ISRN oncology最新文献

{"title":"Gene expression profile analysis of t1 and t2 breast cancer reveals different activation pathways.","authors":"Margit L H Riis,&nbsp;Xi Zhao,&nbsp;Fateme Kaveh,&nbsp;Hilde S Vollan,&nbsp;Anne-Jorunn Nesbakken,&nbsp;Hiroko K Solvang,&nbsp;Torben Lüders,&nbsp;Ida R K Bukholm,&nbsp;Vessela N Kristensen","doi":"10.1155/2013/924971","DOIUrl":"https://doi.org/10.1155/2013/924971","url":null,"abstract":"<p><p>Breast cancers today are of predominantly T1 (0.1 ≥ 2.0 cm) or T2 (>2 ≤ 5 cm) categories due to early diagnosis. Molecular profiling using microarrays has led to the notion of breast cancer as a heterogeneous disease both clinically and molecularly. Given the prognostic power and clinical use of tumor size, the purpose of this study was to search for molecular signatures characterizing clinical T1 and T2. In total 46 samples were included in the discovery dataset. After adjusting for hormone receptor status, lymph node status, grade, and tumor subclass 441 genes were differently expressed between T1 and T2 tumors. Focal adhesion and extracellular matrix receptor interaction were upregulated in the smaller tumors while p38MAPK signaling and immune-related pathways were more dominant in the larger tumors. The T-size signature was then tested on a validation set of 947 breast tumor samples. Using the T-size expression signatures instead of tumor size leads to a significant difference in risk for distant metastases (P < 0.001). If further confirmed, this molecular signature can be used to select patients with tumor category T1 who may need more aggressive treatment and patients with tumor category T2 who may have less benefit from it.</p>","PeriodicalId":89399,"journal":{"name":"ISRN oncology","volume":" ","pages":"924971"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/924971","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40230010","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":"Vitamin d: are we ready to supplement for breast cancer prevention and treatment?","authors":"Katherine D Crew","doi":"10.1155/2013/483687","DOIUrl":"10.1155/2013/483687","url":null,"abstract":"<p><p>Vitamin D deficiency is a potentially modifiable risk factor that may be targeted for breast cancer prevention and treatment. Preclinical studies support various antitumor effects of vitamin D in breast cancer. Numerous observational studies have reported an inverse association between vitamin D status, including circulating 25-hydroxyvitamin D (25(OH)D) levels, and breast cancer risk. The relationship between vitamin D and mammographic density, a strong predictor of breast cancer risk, remains unclear. Studies analyzing the link between genetic polymorphisms in vitamin D pathway genes and breast cancer incidence and prognosis have yielded inconsistent results. Vitamin D deficiency among breast cancer patients has been associated with poorer clinical outcomes and increased mortality. Despite a number of clinical trials of vitamin D supplementation, the efficacy, optimal dosage of vitamin D, and target blood level of 25(OH)D for breast cancer prevention have yet to be determined. Even with substantial literature on vitamin D and breast cancer, future studies need to focus on gaining a better understanding of the biologic effects of vitamin D in breast tissue. Despite compelling data from experimental and observational studies, there is still insufficient data from clinical trials to make recommendations for vitamin D supplementation for breast cancer prevention or treatment.</p>","PeriodicalId":89399,"journal":{"name":"ISRN oncology","volume":" ","pages":"483687"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3600307/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40230011","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":"Relationship between Metabolic Syndrome and History of Cervical Cancer among a US National Population.","authors":"Eribeth K Penaranda,&nbsp;Navkiran Shokar,&nbsp;Melchor Ortiz","doi":"10.1155/2013/840964","DOIUrl":"https://doi.org/10.1155/2013/840964","url":null,"abstract":"<p><p>The metabolic changes present in the metabolic syndrome (MetS) have been associated with increased risk of pancreatic and colon cancers; however, there is little information about the association between MetS and cervical cancer risk. We performed a case-control study using data from the National Health and Nutrition Examination Survey (NHANES) between 1999-2010. We identified women 21 years of age and older, of which an estimated 585,924 (2.3% of the sample) self-reported a history of cervical cancer (cases). About half (48.6%) of cases and 33.2% of controls met criteria for MetS. Logistic regression analysis showed increased odds of history of cervical cancer among women with MetS (OR = 1.9; 95% CI 1.06, 3.42; P value ≤ 0.05) for the risk of history of cervical cancer among women with MetS while adjusting for other known risk factors (high number of lifetime sexual partners, multiparty, history of hormonal contraceptive use, and history of smoking) (AOR = 1.82; 95% CI 1.02, 3.26; P value ≤ 0.05). In this US surveyed population we found increased odds of history of cervical cancer among subjects with MetS.