Journal of Carcinogenesis (J Carcinog)

Publications in this journal

• Article: Nicotine and lung cancer.

  Graham W Warren, Anurag K Singh
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  ABSTRACT: Tobacco use in cancer patients is associated with increased cancer treatment failure and decreased survival. Nicotine is one of over 7,000 compounds in tobacco smoke and nicotine is the principal chemical associated with addiction. The purpose of this article is to review the tumor promoting activities of nicotine. Nicotine and its metabolites can promote tumor growth through increased proliferation, angiogenesis, migration, invasion, epithelial to mesenchymal transition, and stimulation of autocrine loops associated with tumor growth. Furthermore, nicotine can decrease the biologic effectiveness of conventional cancer treatments such as chemotherapy and radiotherapy. Common mechanisms appear to involve activation of nicotinic acetylcholine receptors and beta-adrenergic receptors leading to downstream activation of parallel signal transduction pathways that facilitate tumor progression and resistance to treatment. Data suggest that nicotine may be an important mechanism by which tobacco promotes tumor development, progression, and resistance to cancer treatment.
  Journal of Carcinogenesis 01/2013; 12:1.
• Article: Cell of origin of lung cancer.

  Jennifer M Hanna, Mark W Onaitis
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  ABSTRACT: Lung cancer is the leading cause of cancer deaths worldwide, and current therapies are disappointing. Elucidation of the cell(s) of origin of lung cancer may lead to new therapeutics. In addition, the discovery of putative cancer-initiating cells with stem cell properties in solid tumors has emerged as an important area of cancer research that may explain the resistance of these tumors to currently available therapeutics. Progress in our understanding of normal tissue stem cells, tumor cell of origin, and cancer stem cells has been hampered by the heterogeneity of the disease, the lack of good in vivo transplantation models to assess stem cell behavior, and an overall incomplete understanding of the epithelial stem cell hierarchy. As such, a systematic computerized literature search of the MEDLINE database was used to identify articles discussing current knowledge about normal lung and lung cancer stem cells or progenitor cells. In this review, we discuss what is currently known about the role of cancer-initiating cells and normal stem cells in the development of lung tumors.
  Journal of Carcinogenesis 01/2013; 12:6.
• Article: Lung cancer screening update.

  Samjot Singh Dhillon, Gregory Loewen, Vijayvel Jayaprakash, Mary E Reid
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  ABSTRACT: Lung cancer is the leading cause of cancer-related mortality globally and the American cancer society estimates approximately 226,160 new cases and 160,340 deaths from lung cancer in the USA in the year 2012. The majority of lung cancers are diagnosed in the later stages which impacts the overall survival. The 5-year survival rate for pathological st age IA lung cancer is 73% but drops to only 13% for stage IV. Thus, early detection through screening and prevention are the keys to reduce the global burden of lung cancer. This article discusses the current state of lung cancer screening, including the results of the National Lung Cancer Screening Trial, the consideration of implementing computed tomography screening, and a brief overview of the role of bronchoscopy in early detection and potential biomarkers that may aid in the early diagnosis of lung cancer.
  Journal of Carcinogenesis 01/2013; 12:2.
• Article: Human endogenous retroviral K element encodes fusogenic activity in melanoma cells.

  Gengming Huang, Zhongwu Li, Xiaohua Wan, Yue Wang, Jianli Dong
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  ABSTRACT: Nuclear atypia with features of multi nuclei have been detected in human melanoma specimens. We found that the K type human endogenous retroviral element (HERV K) is expressed in such cells. Since cellular syncytia can form when cells are infected with retroviruses, we hypothesized that HERV K expressed in melanoma cells may contribute to the formation of multinuclear atypia cells in melanoma. We specifically inhibited HERV K expression using RNA interference (RNAi) and monoclonal antibodies and observed dramatic reduction of intercellular fusion of cultured melanoma cells. Importantly, we identified loss of heterozygosity (LOH)of D19S433 in a cell clone that survived and proliferated after cell fusion. Our results support the notion that proteins encoded by HERV K can mediate intercellular fusion of melanoma cells, which may generate multinuclear cells and drive the evolution of genetic changes that provide growth and survival advantages.
  Journal of Carcinogenesis 01/2013; 12:5.
• Article: Targeted agents in non-small cell lung cancer therapy: What is there on the horizon?

