Journal of Carcinogenesis最新文献

{"title":"Cancer review: Cholangiocarcinoma.","authors":"Yezaz Ahmed Ghouri, Idrees Mian, Boris Blechacz","doi":"10.4103/1477-3163.151940","DOIUrl":"10.4103/1477-3163.151940","url":null,"abstract":"<p><p>Cholangiocarcinoma (CCA) is the most common biliary tract malignancy. CCA is classified as intrahepatic, perihilar or distal extrahepatic; the individual subtypes differ in their biologic behavior, clinical presentation, and management. Throughout the last decades, CCA incidence rates had significantly increased. In addition to known established risk factors, novel possible risk factors (i.e. obesity, hepatitis C virus) have been identified that are of high importance in developed countries where CCA prevalence rates have been low. CCA tends to develop on the background of inflammation and cholestasis. In recent years, our understanding of the molecular mechanisms of cholangiocarcinogenesis has increased, thereby, providing the basis for molecularly targeted therapies. In its diagnostic evaluation, imaging techniques have improved, and the role of complementary techniques has been defined. There is a need for improved CCA biomarkers as currently used ones are suboptimal. Multiple staging systems have been developed, but none of these is optimal. The prognosis of CCA is considered dismal. However, treatment options have improved throughout the last two decades for carefully selected subgroups of CCA patients. Perihilar CCA can now be treated with orthotopic liver transplantation with neoadjuvant chemoradiation achieving 5-year survival rates of 68%. Classically considered chemotherapy-resistant, the ABC-02 trial has shown the therapeutic benefit of combination therapy with gemcitabine and cisplatin. The benefits of adjuvant treatments for resectable CCA, local ablative therapies and molecularly targeted therapies still need to be defined. In this article, we will provide the reader with an overview over CCA, and discuss the latest developments and controversies. </p>","PeriodicalId":52464,"journal":{"name":"Journal of Carcinogenesis","volume":"14 ","pages":"1"},"PeriodicalIF":0.0,"publicationDate":"2015-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4360553/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33143391","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}

{"title":"Gastric cancer review.","authors":"Lauren Peirce Carcas","doi":"10.4103/1477-3163.146506","DOIUrl":"https://doi.org/10.4103/1477-3163.146506","url":null,"abstract":"<p><p>Gastric cancer is an aggressive disease that continues to have a daunting impact on global health. Despite an overall decline in incidence over the last several decades, gastric cancer remains the fourth most common type of cancer and is the second leading cause of cancer-related death worldwide. This review aims to discuss the global distribution of the disease and the trend of decreasing incidence of disease, delineate the different pathologic subtypes and their immunohistochemical (IHC) staining patterns and molecular signatures and mutations, explore the role of the pathogen H. pylori in tumorgenesis, discuss the increasing incidence of the disease in the young, western populations and define the role of biologic agents in the treatment of the disease. </p>","PeriodicalId":52464,"journal":{"name":"Journal of Carcinogenesis","volume":"13 ","pages":"14"},"PeriodicalIF":0.0,"publicationDate":"2014-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4278094/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32976662","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}

{"title":"The advent of precision therapy in gastrointestinal malignancies: Targeting the human epidermal growth factor receptor family in colorectal and esophagogastric cancer.","authors":"Danielle Desautels,&nbsp;Craig Harlos,&nbsp;Piotr Czaykowski","doi":"10.4103/1477-3163.145609","DOIUrl":"https://doi.org/10.4103/1477-3163.145609","url":null,"abstract":"<p><p>Until recently, systemic therapy for gastrointestinal malignancies was restricted to relatively noncancer-specific cytotoxic chemotherapy. Over the last 15 years targeted therapies have become available, most notably bevacizumab in the case of advanced colorectal cancer. Unfortunately, there are no predictive biomarkers to guide the use of this agent. In this review article, we describe the advent of \"Precision Medicine\" (in part, the use of patient-specific molecular markers to inform treatment) in gastrointestinal cancers: The use of monoclonal antibodies targeting epidermal growth factor receptor in advanced colorectal cancer, and human epidermal growth factor receptor 2-neu in advanced esophagogastric cancer. In both instances, biomarkers help in selecting appropriate patients for such treatment. </p>","PeriodicalId":52464,"journal":{"name":"Journal of Carcinogenesis","volume":"13 ","pages":"13"},"PeriodicalIF":0.0,"publicationDate":"2014-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4258725/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32921126","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}

