Pub Date : 2018-01-01DOI: 10.4172/2157-2518.1000323
Fu Houwei
{"title":"Advances in Surgical Research of Hepatocellular Carcinoma with Bile Duct Tumor Thrombus","authors":"Fu Houwei","doi":"10.4172/2157-2518.1000323","DOIUrl":"https://doi.org/10.4172/2157-2518.1000323","url":null,"abstract":"","PeriodicalId":15209,"journal":{"name":"Journal of carcinogenesis & mutagenesis","volume":"63 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80739784","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}
Pub Date : 2017-12-15DOI: 10.4172/2157-2518.1000309
K. U. Rahman, A. Jesrani, Mubarak Ali
Background: Renal cell carcinoma (RCC) accounts for 3% of all human malignant tumors. The behavior of RCC apparently depends on its subtype. CT scan can provide detailed information about the tumor itself and regarding its precise extension. The pre-histological diagnosis of clear cell renal carcinoma could be made with more precision on the basis of CT scan features and would ultimately play a major role in the prognosis and management of the disease. Objective: To determine the diagnostic accuracy of computed tomography in the diagnosis of clear cell renal carcinoma taking histopathological findings as gold standard. Methods: Total 100 patients had renal mass were included. All patients underwent contrast enhanced CT scan. On the basis of CT scan features a pre-surgical diagnosis of histological subtype of RCC, clear cell renal carcinoma was made. The patients were followed by nephrectomy. The diagnostic accuracy of CT scan was determined. Results: The male to female ratio was 3.2:1.0. Out of total study subjects 85.0% patients turned out to be renal cell carcinomas and among these 40 (47%) were right sided and 45 (53%) were left sided. The mean size of tumor was 12.75 cm. The sensitivity, specificity, and diagnostic accuracy of CT scan were 89.0%, 72.7%, and 86.0% respectively. Conclusion: The CT scan was helpful in diagnosing clear cell renal carcinoma. The most valuable parameter was the degree of enhancement of clear cell renal carcinoma with other parameters playing supplemental role.
{"title":"Role of Computed Tomography in the Pre operative Diagnosis of Clear Cell Renal Carcinoma","authors":"K. U. Rahman, A. Jesrani, Mubarak Ali","doi":"10.4172/2157-2518.1000309","DOIUrl":"https://doi.org/10.4172/2157-2518.1000309","url":null,"abstract":"Background: Renal cell carcinoma (RCC) accounts for 3% of all human malignant tumors. The behavior of RCC apparently depends on its subtype. CT scan can provide detailed information about the tumor itself and regarding its precise extension. The pre-histological diagnosis of clear cell renal carcinoma could be made with more precision on the basis of CT scan features and would ultimately play a major role in the prognosis and management of the disease. Objective: To determine the diagnostic accuracy of computed tomography in the diagnosis of clear cell renal carcinoma taking histopathological findings as gold standard. Methods: Total 100 patients had renal mass were included. All patients underwent contrast enhanced CT scan. On the basis of CT scan features a pre-surgical diagnosis of histological subtype of RCC, clear cell renal carcinoma was made. The patients were followed by nephrectomy. The diagnostic accuracy of CT scan was determined. Results: The male to female ratio was 3.2:1.0. Out of total study subjects 85.0% patients turned out to be renal cell carcinomas and among these 40 (47%) were right sided and 45 (53%) were left sided. The mean size of tumor was 12.75 cm. The sensitivity, specificity, and diagnostic accuracy of CT scan were 89.0%, 72.7%, and 86.0% respectively. Conclusion: The CT scan was helpful in diagnosing clear cell renal carcinoma. The most valuable parameter was the degree of enhancement of clear cell renal carcinoma with other parameters playing supplemental role.","PeriodicalId":15209,"journal":{"name":"Journal of carcinogenesis & mutagenesis","volume":"31 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2017-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74535233","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}
Pub Date : 2017-10-18DOI: 10.4172/2157-2518.1000307
M. Pawlikowski, M. Miler
Investigation of Carcinoma basocellulare solidum exulcerans, Carcinoma basocellulare superficiale multicentricum, and Trichoepithelioma was performed using histology and bio-mineralogical methods. Obtained data confirmed elevated levels of some elements in altered skin tissues. Moreover, rare micrograins of phosphates were observed. Additionally, examination of bio mineralization of human tissues suggests that higher local mineralization (of tissue fluids) may lead to mistakes in DNA code at the moment of cell division. It is possible that cancer tissues are secondarily mineralized by activity of cancer cells. Further research is needed to answer questions that arose.