</p>","PeriodicalId":89399,"journal":{"name":"ISRN oncology","volume":"2013 ","pages":"840964"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/840964","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31257595","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":"Decreasing frequency of osteonecrosis of the jaw in cancer and myeloma patients treated with bisphosphonates: the experience of the oncology network of piedmont and aosta valley (north-Western Italy).","authors":"Vittorio Fusco,&nbsp;Claudia Galassi,&nbsp;Alfredo Berruti,&nbsp;Cinzia Ortega,&nbsp;Libero Ciuffreda,&nbsp;Matteo Scoletta,&nbsp;Franco Goia,&nbsp;Mario Migliario,&nbsp;Anna Baraldi,&nbsp;Mario Boccadoro,&nbsp;Anastasios Loidoris,&nbsp;Oscar Bertetto","doi":"10.1155/2013/672027","DOIUrl":"https://doi.org/10.1155/2013/672027","url":null,"abstract":"<p><p>Background. Data concerning frequency of Osteonecrosis of Jaws (ONJ) are mostly based on single center experiences. Patients and Methods. Since 2005 a multidisciplinary study group collected data of cases of ONJ in patients treated with Bisphosphonates (BP) and observed in oncology and hematology centers of a regional network. Results. By December 2008, 221 cases were registered. We report details of 200 cases, identified after cross-checking reports from centres of medical oncology, haematology, and oral care. Primary neoplasm was breast cancer (39%), myeloma (32%), prostate cancer (16%), and other types of cancer (8%). In about 50% of the cases a history of dental extraction was present. Zoledronic acid was administered (alone or with other BP) to 178 patients (89%). Median time from first infusion to ONJ diagnosis was 21.0 (zoledronic acid only) and 39.0 months (pamidronate only). The number of ONJ cases per year was 3 in 2003, 21 in 2004, 58 in 2005, 60 in 2006, 37 in 2007, and 21 in 2008. Conclusion. The number of new ONJ cases in cancer and myeloma patients increased until 2006 and then reduced. The possible reasons of this trend (introduction of zoledronic acid; increase of ONJ awareness; diffusion of preventive dental measures; late modifications of BP prescription) are herein discussed.</p>","PeriodicalId":89399,"journal":{"name":"ISRN oncology","volume":" ","pages":"672027"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/672027","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40228976","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":"Epigenetic influences in the aetiology of cancers arising from breast and prostate: a hypothesised transgenerational evolution in chromatin accessibility.","authors":"Francis L Martin","doi":"10.1155/2013/624794","DOIUrl":"10.1155/2013/624794","url":null,"abstract":"<p><p>Epidemiological studies have consistently supported the notion that environmental and/or dietary factors play a central role in the aetiology of cancers of the breast and prostate. However, for more than five decades investigators have failed to identify a single cause-and-effect factor, which could be implicated; identification of a causative entity would allow the implementation of an intervention strategy in at-risk populations. This suggests a more complex pathoaetiology for these cancer sites, compared to others. When one examines the increases or decreases in incidence of specific cancers amongst migrant populations, it is notable that disease arising in colon or stomach requires one or at most two generations to exhibit a change in incidence to match that of high-incidence regions, whereas for breast or prostate cancer, at least three generations are required. This generational threshold could suggest a requirement for nonmutation-driven epigenetic alterations in the F0/F1 generations (parental/offspring adopting a more westernized lifestyle), which then predisposes the inherited genome of subsequent generations to mutagenic/genotoxic alterations leading to the development of sporadic cancer in these target sites. As such, individual susceptibility to carcinogen insult would not be based per se on polymorphisms in activating/detoxifying/repair enzymes, but on elevated accessibility of crucial target genes (e.g., oncogenes, tumour suppressor genes) or hotspots therein to mutation events. This could be termed a genomic susceptibility organizational structure (SOS). Several exposures including alcohol and heavy metals are epigens (i.e., modifiers of the epigenome), whereas others are mutagenic/genotoxic, for example, heterocyclic aromatic amines; humans are continuously and variously exposed to mixtures of these agents. Within such a transgenerational multistage model of cancer development, determining the interaction between epigenetic modification to generate a genomic SOS and genotoxic insult will facilitate a new level of understanding in the aetiology of cancer.