{"title":"Reducing inequities in colorectal cancer screening in North America.","authors":"Kathleen M Decker,&nbsp;Harminder Singh","doi":"10.4103/1477-3163.144576","DOIUrl":"https://doi.org/10.4103/1477-3163.144576","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is an important cause of mortality and morbidity in North America. Screening using a fecal occult blood test, flexible sigmoidoscopy, or colonoscopy reduces CRC mortality through the detection and treatment of precancerous polyps and early stage CRC. Although CRC screening participation has increased in recent years, large inequities still exist. Minorities, new immigrants, and those with lower levels of education or income are much less likely to be screened. This review provides an overview of the commonly used tests for CRC screening, disparities in CRC screening, and promising methods at the individual, provider, and system levels to reduce these disparities. Overall, to achieve high CRC participation rates and reduce the burden of CRC in the population, a multi-faceted approach that uses strategies at all levels to reduce CRC screening disparities is urgently required. </p>","PeriodicalId":52464,"journal":{"name":"Journal of Carcinogenesis","volume":"13 ","pages":"12"},"PeriodicalIF":0.0,"publicationDate":"2014-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4253036/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32907426","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}

{"title":"Esophageal cancer: Recent advances in screening, targeted therapy, and management.","authors":"Puja Gaur,&nbsp;Min P Kim,&nbsp;Brian J Dunkin","doi":"10.4103/1477-3163.143720","DOIUrl":"https://doi.org/10.4103/1477-3163.143720","url":null,"abstract":"<p><p>The incidence of esophageal cancer remains on the rise worldwide and despite aggressive research in the field of gastrointestinal oncology, the survival remains poor. Much remains to be defined in esophageal cancer, including the development of an effective screening tool, identifying a good tumor marker for surveillance purposes, ways to target esophageal cancer stem cells as well as circulating tumor cells, and developing minimally invasive protocols to treat early-stage disease. The goal of this chapter is to highlight some of the recent advances and ongoing research in the field of esophageal cancer. </p>","PeriodicalId":52464,"journal":{"name":"Journal of Carcinogenesis","volume":"13 ","pages":"11"},"PeriodicalIF":0.0,"publicationDate":"2014-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4229783/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32814307","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}