{"title":"Bio-mineralogy of Selected Skin Cancers","authors":"M. Pawlikowski, M. Miler","doi":"10.4172/2157-2518.1000307","DOIUrl":"https://doi.org/10.4172/2157-2518.1000307","url":null,"abstract":"Investigation of Carcinoma basocellulare solidum exulcerans, Carcinoma basocellulare superficiale multicentricum, and Trichoepithelioma was performed using histology and bio-mineralogical methods. Obtained data confirmed elevated levels of some elements in altered skin tissues. Moreover, rare micrograins of phosphates were observed. Additionally, examination of bio mineralization of human tissues suggests that higher local mineralization (of tissue fluids) may lead to mistakes in DNA code at the moment of cell division. It is possible that cancer tissues are secondarily mineralized by activity of cancer cells. Further research is needed to answer questions that arose.","PeriodicalId":15209,"journal":{"name":"Journal of carcinogenesis & mutagenesis","volume":"14 1","pages":"1-9"},"PeriodicalIF":0.0,"publicationDate":"2017-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78445840","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}
Pub Date : 2017-10-16DOI: 10.4172/2157-2518.1000305
Bo Zhang, Sai Hu, Lantao Liu, Zi-jian Yu, H. Guan, Lijing Geng, P. Zhou
In order to study the mechanism of a novel vanillin derivative BVAN08, provide evidence and experimental data for developing it as a new potential anticancer drug. Hepatic cancer HepG2 cells and normal LO2 cells were used to investigate cytotoxicity of BVAN08. The MTT and colony-forming ability assays showed that BVAN08 significantly sensitized HepG2 cells to radiation rather than LO2 cells. Moreover, BVAN08 inhibited the growth of HepG2 cells in nude mice and exerted no effects on body weight and the number of the peripheral white blood cells. The immunohistochemistry results indicated that the DNA-PKcs expression the BVAN08 group tumor was lower than that of control group. BVAN08 obviously inhibits proliferation of HepG2 cells in vitro and in vivo supporting it as a promising anticancer drug candidate.
{"title":"Inhibitory Effects of BVAN08 on the Growth of Experimental Tumor Cell Lines both In Vivo and In Vitro","authors":"Bo Zhang, Sai Hu, Lantao Liu, Zi-jian Yu, H. Guan, Lijing Geng, P. Zhou","doi":"10.4172/2157-2518.1000305","DOIUrl":"https://doi.org/10.4172/2157-2518.1000305","url":null,"abstract":"In order to study the mechanism of a novel vanillin derivative BVAN08, provide evidence and experimental data for developing it as a new potential anticancer drug. Hepatic cancer HepG2 cells and normal LO2 cells were used to investigate cytotoxicity of BVAN08. The MTT and colony-forming ability assays showed that BVAN08 significantly sensitized HepG2 cells to radiation rather than LO2 cells. Moreover, BVAN08 inhibited the growth of HepG2 cells in nude mice and exerted no effects on body weight and the number of the peripheral white blood cells. The immunohistochemistry results indicated that the DNA-PKcs expression the BVAN08 group tumor was lower than that of control group. BVAN08 obviously inhibits proliferation of HepG2 cells in vitro and in vivo supporting it as a promising anticancer drug candidate.","PeriodicalId":15209,"journal":{"name":"Journal of carcinogenesis & mutagenesis","volume":"43 1","pages":"1-5"},"PeriodicalIF":0.0,"publicationDate":"2017-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88067684","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}
Pub Date : 2017-10-16DOI: 10.4172/2157-2518.1000306
Jing Sun, Shaohua He, P. Lin, Ping Li, Xiaomin Cai, Lele Li, J. Qian, Chong Liu, Xiao Li, Yi-qian Liu, O. Røe, Y. Shu, Yanhong Gu, Xiaofeng Chen
Objective: This retrospective study was carried out to compare the safety and efficacy of adjuvant capecitabine/ oxaliplatin (XELOX) versus capecitabine/paclitaxel (XP) in gastric cancer patients after D2 gastrectomy. Methods: The hospital records of the First Affiliated Hospital of Nanjing Medical University from 2008-2012 were searched to identify patients treated with adjuvant XELOX or XP after D2 gastrectomy and their clinicopathological data were retrieved. Disease-free survival (DFS) and overall survival (OS) were analyzed by Kaplan-Meier method with log-rank test. Results: A total of 144 stage I-III patients who received adjuvant XELOX (n=89) or XP (n=55) after D2 gastrectomy were identified. The median follow-up time was 47.0 (25.0-80.0) months. The 3-year DFS and OS rate was 67.0% versus 50.8% (p=0.047) and 74.8% versus 63.5% (p=0.184) in the XELOX and XP group respectively. XELOX significantly reduced the risk of relapse at three years (HR 0.60, 95% CI 0.36-0.99) but did not reduced the risk of death at the third year (HR 0.66, 95% CI 0.36-1.22) compared with that treated with XP. Conclusions: These results indicate that adjuvant XELOX after D2 gastrectomy has a clinical advantage over XP; however, prospective studies are needed to verify this finding.