  Victoria M Villaflor, Ravi Salgia
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  ABSTRACT: Lung cancer is a heterogeneous group of diseases. There has been much research in lung cancer over the past decade which has advanced our ability to treat these patients with a more personalized approach. The scope of this paper is to review the literature and give a broad understanding of the current molecular targets for which we currently have therapies as well as other targets for which we may soon have therapies. Additionally, we will cover some of the issues of resistance with these targeted therapies. The molecular targets we intend to discuss are epidermal growth factor receptor (EGFR), Vascular endothelial growth factor (VEGF), anaplastic large-cell lymphoma kinase (ALK), KRAS, C-MET/RON, PIK3CA. ROS-1, RET Fibroblast growth factor receptor (FGFR). Ephrins and their receptors, BRAF, and immunotherapies/vaccines. This manuscript only summarizes the work which has been done to date and in no way is meant to be comprehensive.
  Journal of Carcinogenesis 01/2013; 12:7.
• Article: Lung cancer biomarkers: State of the art.

  Sangeetha Subramaniam, Ram Krishna Thakur, Vinod Kumar Yadav, Ranjan Nanda, Shantanu Chowdhury, Anurag Agrawal
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  ABSTRACT: Lung cancer is one of the deadliest cancers worldwide, with the highest incidence and mortality amongst all cancers. While the prognosis of lung cancer is generally grim, with 5-year survival rates of only 15%, there is hope, and evidence, that early detection of lung cancer can reduce mortality. Today, only computed tomography screening has shown to lead to early detection and reduction in mortality, but is limited by being anatomic in nature, unable to differentiate between inflammatory and neoplastic pathways, and therefore, susceptible to false positives. There is increasing interest in biomarkers for lung cancer, especially those that predict metastatic risk. Some biomarkers like DNA mutations and epigenetic changes potentially require tissue from the at-risk site; some like serum proteins and miRNAs are minimally invasive, but may not be specific to the lung. In comparison, emerging biomarkers from exhaled breath, like volatile organic compounds (VOC), and exhaled breath condensate, e.g., small molecules and nucleic acids, have the potential to combine the best of both. This mini review is intended to provide an overview of the field, briefly discussing the potential of what is known and highlighting the exciting recent developments, particularly with miRNAs and VOCs.
  Journal of Carcinogenesis 01/2013; 12:3.
• Article: Missense allele of a single nucleotide polymorphism rs2294008 attenuated antitumor effects of prostate stem cell antigen in gallbladder cancer cells.

  Hiroe Ono, Dai Chihara, Fumiko Chiwaki, Kazuyoshi Yanagihara, Hiroki Sasaki, Hiromi Sakamoto, Hideo Tanaka, Teruhiko Yoshida, Norihisa Saeki, Keitaro Matsuo
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  ABSTRACT: Prostate stem cell antigen (PSCA), an organ-dependent tumor suppressor, is down regulated in gallbladder cancer (GBC). It is anticipated that the missense allele C of the single nucleotide polymorphism (SNP) rs2294008 (T/C) in the translation initiation codon of the gene affects the gene's biological function and has some influence on GBC susceptibility. We examined the biological effect of the C allele on the function of the gene and the relation between the C allele and GBC susceptibility. Functional analysis of the SNP was conducted by introducing PSCA cDNA harboring the allele to a GBC cell line TGBC- 1TKB and performing colony formation assays in vitro and tumor formation assays in mice. The effect on transcriptional regulation was assessed by reporter assays. The association study was conducted on 44 Japanese GBC cases and 173 controls. The PSCA cDNA harboring the C allele showed lower cell growth inhibition activity (20% reduction) than that with the T allele. Concordantly, when injected into subcutaneous tissues of mice, the GBC cell line stably expressing the cDNA with the C allele formed tumors of almost the same size as that of the control cells, but the cell line expressing the cDNA with the T allele showed slower growth. The upstream DNA fragment harboring the C allele had more transcriptional activity than that with the T allele. The C allele showed positive correlation to GBC but no statistical significant odds ratio (OR = 1.77, 95% confidence interval 0.85-3.70, P value = 0.127 in dominant model). The missense allele was shown to have a biological effect, attenuating antitumor activities of PSCA, and consequently it may be a potential risk for GBC development. An association study in a larger sample size may reveal a significant association between the allele and GBC.
  Journal of Carcinogenesis 01/2013; 12:4.
• Article: Constitutive over expression of IL-1β, IL-6, NF-κB, and Stat3 is a potential cause of lung tumorgenesis in urethane (ethyl carbamate) induced Balb/c mice.