{"title":"Expression of epidermal growth factor receptor, p53, Bcl2, vascular endothelial growth factor, cyclooxygenase-2, cyclin D1, human epidermal receptor-2 and Ki-67: Association with clinicopathological profiles and outcomes in gallbladder carcinoma.","authors":"Dinesh Chandra Doval,&nbsp;Saud Azam,&nbsp;Rupal Sinha,&nbsp;Ullas Batra,&nbsp;Anurag Mehta","doi":"10.4103/1477-3163.139450","DOIUrl":"https://doi.org/10.4103/1477-3163.139450","url":null,"abstract":"<p><strong>Background: </strong>The present study observed the expression levels of epidermal growth factor receptor (EGFR), p53, Bcl2, vascular endothelial growth factor (VEGF), cyclooxygenase-2 (cox-2), cyclin D1, human epidermal receptor-2 (HER-2) and Ki-67 in gallbladder carcinoma (GBC) and their association with clinicopathological profiles and disease outcomes.</p><p><strong>Materials and methods: </strong>Fifty consecutive samples of cholecystectomy/biopsies from GB bed (archived formalin fixed paraffin embedded tissue blocks of different stages of GBC) were included, and patient details related to their demographic profile, investigations, tumor profile, treatment, and follow-up were recorded. Immunohistochemistry was performed to study the expression levels.</p><p><strong>Results: </strong>Overexpression of EGFR, p53, Bcl2, VEGF, cox-2, cyclin D1 and HER-2 was observed as 74%, 44%, 8%, 34%, 66%, 64%, and 4%, respectively. Association of Bcl2 overexpression in mucinous morphology (40%, P = 0.045), cox-2 overexpression in early stage (I/II) tumors (87.5%, P = 0.028) and VEGF overexpression in alive patients (47.1%, P = 0.044) was observed. Co-expression of EGFR and p53 were statistically significant (P = 0.033). Ki-67 labeling index was significantly higher in patients in age group <40 years (P = 0.027), and poorly differentiated tumors (P = 0.023). Advanced disease and poorly differentiated tumors showed a significantly poor median survival (P < 0.05).</p><p><strong>Conclusion: </strong>EGFR, cox-2 and cyclin D1 were largely overexpressed. Advanced tumor stages and poorly differentiated tumors are predictors of poor survival.</p>","PeriodicalId":52464,"journal":{"name":"Journal of Carcinogenesis","volume":"13 ","pages":"10"},"PeriodicalIF":0.0,"publicationDate":"2014-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4163917/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32671792","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}

{"title":"Doenjang prepared with mixed starter cultures attenuates azoxymethane and dextran sulfate sodium-induced colitis-associated colon carcinogenesis in mice.","authors":"Ji-Kang Jeong,&nbsp;Hee-Kyung Chang,&nbsp;Kun-Young Park","doi":"10.4103/1477-3163.137699","DOIUrl":"https://doi.org/10.4103/1477-3163.137699","url":null,"abstract":"<p><strong>Backgrounds: </strong>Doenjang is traditional Korean fermented soybean paste and widely known for its various health benefits including anticancer effect. In this study, we manufactured doenjang with the grain-type meju using probiotic mixed starter cultures of Aspegillus oryzae, Bacillus subtilis-SKm, and Lactococcus lactis-GAm to improve the qualities and beneficial properties of doenjang.</p><p><strong>Materials and methods: </strong>The inhibitory effects of the doenjang prepared with the grain-type meju using mixed starter cultures were investigated in azoxymethane (AOM) and dextran sulfate sodium (DSS)-induced colon carcinogenesis mice model. AOM and DSS colon carcinogenesis was induced in female C57BL/6 mice, and doenjang was orally administered for 4 weeks. Body weight, colon length, and colon weight of mice were determined, and colonic tissues were histologically evaluated. The serum levels of proinflammatory cytokines as well as the expression of inflammation- and apoptosis-related genes in colonic tissue were also analyzed.</p><p><strong>Results: </strong>Administration of the doenjang using probiotic mixed starter cultures ameliorated the symptoms of colon cancer, and reduced the incidence of neoplasia, and reduced the levels of serum proinflammatory cytokines such as interleukin-6, and tumor necrosis factor-α and inducible nitric oxide synthase and cycloooxygenase-2 expression levels in colonic tissue. In addition, it increased Bax and reduced Bcl-2 expression levels and increased p21 and p53 expression in the colonic tissues.</p><p><strong>Conclusion: </strong>These findings indicate that the doenjang attenuated colon carcinogenesis induced by AOM and DSS by ameliorating the symptoms of colon cancer, reducing the occurrence of neoplasia, regulating proinflammatory cytokine levels, and controlling the expressions of inflammation- and apoptosis-related genes in the colonic tissue.</p>","PeriodicalId":52464,"journal":{"name":"Journal of Carcinogenesis","volume":"13 ","pages":"9"},"PeriodicalIF":0.0,"publicationDate":"2014-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4103/1477-3163.137699","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32642683","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}