目的:本回顾性研究比较D2胃切除术后辅助卡培他滨/奥沙利铂(XELOX)与卡培他滨/紫杉醇(XP)在胃癌患者中的安全性和有效性。方法:检索南京医科大学附属第一医院2008-2012年的住院记录，找出D2胃切除术后辅助使用XELOX或XP的患者，并检索其临床病理资料。采用Kaplan-Meier法和log-rank检验分析无病生存期(DFS)和总生存期(OS)。结果:共有144例I-III期患者在D2胃切除术后接受辅助XELOX (n=89)或XP (n=55)。中位随访时间为47.0(25.0 ~ 80.0)个月。XELOX组和XP组3年DFS和OS分别为67.0%和50.8% (p=0.047)和74.8%和63.5% (p=0.184)。与接受XP治疗的患者相比，XELOX显著降低了三年复发风险(HR 0.60, 95% CI 0.36-0.99)，但未降低第三年死亡风险(HR 0.66, 95% CI 0.36-1.22)。结论:D2胃切除术后辅助XELOX较XP有临床优势;然而，需要前瞻性研究来验证这一发现。
{"title":"Adjuvant Capecitabine and Oxaliplatin vs. Capecitabine and Paclitaxel in Gastric Cancer Patients after D2 Gastrectomy","authors":"Jing Sun, Shaohua He, P. Lin, Ping Li, Xiaomin Cai, Lele Li, J. Qian, Chong Liu, Xiao Li, Yi-qian Liu, O. Røe, Y. Shu, Yanhong Gu, Xiaofeng Chen","doi":"10.4172/2157-2518.1000306","DOIUrl":"https://doi.org/10.4172/2157-2518.1000306","url":null,"abstract":"Objective: This retrospective study was carried out to compare the safety and efficacy of adjuvant capecitabine/ \u0000 oxaliplatin (XELOX) versus capecitabine/paclitaxel (XP) in gastric cancer patients after D2 gastrectomy. \u0000Methods: The hospital records of the First Affiliated Hospital of Nanjing Medical University from 2008-2012 were \u0000 searched to identify patients treated with adjuvant XELOX or XP after D2 gastrectomy and their clinicopathological \u0000 data were retrieved. Disease-free survival (DFS) and overall survival (OS) were analyzed by Kaplan-Meier method \u0000 with log-rank test. \u0000Results: A total of 144 stage I-III patients who received adjuvant XELOX (n=89) or XP (n=55) after D2 \u0000 gastrectomy were identified. The median follow-up time was 47.0 (25.0-80.0) months. The 3-year DFS and OS rate \u0000 was 67.0% versus 50.8% (p=0.047) and 74.8% versus 63.5% (p=0.184) in the XELOX and XP group respectively. \u0000 XELOX significantly reduced the risk of relapse at three years (HR 0.60, 95% CI 0.36-0.99) but did not reduced the \u0000 risk of death at the third year (HR 0.66, 95% CI 0.36-1.22) compared with that treated with XP. \u0000Conclusions: These results indicate that adjuvant XELOX after D2 gastrectomy has a clinical advantage over \u0000 XP; however, prospective studies are needed to verify this finding.","PeriodicalId":15209,"journal":{"name":"Journal of carcinogenesis & mutagenesis","volume":"126 1","pages":"1-7"},"PeriodicalIF":0.0,"publicationDate":"2017-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85708861","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}
Pub Date : 2017-08-21DOI: 10.4172/2157-2518.1000304
A. Taddei, T. Lottini, M. Fazi, M. Ringressi, E. Lastraioli, P. Bechi, A. Arcangeli
Purpose: Barrett’s esophagus (BE) is the sole precursor lesion of esophageal adenocarcinoma (EA) identified so far. The progression towards EA is estimated to affect 2 to 10% of BE patients, hence endoscopic surveillance of at-risk subjects is mandatory. Surveillance endoscopic procedures imply high cost, discomfort and risks for the patient, as well as the non-infrequent missing of small, focal lesions signaling progression to EA. Hence, it is important to search for new potential markers to better identify BE patients at risk of EA progression. The aim of this study was to produce a mouse model of BE, suitable for further molecular and genetic analyses. Methods: Forty-four CD1 mice were operated upon by means of an esophago-jejunal anastomosis. Five CD1 mice underwent a sham operation. The animals were sacrificed 10 months later and histological analysis was performed with Hematoxylin & Eosin and Alcian Blue staining. Results: The overall postoperative mortality rate was 11%. Of the 39 operated animals 14% developed histologically detectable intestinal metaplasia in the lower esophagus. No histologically detectable lesions were shown in the sham group. Conclusions: The mice model we propose could be applied because of its technical feasibility and acceptable mortality and can be used in transgenic mice too, in order to better understand molecular progression from BE to esophageal adenocarcinoma.