</p>","PeriodicalId":89399,"journal":{"name":"ISRN oncology","volume":"2013 ","pages":"624794"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3574745/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31257133","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":"Intercostobrachial nerves as a novel anatomic landmark for dividing the axillary space in lymph node dissection.","authors":"Jianyi Li,&nbsp;Yang Zhang,&nbsp;Wenhai Zhang,&nbsp;Shi Jia,&nbsp;Xi Gu,&nbsp;Yan Ma,&nbsp;Dan Li","doi":"10.1155/2013/279013","DOIUrl":"https://doi.org/10.1155/2013/279013","url":null,"abstract":"<p><p>Purpose. Our aim was to assess the feasibility of using the intercostobrachial nerves (ICBNs) as a possible new anatomic landmark for axillaries lymph node dissection in breast cancer patients. Background Data Summary. The preservation of ICBN is now an accepted procedure in this type of dissection; however, it could be improved further to reduce the number of postoperative complications. The axillary space is divided into lower and upper parts by the ICBN-a thorough investigation of the metastasis patterns in lymph nodes found in this area could supply new information leading to such improvements. Methods. Seventy-two breast cancer patients, all about to undergo lymph node dissection and with sentinel lymph nodes identified, were included in this trial. The lymph nodes were collected in two groups, from lower and upper axillary spaces, relative to the intercostobrachial nerves. The first group was further subdivided into sentinel (SLN) and nonsentinel (non-SLN) nodes. All lymph nodes were tested to detect macro- and micrometastasis. Results. All the sentinel lymph nodes were found under the intercostobrachial nerves; more than 10 lymph nodes were located in that space. Moreover, when lymph nodes macrometastasize or micrometastasize above the intercostobrachial nerves, we also observe metastasis-positive nodes under the nerves; when the lower group nodes show no metastasis, the upper group is also metastasis free. Conclusions. Our results show that the intercostobrachial nerves are good candidates for a new anatomic landmark to be used in lymph node dissection procedure.</p>","PeriodicalId":89399,"journal":{"name":"ISRN oncology","volume":"2013 ","pages":"279013"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/279013","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31231715","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":"ENETS TNM Staging Predicts Prognosis in Small Bowel Neuroendocrine Tumours.","authors":"Rajaventhan Srirajaskanthan,&nbsp;A Ahmed,&nbsp;A Prachialias,&nbsp;P Srinivasan,&nbsp;N Heaton,&nbsp;N Jervis,&nbsp;A Quaglia,&nbsp;G Vivian,&nbsp;J K Ramage","doi":"10.1155/2013/420795","DOIUrl":"https://doi.org/10.1155/2013/420795","url":null,"abstract":"<p><p>Introduction. Small bowel neuroendocrine tumours (NETs) are the most common type of gastrointestinal neuroendocrine tumours. The incidence and prevalence of these tumours are on the rise. The aims of this study were to determine prognostic clinicopathological features and whether the ENETS TNM staging system predicts prognosis and also. Method. Clinical data was collected retrospectively from 138 patients with histologically proven small bowel NETs managed at King's College Hospital. Histology was reviewed and small bowels tumours, were staged according to the ENETS TNM staging system. Results. Median age was 65 years (range 29-87). The 5-year survival was 79.5% and the 10-year survival was 48.5%. Resection of the primary tumour was associated with improved survival (120 versus 56 months, P < 0.05). On multivariate analysis prognostic factors were primary tumour resection and not having a carcinoid heart disease. TNM staging significantly separated survival of stage 2 and stage 3 from stage 4 NETs. Conclusion. Small bowel primary tumour resection and not having carcinoid heart disease are prognostic factors. The ENETS TNM staging and grading system appears to be of prognostic relevance to small bowel NETs.