{"title":"Circulating tumor cells in breast cancer.","authors":"Geetha Pukazhendhi,&nbsp;Stefan Glück","doi":"10.4103/1477-3163.135578","DOIUrl":"https://doi.org/10.4103/1477-3163.135578","url":null,"abstract":"<p><p>Circulating tumor cell (CTC) measurement in peripheral blood of patients with breast cancer offers prognostic information. In this review, we will try to identify evidence that could be used for prognosis, predictive power to draw this tool to clinical utility. We reviewed 81 manuscripts, and categorized those in discovery datasets, prognostic factors in metastatic breast cancer, identification of clinical utility in early breast cancer and in novel approaches. With each patient responding differently to chemotherapy, more efficient markers would improve clinical outcome. Current CTC diagnostic techniques use epithelial markers predominantly; however, the most appropriate method is the measurement of circulating DNA. It has been hypothesized that micrometastasis occurs early in the development of tumors. That implies the presence of CTCs in nonmetastatic setting. The origin of stimulus for malignant transformation is yet unknown. The role of microenvironment as a stimulus is also being investigated. It has been shown that CTCs vary in numbers with chemotherapy. The markers, which are followed-up in the primary tumors, are also being studied on the CTCs. There is discordance of the human epidermal growth factor receptor-2 status between the primary tumor and CTCs. This review summarizes our current knowledge about the CTCs. With genetic profiling and molecular characterization of CTCs, it is possible to overcome the diagnostic difficulties. Evidence for clinical utility of CTC as prognostic and predictive marker is increasing. Appropriate patient stratification according to CTC determination among other tests, would make personalized cancer therapy more feasible. </p>","PeriodicalId":52464,"journal":{"name":"Journal of Carcinogenesis","volume":"13 ","pages":"8"},"PeriodicalIF":0.0,"publicationDate":"2014-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4103/1477-3163.135578","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32642682","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}

{"title":"Inhibitory potential of methanolic extracts of Aristolochia tagala and Curcuma caesia on hepatocellular carcinoma induced by diethylnitrosamine in BALB/c mice.","authors":"Khetbadei Lysinia Hynniewta Hadem, Rajeshwar Nath Sharan, Lakhan Kma","doi":"10.4103/1477-3163.133520","DOIUrl":"10.4103/1477-3163.133520","url":null,"abstract":"<p><strong>Context: </strong>Aristolochia tagala (AT) and Curcuma caesia (CC) have been used traditionally by local herbal practitioners for cancer treatment and as chief ingredients of many polyherbal formulations for various types of ailments. However, there is void in scientific study to evaluate their anti-cancer property.</p><p><strong>Aims: </strong>The aim of this study was to evaluate the anti-carcinogenic properties of the crude methanolic extracts of roots of AT and rhizomes of CC in BALB/c mice exposed to a hepatocarcinogen, diethylnitrosamine (DEN).</p><p><strong>Settings and design: </strong>(I) Toxicity of herbal plant extracts (HPE); (II) Anticancer studies; (III) Histological studies; and (IV) Biochemical studies.</p><p><strong>Materials and methods: </strong>To evaluate the effects of these two HPE either alone or following DEN exposure, serum transaminases (aspartate aminotransferase [AST], alanine aminotransferase [ALT]), alkaline phosphatase (ALP), and cancer marker enzyme acetylcholine esterase (AChE) were assayed in mice. In addition, histological study was also carried out under similar conditions. The antioxidant potentials of the HPE were evaluated by monitoring the activity of antioxidant enzymes and metabolites, such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione (GSH).</p><p><strong>Statistical analysis used: </strong>Statistical analysis was performed by GraphPad Prism 6 Software using one-way analysis of variance followed by the Tukey's multiple comparisons test. Significance was set at P < 0.05.</p><p><strong>Results: </strong>Our findings show that DEN administration elevated AST, ALT, ALP, and AChE activities. CC or AT extracts attenuated the increased activities of these marker enzymes. The activities of antioxidant enzymes, which were decreased following DEN administration, were significantly increased in mice treated with CC or AT.</p><p><strong>Conclusions: </strong>The present study clearly documents anticarcinogenic and antioxidant properties of AT and CC in DEN-induced mouse liver cancer in vivo.</p>","PeriodicalId":52464,"journal":{"name":"Journal of Carcinogenesis","volume":"13 ","pages":"7"},"PeriodicalIF":0.0,"publicationDate":"2014-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4141361/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32642681","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}

