ISRN oncologyPub Date : 2013-06-25Print Date: 2013-01-01DOI: 10.1155/2013/463594
M Galukande, H Wabinga, F Mirembe, C Karamagi, A Asea
{"title":"Difference in Risk Factors for Breast Cancer by ER Status in an Indigenous African Population.","authors":"M Galukande, H Wabinga, F Mirembe, C Karamagi, A Asea","doi":"10.1155/2013/463594","DOIUrl":"10.1155/2013/463594","url":null,"abstract":"<p><p>Introduction. Breast cancer is the commonest cancer among women globally. In Uganda, it is on the rise, projected at a 4.5% annual ASR increase (age standardized incidence rate). The reasons for this steep increase are not fully established. In the recent past, gene profiling in tumor tissues suggests that breast cancers are divided into subtypes dependent on the presence or absence of oestrogen receptor, progesterone, and human epidermal growth factor receptor 2 (HER 2). These subtypes do have distinctive clinical outcomes and perhaps risk factors from past studies. There is paucity of data on hormonal receptor status and the traditionally known risk factors in sub-Saharan Africa. The purpose of this study therefore was to establish the differences between ER status and the traditionally known risk factors for breast cancer in Uganda. Methods. An observational analytical hospital, based study, carried out at Makerere University, College of Health Sciences. Formalin fixed and paraffin imbedded sections were prepared for haemotoxylin and eosin (H&E) stains and immunohistochemistry (IHC). Ethical approval was obtained. Results. A total of 113 women were recruited. Mean age was 45 years (SD14). There were no significant differences in selected risk factors (setting, age, contraceptive use, parity, breast feeding, or menarche) by ER status although ER negative tumors had significantly higher grade tumors (by a factor of two) compared to ER positive tumors. Conclusion. There were no significant differences among risk factors by ER status contrary to what several other studies suggest. The manifestation of breast cancer in Africa warrants further extensive inquiry. </p>","PeriodicalId":89399,"journal":{"name":"ISRN oncology","volume":"2013 ","pages":"463594"},"PeriodicalIF":0.0,"publicationDate":"2013-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3708443/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31649960","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}
ISRN oncologyPub Date : 2013-06-16Print Date: 2013-01-01DOI: 10.1155/2013/238017
Natasha D Buchanan, Jessica B King, Juan L Rodriguez, Arica White, Katrina F Trivers, Laura P Forsythe, Erin E Kent, Julia H Rowland, Susan A Sabatino
{"title":"Changes among US Cancer Survivors: Comparing Demographic, Diagnostic, and Health Care Findings from the 1992 and 2010 National Health Interview Surveys.","authors":"Natasha D Buchanan, Jessica B King, Juan L Rodriguez, Arica White, Katrina F Trivers, Laura P Forsythe, Erin E Kent, Julia H Rowland, Susan A Sabatino","doi":"10.1155/2013/238017","DOIUrl":"10.1155/2013/238017","url":null,"abstract":"<p><p>Background. Differences in healthcare and cancer treatment for cancer survivors in the United States (US) have not been routinely examined in nationally representative samples or studied before and after important Institute of Medicine (IOM) recommendations calling for higher quality care provision and attention to comprehensive cancer care for cancer survivors. Methods. To assess differences between survivor characteristics in 1992 and 2010, we conducted descriptive analyses of 1992 and 2010 National Health Interview Survey (NHIS) data. Our study sample consisted of 1018 self-reported cancer survivors from the 1992 NHIS and 1718 self-reported cancer survivors from the 2010 NHIS who completed the Cancer Control (CCS) and Cancer Epidemiology (CES) Supplements. Results. The prevalence of reported survivors increased from 1992 to 2010 (4.2% versus 6.3%). From 1992 to 2010, there was an increase in long-term cancer survivors and a drop in multiple malignancies, and surgery remained the most widely used treatment. Significantly fewer survivors (<10 years after diagnosis) were denied insurance coverage. Survivors continue to report low participation in counseling or support groups. Conclusions. As the prevalence of cancer survivors continues to grow, monitoring differences in survivor characteristics can be useful in evaluating the effects of policy recommendations and the quality of clinical care. </p>","PeriodicalId":89399,"journal":{"name":"ISRN oncology","volume":"2013 ","pages":"238017"},"PeriodicalIF":0.0,"publicationDate":"2013-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/238017","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31572052","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}
ISRN oncologyPub Date : 2013-06-12Print Date: 2013-01-01DOI: 10.1155/2013/385398
Deimante Tamkus, Alla Sikorskii, Kathleen A Gallo, David A Wiese, Cheryl Leece, Burra V Madhukar, Simona C Chivu, Shalini Chitneni, Nikolay V Dimitrov