</p>","PeriodicalId":89399,"journal":{"name":"ISRN oncology","volume":" ","pages":"420795"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/420795","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40228975","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":"Tumor Inhibition by DepoVax-Based Cancer Vaccine Is Accompanied by Reduced Regulatory/Suppressor Cell Proliferation and Tumor Infiltration.","authors":"Mohan Karkada,&nbsp;Tara Quinton,&nbsp;Rachelle Blackman,&nbsp;Marc Mansour","doi":"10.1155/2013/753427","DOIUrl":"https://doi.org/10.1155/2013/753427","url":null,"abstract":"<p><p>A successful cancer vaccine needs to overcome the effects of immune-suppressor cells such as Treg lymphocytes, suppressive cytokine-secreting Tr1 cells, and myeloid-derived suppressor cells (MDSCs), while enhancing tumor-specific immune responses. Given the relative poor efficacy associated with current cancer vaccines, a novel vaccine platform called DepoVax(TM) (DPX) was developed. C3 tumor-challenged mice were immunized with HPV-E7 peptide in DPX- or conventional-emulsion- (CE-) based vaccine. While control mice showed marked increase in Treg/MDSCs in spleen and blood, in mice treated with DPX-E7 the levels remained similar to tumor-free naive mice. Such differences were also seen within the tumor. Antigen-specific IL10-secreting CD4/CD8 T cells and TGF- β (+)CD8(+) T cell frequencies were increased significantly in CE-treated and control mice in contrast to DPX-E7-immunized mice. Analysis of tumor-infiltrating cells revealed higher frequency of suppressor cells in untreated controls than in DPX-E7 group while the converse was true for tumor-infiltrating CD8 T cells. Immunization of tumor-bearing HLA-A2 transgenic mice with human vaccine DPX-0907, a peptide-based vaccine for breast/ovarian/prostate cancers, showed efficient induction of immune response to cancer peptides despite the presence of suppressor cells. Thus, this study provides the rationale for using DPX-based cancer vaccines in immune-suppressed cancer patients, to induce effective anticancer immunity.</p>","PeriodicalId":89399,"journal":{"name":"ISRN oncology","volume":" ","pages":"753427"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/753427","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40228977","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":"Diabetes and risk of cancer.","authors":"Samy L Habib,&nbsp;Maciej Rojna","doi":"10.1155/2013/583786","DOIUrl":"https://doi.org/10.1155/2013/583786","url":null,"abstract":"<p><p>Diabetes and cancer represent two complex, diverse, chronic, and potentially fatal diseases. Cancer is the second leading cause of death, while diabetes is the seventh leading cause of death with the latter still likely underreported. There is a growing body of evidence published in recent years that suggest substantial increase in cancer incidence in diabetic patients. The worldwide prevalence of diabetes was estimated to rise from 171 million in 2000 to 366 million in 2030. About 26.9% of all people over 65 have diabetes and 60% have cancer. Overall, 8-18% of cancer patients have diabetes. In the context of epidemiology, the burden of both diseases, small association between diabetes and cancer will be clinically relevant and should translate into significant consequences for future health care solutions. This paper summarizes most of the epidemiological association studies between diabetes and cancer including studies relating to the general all-site increase of malignancies in diabetes and elevated organ-specific cancer rate in diabetes as comorbidity. Additionally, we have discussed the possible pathophysiological mechanisms that likely may be involved in promoting carcinogenesis in diabetes and the potential of different antidiabetic therapies to influence cancer incidence.</p>","PeriodicalId":89399,"journal":{"name":"ISRN oncology","volume":"2013 ","pages":"583786"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/583786","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31296163","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":"Pathways to breast cancer recurrence.","authors":"Aamir Ahmad","doi":"10.1155/2013/290568","DOIUrl":"https://doi.org/10.1155/2013/290568","url":null,"abstract":"<p><p>Breast cancer remains a deadly disease, even with all the recent technological advancements. Early intervention has made an impact, but an overwhelmingly large number of breast cancer patients still live under the fear of \"recurrent\" disease. Breast cancer recurrence is clinically a huge problem and one that is largely not well understood. Over the years, a number of factors have been studied with an overarching aim of being able to prognose recurrent disease. This paper attempts to provide an overview of our current knowledge of breast cancer recurrence and its associated challenges. Through a survey of the literature on cancer stem cells (CSCs), epithelial-mesenchymal transition (EMT), various signaling pathways such as Notch/Wnt/hedgehog, and microRNAs (miRNAs), we also examine the hypotheses that are currently under investigation for the prevention of breast cancer recurrence.</p>","PeriodicalId":89399,"journal":{"name":"ISRN oncology","volume":" ","pages":"290568"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/290568","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40228974","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}