  Chandradeo Narayan, Arvind Kumar
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  ABSTRACT: Lung cancer is a leading cause of cancer death. There has been found a substantial gap in the understanding of lung cancer genesis at the molecular level. We developed urethane (ethyl carbamate) induced lung tumor mice model to understand the mechanism and molecules involved in the cancer genesis. There might be many molecules involved, but we subsequently emphasized here the study of alternation in the expression of NF-κB, Stat3, and inflammatory cytokines interleukin-1β and interleukin-6 to hypothesize that the microenvironment created by these molecules is promoting tumor formation. 7-8 week old Balb/c mice of either sex were given intraperitoneal (i.p.) injection of urethane (1g/kgbw) for eight consecutive weeks. Histopathological analysis was done to detect abnormality or invasions occurred in the lung tissues. Automated cell counter was used to count the number of inflammatory cells. The expression of NF-κB, Stat3, and IL-1β was observed at translational level by western blot, while the expression of IL-1β and IL-6 was observed at transcriptional level by semiquantitative reverse transcriptase polymerase chain reaction (RT-PCR) method. Secretion of IL-1β and IL-6 in the blood was measured by enzyme-linked immunosorbent assay (ELISA) method at different time intervals. Histopathological analysis showed various lung cancer stages hyperplasia, atypical adenomatous hyperplasia, and adenocarcinoma. Increased population of inflammatory cells, persistant expression of NF-κB, Stat3, pStat3, and IL-1β at translational level, while at transcriptional level constitutive enhanced expression of IL-1β and IL-6 followed by increased secretion of IL-1β and IL-6 in the blood were observed in urethane-injected mice in comparison to phosphate buffer saline (PBS) injected mice at 12, 24, and 36 weeks Overexpression of key molecules such as NF-κB, Stat3, pStat3, IL-1β, and IL-6 might have caused chronic inflammation, leading to the progression of lung cancer.
  Journal of Carcinogenesis 01/2012; 11:9.
• Article: Advances in lung cancer surgery.

  Mark W Hennon, Sai Yendamuri
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  ABSTRACT: The last few years have witnessed an explosion of the use of minimally invasive techniques for the detection, diagnosis, and treatment of all stages of lung Cancer. The use of these techniques has improved the risk-benefit ratio of surgery and has made it more acceptable to patients considering lung surgery. They have also facilitated the delivery of multi-modality therapy to patients with advanced lung cancer. This review article summarizes current surgical techniques that represent the "cutting edge" of thoracic surgery for lung cancer.
  Journal of Carcinogenesis 01/2012; 11:21.
• Article: Meat consumption, ornithine decarboxylase gene polymorphism, and outcomes after colorectal cancer diagnosis.