{"title":"A Mouse Model for Barrett’s Esophagus: Surgery and Histology","authors":"A. Taddei, T. Lottini, M. Fazi, M. Ringressi, E. Lastraioli, P. Bechi, A. Arcangeli","doi":"10.4172/2157-2518.1000304","DOIUrl":"https://doi.org/10.4172/2157-2518.1000304","url":null,"abstract":"Purpose: Barrett’s esophagus (BE) is the sole precursor lesion of esophageal adenocarcinoma (EA) identified \u0000 so far. The progression towards EA is estimated to affect 2 to 10% of BE patients, hence endoscopic surveillance \u0000 of at-risk subjects is mandatory. Surveillance endoscopic procedures imply high cost, discomfort and risks for \u0000 the patient, as well as the non-infrequent missing of small, focal lesions signaling progression to EA. Hence, it is \u0000 important to search for new potential markers to better identify BE patients at risk of EA progression. The aim of this \u0000 study was to produce a mouse model of BE, suitable for further molecular and genetic analyses. \u0000Methods: Forty-four CD1 mice were operated upon by means of an esophago-jejunal anastomosis. Five CD1 \u0000 mice underwent a sham operation. The animals were sacrificed 10 months later and histological analysis was \u0000 performed with Hematoxylin & Eosin and Alcian Blue staining. \u0000Results: The overall postoperative mortality rate was 11%. Of the 39 operated animals 14% developed \u0000 histologically detectable intestinal metaplasia in the lower esophagus. No histologically detectable lesions were \u0000 shown in the sham group. \u0000Conclusions: The mice model we propose could be applied because of its technical feasibility and acceptable \u0000 mortality and can be used in transgenic mice too, in order to better understand molecular progression from BE to \u0000 esophageal adenocarcinoma.","PeriodicalId":15209,"journal":{"name":"Journal of carcinogenesis & mutagenesis","volume":"13 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2017-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89730085","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}
Pub Date : 2017-07-25DOI: 10.4172/2157-2518.1000299
I. S. Guimarães, N. Tessarollo, Di, ra Zipinotti dos Santos, M. L. L. D. Souza, T. B. Henriques, I. V. Silva, L. B. Rangel
Cancer is one of the leading causes of death worldwide. Every year 8.2 million people die from the disease. In this context, breast and ovarian cancer are the most incidental among women. Elucidation of cell growth pathways and the observation that these pathways are altered in human cancer have encouraged the search for specific inhibitors. The phosphatidylinositol-3cinase (PI3K)/Protein kinase b (AKT)/Mammalian Target of Rapamycin (mTOR) is an important pathway involved in cell growth, tumorigenesis, cell invasion, and resistance to therapies. This pathway is often activated in breast and ovarian cancers and the deregulation of its signaling can contribute to tumor growth, angiogenesis and metastasis. Metformin is one of the most commonly prescribed antidiabetic drugs in the world whose anticancer effects, mediated by reduced mTOR signaling, have become notable. Therefore, this review provides an overview of signaling pathway PI3K/AKT/mTOR in the ovarian and breast cancers as well as for target therapies of mTOR signaling, with an emphasis on its mechanisms, clinical applicability and future perspectives.