{"title":"Endothelin-1 enriched tumor phenotype predicts breast cancer recurrence.","authors":"Deimante Tamkus, Alla Sikorskii, Kathleen A Gallo, David A Wiese, Cheryl Leece, Burra V Madhukar, Simona C Chivu, Shalini Chitneni, Nikolay V Dimitrov","doi":"10.1155/2013/385398","DOIUrl":"https://doi.org/10.1155/2013/385398","url":null,"abstract":"<p><p>Introduction. Breast cancer recurrence can develop years after primary treatment. Crosstalk between breast cancer cells and their stromal microenvironment may influence tumor progression. Our primary study aim was to determine whether endothelin-1 (ET-1) expression in tumor and stroma predicts breast cancer relapse. The secondary aim was to determine ET-1/endothelin receptor A (ETAR) role on signaling pathways and apoptosis in breast cancer. Experimental Design. Patients with histologically documented stages I-III invasive breast cancer were included in the study. ET-1 expression by immunohistochemistry (IHC) in tumor cells and stroma was analyzed. Association between ET-1 expression and clinical outcome was assessed using multivariate Cox proportional hazard model. Kaplan-Meier curves were used to estimate disease-free survival (DFS). In addition, the effect of ET-1/ETAR on signaling pathways and apoptosis was evaluated in MCF-7 and MDA-MB-231 breast cancer cells. Results. With a median followup of 7 years, ET-1 non-enriched tumor phenotype had a significant association with favorable disease-free survival (HR = 0.16; 95% CI 0.03-0.77; P value <0.02). ER negativity, advanced stage of disease and ET-1-enriched tumor phenotype were all associated with a higher risk for recurrence. Experimental study demonstrated that ET-1 stimulation promoted Akt activation in MCF-7 and MDA-MB-231 cells. Furthermore, silencing of ETAR induced apoptosis in both hormone receptor negative and hormone receptor positive breast cancer cells. Conclusions. We found ET-1 expression in tumor and stroma to be an independent prognostic marker for breast cancer recurrence. Prospective studies are warranted to examine whether ET-1 expression in tumor/stroma could assist in stratifying patients with hormone receptor positive breast cancer for adjuvant therapy. </p>","PeriodicalId":89399,"journal":{"name":"ISRN oncology","volume":"2013 ","pages":"385398"},"PeriodicalIF":0.0,"publicationDate":"2013-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/385398","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31572053","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}
ISRN oncologyPub Date : 2013-06-11Print Date: 2013-01-01DOI: 10.1155/2013/371854
Edwin Bremer
{"title":"Targeting of the tumor necrosis factor receptor superfamily for cancer immunotherapy.","authors":"Edwin Bremer","doi":"10.1155/2013/371854","DOIUrl":"https://doi.org/10.1155/2013/371854","url":null,"abstract":"<p><p>The tumor necrosis factor (TNF) ligand and cognate TNF receptor superfamilies constitute an important regulatory axis that is pivotal for immune homeostasis and correct execution of immune responses. TNF ligands and receptors are involved in diverse biological processes ranging from the selective induction of cell death in potentially dangerous and superfluous cells to providing costimulatory signals that help mount an effective immune response. This diverse and important regulatory role in immunity has sparked great interest in the development of TNFL/TNFR-targeted cancer immunotherapeutics. In this review, I will discuss the biology of the most prominent proapoptotic and co-stimulatory TNF ligands and review their current status in cancer immunotherapy. </p>","PeriodicalId":89399,"journal":{"name":"ISRN oncology","volume":"2013 ","pages":"371854"},"PeriodicalIF":0.0,"publicationDate":"2013-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/371854","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31569398","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}
ISRN oncologyPub Date : 2013-06-06Print Date: 2013-01-01DOI: 10.1155/2013/305371
Gaetano Romano
{"title":"Deregulations in the cyclin-dependent kinase-9-related pathway in cancer: implications for drug discovery and development.","authors":"Gaetano Romano","doi":"10.1155/2013/305371","DOIUrl":"https://doi.org/10.1155/2013/305371","url":null,"abstract":"<p><p>The CDK9-related pathway is an important regulator of mammalian cell biology and is also involved in the replication cycle of several viruses, including the human immunodeficiency virus type 1. CDK9 is present in two isoforms termed CDK9-42 and CDK9-55 that bind noncovalently type T cyclins and cyclin K. This association forms a heterodimer, where CDK9 carries the enzymatic site and the cyclin partner functions as a regulatory subunit. This heterodimer is the main component of the positive transcription elongation factor b, which stabilizes RNA elongation via phosphorylation of the RNA pol II carboxyl terminal domain. Abnormal activities in the CDK9-related pathway were observed in human malignancies and cardiac hypertrophies. Thus, the elucidation of the CDK9 pathway deregulations may provide useful insights into the pathogenesis and progression of human malignancies, cardiac hypertrophy, AIDS and other viral-related maladies. These studies may lead to the improvement of kinase inhibitors for the treatment of the previously mentioned pathological conditions. This review describes the CDK9-related pathway deregulations in malignancies and the development of kinase inhibitors in cancer therapy, which can be classified into three categories: antagonists that block the ATP binding site of the catalytic domain, allosteric inhibitors, and small molecules that disrupt protein-protein interactions. </p>","PeriodicalId":89399,"journal":{"name":"ISRN oncology","volume":"2013 ","pages":"305371"},"PeriodicalIF":0.0,"publicationDate":"2013-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/305371","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31569396","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}