  Jason A Zell, Bruce S Lin, Argyrios Ziogas, Hoda Anton-Culver
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  ABSTRACT: Dietary arginine and meat consumption are implicated in colorectal cancer (CRC) progression via polyamine-dependent processes. Polymorphism in the polyamine-regulatory gene, ornithine decarboxylase 1 (Odc1, rs2302615) is prognostic for CRC-specific mortality. Here, we examined joint effects of meat consumption and Odc1 polymorphism on CRC-specific mortality. The analytic cohort was comprised of 329 incident stage I-III CRC cases diagnosed 1994-1996 with follow- up through March 2008. Odc1 genotyping was conducted using primers that amplify a 172-bp fragment containing the polymorphic base at +316. Dietary questionnaires were administered at cohort entry. Multivariate Cox proportional hazards regression analysis for CRC-specific mortality was stratified by tumor, node, metastasis (TNM) stage, and adjusted for clinically relevant variables, plus meat consumption (as a continuous variable, i.e., the number of medium-sized servings/week), Odc1 genotype, and a term representing the meat consumption and Odc1 genotype interaction. The primary outcome was the interaction of Odc1 and meat intake on CRC-specific mortality, as assessed by departures from multiplicative joint effects. Odc1 genotype distribution was 51% GG, 49% GA/AA. In the multivariate model, there was a significant interaction between meat consumption and Odc1 genotype, P-int = 0.01. Among Odc1 GA/AA CRC cases in meat consumption Quartiles 1-3, increased mortality risk was observed when compared to GG cases (adjusted hazards ratio (HR) = 7.06 [95% CI 2.34-21.28]) - a difference not found among cases in the highest dietary meat consumption Quartile 4. Effects of meat consumption on CRC-specific mortality risk differ based on genetic polymorphism at Odc1. These results provide further evidence that polyamine metabolism and its modulation by dietary factors such as meat may have relevance to CRC outcomes.
  Journal of Carcinogenesis 01/2012; 11:17.
• Article: The cellular functions of RASSF1A and its inactivation in prostate cancer.

  Karishma S Amin, Partha P Banerjee
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  ABSTRACT: Epigenetic events significantly impact the transcriptome of cells and often contribute to the onset and progression of human cancers. RASSF1A (Ras-association domain family 1 isoform A), a well-known tumor suppressor gene, is frequently silenced by epigenetic mechanisms such as promoter hypermethylation in a wide range of cancers. In the past decade a vast body of literature has emerged describing the silencing of RASSF1A expression in various cancers and demonstrating its ability to reverse the cancerous phenotype when re-expressed in cancer cells. However, the mechanisms by which RASSF1A exerts its tumor suppressive properties have not been entirely defined. RASSF1A appears to mediate three important cellular processes: microtubule stability, cell cycle progression, and the induction of apoptosis through specific molecular interactions with key factors involved in these processes. Loss of function of RASSF1A leads to accelerated cell cycle progression and resistance to apoptotic signals, resulting in increased cell proliferation. In this review, we attempt to summarize the current understanding of the biological functions of RASSF1A and provide insight that the development of targeted drugs to restore RASSF1A function holds promise for the treatment of prostate cancer.
  Journal of Carcinogenesis 01/2012; 11:3.
• Article: Comparative metabolism of benzo[a]pyrene by human keratinocytes infected with high-risk human papillomavirus types 16 and 18 as episomal or integrated genomes.

  Neil Trushin, Samina Alam, Karam El-Bayoumy, Jacek Krzeminski, Shantu G Amin, Jenny Gullett, Craig Meyers, Bogdan Prokopczyk
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  ABSTRACT: Infection with human papillomavirus (HPV) is a critical factor in the development of cervical cancer. Smoking is an additional risk factor. Tobacco smoke carcinogens, such as benzo[a]pyrene (B[a]P), and their cytochrome P450-related metabolites are present in significantly higher levels in the cervical mucus of women smokers than in nonsmokers. We determined the metabolism and P450 expression of B[a]P-treated human keratinocytes infected with HPV-16 or -18. Monolayer cultures of uninfected primary human foreskin keratinocytes, human vaginal and cervical keratinocytes carrying episomal genomes of HPV-16 and -18, respectively, and invasive cervical carcinoma cell lines carrying either HPV-16 or -18 genomes integrated into the host DNA, were incubated with 0.1 μM [(3)H]B[a]P. The resulting oxidative metabolites were analyzed and quantified by radioflow high-performance liquid chromatography. Additionally, all cell lines were incubated with unlabeled 0.1 μM B[a]P for Western blot analysis of cytochrome P450 1A1 and 1B1. Significant enhancement in levels of both detoxification and activation metabolites was found in incubations with all types of HPV-infected cells compared with control incubations (P < 0.05). The highest capacity to metabolize B[a]P was observed with cells containing integrated HPV-18 genomes. Induction of cytochrome 1B1 was observed in HPV-16 and -18 integrated, and in HPV-16 episomal cell types. Both viral genotype and genomic status in the host cell affect B[a]P metabolism and cytochrome P450 1B1 expression. An increase of DNA-damaging metabolites might result from exposure of HPV-infected women to cigarette smoke carcinogens.
  Journal of Carcinogenesis 01/2012; 11:1.
• Article: Acyclic retinoid in chemoprevention of hepatocellular carcinoma: Targeting phosphorylated retinoid X receptor-α for prevention of liver carcinogenesis.

