apoptosis enhancing activity thereof.Methods: We used human OSCC cell lines treated with cetuximab (500 mg/ml) and several HDAC inhibitors. The WST assay and ApoToxGlo™ Triplex Assay determined cell survival. We employed the TdT-mediated dUTP-biotin nick end labeling method to detect apoptosis. We used western blotting to examine the histone acetylation status, ER stress markers, and epidermal growth factor receptor (EGFR) signaling pathways.Results: Cetuximab in combination with 4-phenyl butyric acid (4-PBA) remarkably decreases cell growth in vitro. In addition, the combined treatment resulted in increased EGFR mRNA expression, and it promoted the activation of ERK. The combination treatment induced apoptosis at a significantly higher frequency than did either agent alone.Conclusions: The combination of cetuximab and 4-PBA is more effective against human OSCC cells than either agent alone, suggesting a potential clinical applicability of combination treatment in OSCC therapies.
{"title":"Efficacy of Cetuximab and 4-PBA Combination Therapy in Human Oral Squamous Cell Carcinoma Cells","authors":"A. Noguchi, T. Nishida, Hideki Hatta, Kohji Takagi, Toshiko Kakiuchi, Shinichi Tanaka, Takashi Minamisaka, T. Nakajima, J. Imura","doi":"10.21203/RS.3.RS-536721/V1","DOIUrl":"https://doi.org/10.21203/RS.3.RS-536721/V1","url":null,"abstract":"\u0000 Background: Cetuximab is a powerful anti-neoplastic agent that can inhibit cell growth in oral squamous cell carcinomas (OSCCs). Unfortunately, there are cases with unfavorable outcomes. Because few studies have focused on the combined effects of cetuximab and histone deacetylase (HDAC) inhibitors, we aimed to evaluate the antitumor effect of cetuximab in combination with HDAC inhibitors in human OSCC cell lines, and investigate the mechanism of apoptosis enhancing activity thereof.Methods: We used human OSCC cell lines treated with cetuximab (500 mg/ml) and several HDAC inhibitors. The WST assay and ApoToxGlo™ Triplex Assay determined cell survival. We employed the TdT-mediated dUTP-biotin nick end labeling method to detect apoptosis. We used western blotting to examine the histone acetylation status, ER stress markers, and epidermal growth factor receptor (EGFR) signaling pathways.Results: Cetuximab in combination with 4-phenyl butyric acid (4-PBA) remarkably decreases cell growth in vitro. In addition, the combined treatment resulted in increased EGFR mRNA expression, and it promoted the activation of ERK. The combination treatment induced apoptosis at a significantly higher frequency than did either agent alone.Conclusions: The combination of cetuximab and 4-PBA is more effective against human OSCC cells than either agent alone, suggesting a potential clinical applicability of combination treatment in OSCC therapies.","PeriodicalId":73634,"journal":{"name":"Journal of cancer science and clinical therapeutics","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46037038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
TP53 gene is often mutated in gastric cancer (GC), nonetheless its relationship with clinicopathological characteristics and prognosis is still unclear. Here, we sought to ascertain the difference in clinical phenotypes between TP53 wild-type and mutant tumors in confirmed gastric cancer patients. To this end, we analyzed TP53 mutation status of 415 TCGA GC patients in relation to their clinical and pathological features as well as prognosis. Longrank Test showed that the survival rate of gastric cancer patients with TP53 WT was significantly lower than that of TP53 mut. Compared with TP53 mut gastric cancer patients with low mRNA expression, TP53 WT patients with low mRNA expression have lower overall survival rate. The death risk of TP53 WT gastric cancer patients is 1.395 times that of TP53 mut gastric cancer patients. The death risk of TP53 mut gastric cancer patients is not related to age, and advanced age is not a risk factor. However, the death risk of TP53 WT patients with gastric cancer increases with age, and the death risk of patients over 70 years old is 1.899 times that of patients under 60 years old. These results suggest that the prognosis of elderly gastric cancer patients with TP53 WT is worse.
Conclusion: our results indicate that the status of TP53 mutation in GC is significantly correlated with clinical or molecular categories and that the prognosis of GC patients with WT TP53 is worse than that of patients with mutant TP53. Therefore, our data emphasize the importance of distinguishing TP53 WT to predict poor overall survival and relapse-free survival in patients with GC.
{"title":"Wild-Type TP53 Predicts Poor Prognosis in Patients with Gastric Cancer.","authors":"Wenhong Deng, Qiongyu Hao, Jaydutt Vadgama, Yong Wu","doi":"10.26502/jcsct.50790107","DOIUrl":"https://doi.org/10.26502/jcsct.50790107","url":null,"abstract":"<p><p>TP53 gene is often mutated in gastric cancer (GC), nonetheless its relationship with clinicopathological characteristics and prognosis is still unclear. Here, we sought to ascertain the difference in clinical phenotypes between TP53 wild-type and mutant tumors in confirmed gastric cancer patients. To this end, we analyzed TP53 mutation status of 415 TCGA GC patients in relation to their clinical and pathological features as well as prognosis. Longrank Test showed that the survival rate of gastric cancer patients with TP53 WT was significantly lower than that of TP53 mut. Compared with TP53 mut gastric cancer patients with low mRNA expression, TP53 WT patients with low mRNA expression have lower overall survival rate. The death risk of TP53 WT gastric cancer patients is 1.395 times that of TP53 mut gastric cancer patients. The death risk of TP53 mut gastric cancer patients is not related to age, and advanced age is not a risk factor. However, the death risk of TP53 WT patients with gastric cancer increases with age, and the death risk of patients over 70 years old is 1.899 times that of patients under 60 years old. These results suggest that the prognosis of elderly gastric cancer patients with TP53 WT is worse.</p><p><strong>Conclusion: </strong>our results indicate that the status of TP53 mutation in GC is significantly correlated with clinical or molecular categories and that the prognosis of GC patients with WT TP53 is worse than that of patients with mutant TP53. Therefore, our data emphasize the importance of distinguishing TP53 WT to predict poor overall survival and relapse-free survival in patients with GC.</p>","PeriodicalId":73634,"journal":{"name":"Journal of cancer science and clinical therapeutics","volume":"5 1","pages":"134-153"},"PeriodicalIF":0.0,"publicationDate":"2021-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8694034/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10726406","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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