{"title":"Systems oncology: A new paradigm in cancer research.","authors":"Gopala Kovvali","doi":"10.4103/1477-3163.128641","DOIUrl":"https://doi.org/10.4103/1477-3163.128641","url":null,"abstract":"Since the time the word oncology was coined in 1857, the field has expanded exponentially metamorphosing the original connotation and intent of the word (Roman word “oncos” (swelling) in relation to the tumors). The word oncology should, then, literally mean the study of swelling or tumors. In a premolecular or pregenomic era, oncology was confined to diagnosing and treating the solid tumors, which was later expanded to include hematological malignancies, which are now referred to as liquid tumors. The word liquid tumor is a misnomer, in that context, but it is a topic for another discussion on another day. The advent of DNA era has focused on seeking answers to the origin of tumors in the genetics under the genetics paradigm or genetics-only paradigm. The rapidly evolved disciplines of molecular biology, biotechnology and related disciplines have enormously contributed to the understanding of tumors and tumorigenesis. The genetic paradigm has recently been sharing its prime spot with the epigenetic phenomenon that could explain the tumorigenesis and has a promise for reversibility of the process. The most recent and exciting paradigm of tumorigenic process relates to cancer stem cells. Therefore, the concepts and models of tumorigenesis are still evolving and the field seems to be far from fully explored. \u0000 \u0000So, I ponder, if cancer is a disease or a phenomenon? I tend to believe that cancer is a phenomenon. The conceptual frameworks used so far to understand cancer, from its origin to the development of therapeutics to treat, are based on the deep-rooted notion that cancer is a single disease with diverse molecular manifestations in different organ sites. This notion seems to be strongly subscribed to and is used for diagnostics and therapeutic development as it offers an opportunity for clinical intervention. Interestingly, a general framework for oncology drug discovery is based on the ability to target an up-regulated molecule, in many cases a protein. A critical gap in this approach is the missing knowledge about the cause of events leading to up-regulation. Expression of a protein resulting from a gene fusion, like BCR-ABL, is easy to address by inhibitors, but they represent a rare genetic phenomenon leading to cancers. Even in those cases where the drugs prove effective, how sure are we that the underlying causes of molecular dysregulation are re-balanced by the therapy? \u0000 \u0000 \u0000THE JOURNEY OF ONCOLOGY AS A FIELD, FROM A FIELD TO STUDY TUMORS OF UNKNOWN ETIOLOGY AND CHARACTERISTICS, HAS BEEN VERY EVENTFUL FOR THE HUMAN RACE, BUT SEEMS BE HIJACKED BY COMPULSIONS OF ONCOONOOMICS, A TERM I SUGGEST TO PARTLY DESCRIBE THE ECONOMICS OF ONCOLOGY DRUG DISCOVERY AND DEVELOPMENT AND THE PAYER DYNAMICS. \u0000 \u0000 \u0000The Journey of Oncology as a field, from a field to study tumors of unknown etiology and characteristics, has been very eventful for the human race, but seems to be hijacked by the compulsions of onconomics, a term I suggest to partly describe the ","PeriodicalId":52464,"journal":{"name":"Journal of Carcinogenesis","volume":"13 ","pages":"6"},"PeriodicalIF":0.0,"publicationDate":"2014-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4103/1477-3163.128641","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32317199","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}