ISRN oncologyPub Date : 2013-05-30Print Date: 2013-01-01DOI: 10.1155/2013/697521
Maria E Ramos-Nino
{"title":"The role of chronic inflammation in obesity-associated cancers.","authors":"Maria E Ramos-Nino","doi":"10.1155/2013/697521","DOIUrl":"10.1155/2013/697521","url":null,"abstract":"<p><p>There is a strong relationship between metabolism and immunity, which can become deleterious under conditions of metabolic stress. Obesity, considered a chronic inflammatory disease, is one example of this link. Chronic inflammation is increasingly being recognized as an etiology in several cancers, particularly those of epithelial origin, and therefore a potential link between obesity and cancer. In this review, the connection between the different factors that can lead to the chronic inflammatory state in the obese individual, as well as their effect in tumorigenesis, is addressed. Furthermore, the association between obesity, inflammation, and esophageal, liver, colon, postmenopausal breast, and endometrial cancers is discussed. </p>","PeriodicalId":89399,"journal":{"name":"ISRN oncology","volume":"2013 ","pages":"697521"},"PeriodicalIF":0.0,"publicationDate":"2013-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/697521","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31550223","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}
ISRN oncologyPub Date : 2013-05-23Print Date: 2013-01-01DOI: 10.1155/2013/362467
Katarina Sevcikova, Bibiana Vertakova-Krakovska, Stanislav Spanik
{"title":"Neoadjuvant Treatment in Patients with HER2-Positive Breast Cancer.","authors":"Katarina Sevcikova, Bibiana Vertakova-Krakovska, Stanislav Spanik","doi":"10.1155/2013/362467","DOIUrl":"10.1155/2013/362467","url":null,"abstract":"<p><p>Approximately 20%-25% of patients with breast cancer demonstrate amplification of the human epidermal receptor type 2 (HER2) gene, resulting in an overexpression of the HER2 receptor. This overexpression is associated with aggressive disease, relatively poor prognosis, and worse clinical outcomes. Neoadjuvant therapy is the standard treatment in patients with locally advanced, inflammatory, or inoperable primary breast cancer. It is generally used to downstage the tumors and therefore to improve surgical options including breast-conserving surgery rather than mastectomy. It has been confirmed that patients with pathological complete response (pCR) to neoadjuvant treatment have better disease-free survival (DFS) and overall survival (OS). Neoadjuvant treatment can also serve as in vivo test of sensitivity to the used therapeutic regimen. The preferred neoadjuvant approach to patients with HER2-positive breast cancer is a sequential anthracycline-taxane-based chemotherapy in combination with trastuzumab. Addition of other anti-HER2 agents has increased pCR rate up to 75% and will probably become a new therapeutic direction. In the first part of this paper, we summarize the information about HER2-positive breast cancer, the various treatment possibilities, and the results of the major neoadjuvant trials. The second part focuses on the data concerning the importance of pCR and the potential risk of cardiotoxicity associated with this treatment.</p>","PeriodicalId":89399,"journal":{"name":"ISRN oncology","volume":"2013 ","pages":"362467"},"PeriodicalIF":0.0,"publicationDate":"2013-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/362467","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31503622","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}
ISRN oncologyPub Date : 2013-05-15Print Date: 2013-01-01DOI: 10.1155/2013/673793
Masahiro Toda
{"title":"Glioma stem cells and immunotherapy for the treatment of malignant gliomas.","authors":"Masahiro Toda","doi":"10.1155/2013/673793","DOIUrl":"https://doi.org/10.1155/2013/673793","url":null,"abstract":"<p><p>Stem cell research has led to the discovery of glioma stem cells (GSCs), and because these cells are resistant to chemotherapy and radiotherapy, analysis of their properties has been rapidly pursued for targeted treatment of malignant glioma. Recent studies have also revealed complex crosstalk between GSCs and their specialized environment (niche). Therefore, targeting not only GSCs but also their niche may be a principle for novel therapies of malignant glioma. One possible novel strategy for targeting GSCs and their niches is immunotherapy with different antitumor mechanism(s) from those of conventional therapy. Recent clinical studies of immunotherapy using peptide vaccines and antibodies have shown promising results. This review describes the recent findings related to GSCs and their niches, as well as immunotherapies for glioma, followed by discussion of immunotherapies that target GSCs for the treatment of malignant glioma.</p>","PeriodicalId":89399,"journal":{"name":"ISRN oncology","volume":"2013 ","pages":"673793"},"PeriodicalIF":0.0,"publicationDate":"2013-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/673793","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31503625","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}