{"title":"Metformin and mTOR Inhibitors: Allies against Ovarian and Breast Cancers","authors":"I. S. Guimarães, N. Tessarollo, Di, ra Zipinotti dos Santos, M. L. L. D. Souza, T. B. Henriques, I. V. Silva, L. B. Rangel","doi":"10.4172/2157-2518.1000299","DOIUrl":"https://doi.org/10.4172/2157-2518.1000299","url":null,"abstract":"Cancer is one of the leading causes of death worldwide. Every year 8.2 million people die from the disease. In this context, breast and ovarian cancer are the most incidental among women. Elucidation of cell growth pathways and the observation that these pathways are altered in human cancer have encouraged the search for specific inhibitors. The phosphatidylinositol-3cinase (PI3K)/Protein kinase b (AKT)/Mammalian Target of Rapamycin (mTOR) is an important pathway involved in cell growth, tumorigenesis, cell invasion, and resistance to therapies. This pathway is often activated in breast and ovarian cancers and the deregulation of its signaling can contribute to tumor growth, angiogenesis and metastasis. Metformin is one of the most commonly prescribed antidiabetic drugs in the world whose anticancer effects, mediated by reduced mTOR signaling, have become notable. Therefore, this review provides an overview of signaling pathway PI3K/AKT/mTOR in the ovarian and breast cancers as well as for target therapies of mTOR signaling, with an emphasis on its mechanisms, clinical applicability and future perspectives.","PeriodicalId":15209,"journal":{"name":"Journal of carcinogenesis & mutagenesis","volume":"24 1","pages":"1-11"},"PeriodicalIF":0.0,"publicationDate":"2017-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80903542","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}
Arachidonic acid can be catalyzed by three different kind of metabolizing enzyme: cyclooxygenase (COX), lipoxygenase (LOX) and/or cytochrome P450 (CYP), and they produce prostaglandins, monohydroxys, leukotrienes and epoxyeicosanoids respectively. Through the cytochrome P450 pathway, arachidonic acid can be converted to two kinds of eicosanoid acids: epoxyeicosanoids acid (EET) by cytochrome P450 and hydroxyeicosatetraenoic acids (HETEs) formed by CYP α-oxidases.
{"title":"Soluble Epoxide Hydrolase: Potential Target for Inflammation and Inflammation-Driven Cancer","authors":"Chao Lou, Liping Zhang, Xiaobin Wang, Xiaoping Ma, Cuiyun Qin, Wei Li, Ting Jia, Qing-ling Nan, R. Qiang","doi":"10.4172/2157-2518.1000294","DOIUrl":"https://doi.org/10.4172/2157-2518.1000294","url":null,"abstract":"Arachidonic acid can be catalyzed by three different kind of metabolizing enzyme: cyclooxygenase (COX), lipoxygenase (LOX) and/or cytochrome P450 (CYP), and they produce prostaglandins, monohydroxys, leukotrienes and epoxyeicosanoids respectively. Through the cytochrome P450 pathway, arachidonic acid can be converted to two kinds of eicosanoid acids: epoxyeicosanoids acid (EET) by cytochrome P450 and hydroxyeicosatetraenoic acids (HETEs) formed by CYP α-oxidases.","PeriodicalId":15209,"journal":{"name":"Journal of carcinogenesis & mutagenesis","volume":"58 1","pages":"1-5"},"PeriodicalIF":0.0,"publicationDate":"2017-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74642160","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}
Pub Date : 2017-05-19DOI: 10.4172/2157-2518.1000293
Firdous Hussain, A. Hamid, Rita Singh Majumdhar
Cyclin D1 (CCND1) is a critical gene in regulating the progression of cell cycle from G1 to S phases. Like other cyclins, cyclin D1 is frequently dysregulated in multiple cancers. Various clinical and epidemiological studies have suggested the possible association of cyclin D1 A870G polymorphism with the development of various cancers. Hence, we investigated the role of cyclin D1 A870G polymorphism in modulating the risk of prostate cancer (CaP) in a Kashmiri population. We examined a case–control study in which 129 CaP cases were studied for cyclin D1 A870G polymorphism against 221 controls taken from the general population by employing the polymerase chain reaction–restriction length fragment polymorphism technique. We observed the cyclin D1 A allele was more frequently present in the CaP group than the control group. Furthermore, men with AA genotype have an increased risk for developing CaP as compared to the control groups. We found AA genotype statistically significantly associated with dwelling, lymph node metastases, histopathological grade, and PSA levels. Therefore, our findings suggest that A870G polymorphism is a risk factor for CaP development. Furthermore, men with AA genotype have an increased risk of developing CaP.
