Journal of Carcinogenesis最新文献

{"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}

{"title":"Novel agents in the management of castration resistant prostate cancer.","authors":"Shruti Chaturvedi,&nbsp;Jorge A Garcia","doi":"10.4103/1477-3163.128185","DOIUrl":"https://doi.org/10.4103/1477-3163.128185","url":null,"abstract":"<p><p>Prostate cancer (PCa) is a leading cause of cancer mortality in men and despite high cure rates with surgery and/or radiation, 30-40% of patients will eventually develop advanced disease. Androgen deprivation is the first line therapy for standard of care for men with advanced disease. Eventually however all men will progress to castration-resistant prostate cancer (CRPC). Insight into the molecular mechanisms of androgen resistance has led to the development of alternative novel hormonal agents. Newer hormonal agents such as abiraterone, enzalutamide and TOK-001; and the first cancer vaccine, Sipuleucel T have been approved for use in men with CRPC. The recognition of the importance of bone health and morbidity associated with skeletal related events has led to the introduction of the receptor activator of nuclear factor kappa-B-ligand inhibitor denosumab. Other molecularly targeted therapies have shown promise in pre-clinical studies, but this has not consistently translated into clinical efficacy. It is increasingly evident that CRPC is a heterogeneous disease and an individualized approach directed at identifying primary involvement of specific pathways could maximize the benefit from targeted therapies. This review focuses on targeted therapy for PCa with special emphasis on therapies that have been Food and Drug Administration approved for use in men with CRPC. </p>","PeriodicalId":52464,"journal":{"name":"Journal of Carcinogenesis","volume":"13 ","pages":"5"},"PeriodicalIF":0.0,"publicationDate":"2014-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4103/1477-3163.128185","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32317200","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":"Targeted therapy for renal cell carcinoma: The next lap.","authors":"Ravindran Kanesvaran,&nbsp;Min-Han Tan","doi":"10.4103/1477-3163.127638","DOIUrl":"https://doi.org/10.4103/1477-3163.127638","url":null,"abstract":"<p><p>Advances in rationally targeted therapeutics over the last decade have transformed the clinical care of advanced kidney cancer. While oncologists consolidate the gains of the wave of new agents, comprising a panoply of anti-vascular endothelial growth factor multi-targeted tyrosine kinase inhibitors and inhibitors of the mammalian target of rapamycin (mTOR), there is an increasing sense that a plateau has been reached in the short term. It is sobering that all currently approved targeted therapies have not yielded durable remissions and remain palliative in intent. In the context of recent insights in kidney cancer biology, we review promising ongoing and future approaches for kidney cancer therapeutics aimed toward forging new paths in the systemic management of renal cell carcinoma. Broadly, candidate agents for such innovative strategies include immune check-point inhibitors, anti-cancer stem cell agents, next-generation anti-vascular endothelial growth factor receptor and anti-mTOR agents as well as more investigational agents in the preclinical and early clinical development settings. </p>","PeriodicalId":52464,"journal":{"name":"Journal of Carcinogenesis","volume":"13 ","pages":"3"},"PeriodicalIF":0.0,"publicationDate":"2014-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4103/1477-3163.127638","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32267769","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":"Targeted therapy in gastrointestinal malignancies.","authors":"Ravi Chhatrala,&nbsp;Yasmin Thanavala,&nbsp;Renuka Iyer","doi":"10.4103/1477-3163.127639","DOIUrl":"https://doi.org/10.4103/1477-3163.127639","url":null,"abstract":"<p><p>Increased understanding of cancer pathogenesis has identified several pathways that serve as potential targets for novel targeted agents in development. The selection of targeted cancer therapy based on biomarkers has instigated a new era of personalized medicine and changed the way we practice oncology. Many targeted agents are approved for treatment of gastrointestinal malignancies most targeting tumor angiogenesis, and many more are in different phases of development. Here we briefly summarize nine different targeted agents that are approved currently in the U.S. and several other agents currently being studied in various gastrointestinal cancers. </p>","PeriodicalId":52464,"journal":{"name":"Journal of Carcinogenesis","volume":"13 ","pages":"4"},"PeriodicalIF":0.0,"publicationDate":"2014-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4103/1477-3163.127639","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32267770","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":"Antisense oligonucleotides directed against insulin-like growth factor-II messenger ribonucleic acids delay the progress of rat hepatocarcinogenesis.","authors":"Miltu Kumar Ghosh,&nbsp;Falguni Patra,&nbsp;Shampa Ghosh,&nbsp;Chowdhury Mobaswar Hossain,&nbsp;Biswajit Mukherjee","doi":"10.4103/1477-3163.126761","DOIUrl":"https://doi.org/10.4103/1477-3163.126761","url":null,"abstract":"<p><strong>Background: </strong>Hepatocellular carcinoma (HCC) is a multistep complex process, caused by many of genetic alteration. Insulin-like growth factors and their receptor have been widely implicated to HCC. Insulin-like growth factor-II (IGF-II) is a mitogenic polypeptide, found in various fetal and neonatal tissues of humans and rats and expresses in HCC. Here we investigated anticancer potential of phosphorothioate antisense oligonucleotides (ASOs) against three coding exons (exon-1/exon-2/exon-3) of IGF-II messenger ribonucleic acid in rat hepatocarcinogenesis model.</p><p><strong>Materials and methods: </strong>During diethylnitrosamine and 2-acetylaminofluorene induced hepatocarcinogenesis, rats were treated with ASOs. Various biochemical and histological studies were conducted.</p><p><strong>Results: </strong>About 40% of carcinogen treated rats, which received two oligomers (against exon-1 or-3) did not show any hepatic lesion, hyperplastic nodule or tumor and remaining 60% of those rats showed lesion incidence and had about 59% and 55% reductions in the numbers of hepatic altered foci, respectively. Reductions in the total lesion-area when compared with carcinogen control rats were 64% and 53%, respectively for the animals treated with carcinogen and received the ASOs against exon-1/-3. Fluorescein isothiocyanate-labeled ASO reached in the hepatocytes in 2 h. No predominant IGF-II overexpression was observed in case of rats treated with the two ASOs. Treatment of the antisense IGF-II oligomers in carcinogen treated rats show better hepatocellular integrity along with several preneoplastic/neoplastic marker isoenzyme/enzyme modulations.</p><p><strong>Conclusions: </strong>Two of the three antisense oligomer-types effectively controlled IGF-II overexpression, causing the delay of the development and/or progress of hepatic cancer in rats.</p>","PeriodicalId":52464,"journal":{"name":"Journal of Carcinogenesis","volume":"13 ","pages":"2"},"PeriodicalIF":0.0,"publicationDate":"2014-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4103/1477-3163.126761","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32266755","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}