ISRN oncologyPub Date : 2013-04-18Print Date: 2013-01-01DOI: 10.1155/2013/680136
Anastasia V Suhovskih, Lyudmila A Mostovich, Igor S Kunin, Mekhrozhiddin M Boboev, Galina I Nepomnyashchikh, Svetlana V Aidagulova, Elvira V Grigorieva
{"title":"Proteoglycan expression in normal human prostate tissue and prostate cancer.","authors":"Anastasia V Suhovskih, Lyudmila A Mostovich, Igor S Kunin, Mekhrozhiddin M Boboev, Galina I Nepomnyashchikh, Svetlana V Aidagulova, Elvira V Grigorieva","doi":"10.1155/2013/680136","DOIUrl":"https://doi.org/10.1155/2013/680136","url":null,"abstract":"<p><p>Proteoglycans (PGs) are expressed on the cell surface and extracellular matrix of all mammalian cells and tissues, playing an important role in cell-cell and cell-matrix interactions and signaling. Changes in the expression and functional properties of individual PGs in prostate cancer are shown, although common patterns of PGs expression in normal and tumour prostate tissues remain unknown. In this study, expression of cell surface and stromal proteoglycans (glypican-1, perlecan, syndecan-1, aggrecan, versican, NG2, brevican, decorin, and lumican) in normal tissue and prostate tumours was determined by RT-PCR analysis and immunostaining with core protein- and GAG-specific antibodies. In normal human prostate tissue, versican, decorin, and biglycan were predominant proteoglycans localised in tissue stroma, and syndecan-1 and glypican-1 were expressed mainly by epithelial cells. In prostate tumours, complex changes in proteoglycans occur, with a common trend towards decrease of decorin and lumican expression, overall increase of syndecan-1 and glypican-1 expression in tumour stroma along with its disappearance in tumour epithelial cells, and aggrecan and NG2 expressions in some prostate tumours. All the changes result in the highly individual proteoglycan expression patterns in different prostate tumours, which may be potentially useful as molecular markers for prostate cancer personalised diagnosis and treatment.</p>","PeriodicalId":89399,"journal":{"name":"ISRN oncology","volume":"2013 ","pages":"680136"},"PeriodicalIF":0.0,"publicationDate":"2013-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/680136","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31444812","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}
ISRN oncologyPub Date : 2013-04-11Print Date: 2013-01-01DOI: 10.1155/2013/214304
Carsten Nieder, Oddvar Spanne, Ellinor Haukland, Astrid Dalhaug
{"title":"Does Time between Imaging Diagnosis and Initiation of Radiotherapy Impact Survival after Whole-Brain Radiotherapy for Brain Metastases?","authors":"Carsten Nieder, Oddvar Spanne, Ellinor Haukland, Astrid Dalhaug","doi":"10.1155/2013/214304","DOIUrl":"https://doi.org/10.1155/2013/214304","url":null,"abstract":"<p><p>Aims. To evaluate whether reduced waiting time influences survival of patients treated with whole-brain radiotherapy (WBRT) for brain metastases. Materials and Methods. Retrospective intention-to-treat study including 110 patients treated with primary WBRT (typically 10 fractions of 3 Gy; no other treatment between diagnosis and WBRT). Uni- and multivariate tests were performed. Results. Median delay between imaging diagnosis and WBRT was 12 days (range 0-66 days). WBRT started within 1 week in 36%, during the second week in 28%, and during the third week in 18% of patients. No significant correlation between waiting time and survival was evident, except for one subgroup of patients. Those without extracranial metastases (potentially more threatened by worse intracranial disease control) survived for a median of 2.5 months from WBRT if waiting time was 2 weeks or longer as compared to 5.6 months if waiting time was shorter than 2 weeks (P = 0.03). The same correlation was seen if survival was computed from imaging diagnosis. Conclusion. If departmental resources are not sufficient to provide immediate WBRT within 2 weeks to all patients, those without extracranial metastases should be prioritised. This study did not address the impact of waiting time on quality of life or symptom palliation.</p>","PeriodicalId":89399,"journal":{"name":"ISRN oncology","volume":"2013 ","pages":"214304"},"PeriodicalIF":0.0,"publicationDate":"2013-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2013/214304","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31445439","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}