{"title":"Risk of Prostate Cancer and Cyclin D1 A870G polymorphism; a Study of Correlation","authors":"Firdous Hussain, A. Hamid, Rita Singh Majumdhar","doi":"10.4172/2157-2518.1000293","DOIUrl":"https://doi.org/10.4172/2157-2518.1000293","url":null,"abstract":"Cyclin D1 (CCND1) is a critical gene in regulating the progression of cell cycle from G1 to S phases. Like other \u0000 cyclins, cyclin D1 is frequently dysregulated in multiple cancers. Various clinical and epidemiological studies have \u0000 suggested the possible association of cyclin D1 A870G polymorphism with the development of various cancers. \u0000 Hence, we investigated the role of cyclin D1 A870G polymorphism in modulating the risk of prostate cancer (CaP) in \u0000 a Kashmiri population. We examined a case–control study in which 129 CaP cases were studied for cyclin D1 A870G polymorphism against 221 controls taken from the general population by employing the polymerase chain \u0000 reaction–restriction length fragment polymorphism technique. We observed the cyclin D1 A allele was more \u0000 frequently present in the CaP group than the control group. Furthermore, men with AA genotype have an increased \u0000 risk for developing CaP as compared to the control groups. We found AA genotype statistically significantly \u0000 associated with dwelling, lymph node metastases, histopathological grade, and PSA levels. Therefore, our findings \u0000 suggest that A870G polymorphism is a risk factor for CaP development. Furthermore, men with AA genotype have \u0000 an increased risk of developing CaP.","PeriodicalId":15209,"journal":{"name":"Journal of carcinogenesis & mutagenesis","volume":"10 1","pages":"1-6"},"PeriodicalIF":0.0,"publicationDate":"2017-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86533231","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}
Pub Date : 2017-04-24DOI: 10.4172/2157-2518.1000290
D. Kalasauskas, M. Renovanz, Sven-Ernö Bikár, A. Buzdin, A. Enam, S. Kantelhardt, A. Giese, Ella L. Kim
Glioblastoma is the most common and most malignant type of intrinsic brain tumor in adults. The standard of care for glioblastoma consists of surgical debulking followed by combined radiochemotherapy. The clinical efficacy of standard therapies for newly diagnosed glioblastomas is rather modest with the highest survival rate at 5-years being less than 10%. Inevitable recurrence after cytotoxic therapies poses the major challenge in the clinical management of high grade gliomas. For recurrent glioblastomas, there is no standard therapy with lack of level one evidence for treatment efficacy. Recent evidence indicates that post-therapy recurrence in gliomas is a consequence of a plethora of molecular and cellular factors including intratumoural heterogeneity, functional hierarchy of distinct types of glioma cells, dynamic changes in the molecular landscapes and cellular composition of the tumour during therapy and the impact of particular treatment modalities. There is an emerging consensus that molecular distinctions within and between individual tumours is an important factor determining clinical outcomes. Consequently, integrated approaches based on the combination of molecular profiling with traditional methods such as immunohistochemical phenotyping, karyotyping and/or non-quantitative methylation-specific PCR have emerged as a promising venue towards increasing the predictive value of diagnostics for malignant brain tumors. The high level of inter-and intra-tumoural molecular diversity in gliomas underscores the need of integrating high throughput molecular profiling and pharmacogenomics into a diagnostic paradigm for gliomas and raises the possibility that molecular-instructed personalized treatments may provide clinical benefit to patients with glioblastoma, particularly in the setting of post-treatment recurrence. Here we discuss potential prospects and challenges of patient-tailored diagnostics and personalized treatment strategies for recurrent glioblastomas.
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