  Masahito Shimizu, Yohei Shirakami, Kenji Imai, Koji Takai, Hisataka Moriwaki
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  ABSTRACT: One of the key features of hepatocellular carcinoma (HCC) is the high rate of intrahepatic recurrence that correlates with poor prognosis. Therefore, in order to improve the clinical outcome for patients with HCC, development of a chemopreventive agent that can decrease or delay the incidence of recurrence is a critical issue for urgent investigation. Acyclic retinoid (ACR), a synthetic retinoid, successfully improves HCC patient survival by preventing recurrence and the formation of secondary tumors. A malfunction of the retinoid X receptor-α (RXRα) due to phosphorylation by the Ras-MAPK signaling pathway plays a critical role in liver carcinogenesis, and ACR exerts chemopreventive effects on HCC development by inhibiting RXRα phosphorylation. Here, we review the relationship between retinoid signaling abnormalities and liver disease, the mechanisms of how RXRα phosphorylation contributes to liver carcinogenesis, and the detailed effects of ACR on preventing HCC development, especially based on the results of our basic and clinical research. We also outline the concept of "clonal deletion and inhibition" therapy, which is defined as the removal and inhibition of latent malignant clones from the liver before they expand into clinically detectable HCC, because ACR prevents the development of HCC by implementing this concept. Looking toward the future, we discuss "combination chemoprevention" using ACR as a key drug since it can generate a synergistic effect, and may thus be an effective new strategy for the prevention of HCC.
  Journal of Carcinogenesis 01/2012; 11:11.
• Article: Plastics and carcinogenesis: The example of vinyl chloride.

  Paul Wesley Brandt-Rauf, Yongliang Li, Changmin Long, Regina Monaco, Gopala Kovvali, Marie-Jeanne Marion
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  ABSTRACT: The manufacture, use and disposal of various plastics can pose numerous health risks, including the risk of cancer. A model example of carcinogenic risk from plastics is provided by polyvinyl chloride, since it is composed of the known human carcinogen vinyl chloride (VC). In recent years, much has been learned about the molecular biological pathways of VC carcinogenesis. This has led to molecular epidemiologic studies of VC carcinogenesis in exposed human populations which have identified useful biomarkers of exposure, effect and susceptibility for VC. These studies have in turn provided the basis for new molecular approaches for the prevention and treatment of VC cancers. This model could have much wider applicability for many other carcinogenic exposures and many other human cancers.
  Journal of Carcinogenesis 01/2012; 11:5.
• Article: The burden of prostate cancer in Asian nations.

  Jennifer Cullen, Sally Elsamanoudi, Stephen A Brassell, Yongmei Chen, Monica Colombo, Amita Srivastava, David G McLeod
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  ABSTRACT: In this review, the International Agency for Research on Cancer's cancer epidemiology databases were used to examine prostate cancer (PCa) age-standardized incidence rates (ASIR) in selected Asian nations, including Cancer Incidence in Five Continents (CI5) and GLOBOCAN databases, in an effort to determine whether ASIRs are rising in regions of the world with historically low risk of PCa development. Asian nations with adequate data quality were considered for this review. PCa ASIR estimates from CI5 and GLOBOCAN 2008 public use databases were examined in the four eligible countries: China, Japan, Korea and Singapore. Time trends in PCa ASIRs were examined using CI5 Volumes I-IX. While PCa ASIRs remain much lower in the Asian nations examined than in North America, there is a clear trend of increasing PCa ASIRs in the four countries examined. Efforts to systematically collect cancer incidence data in Asian nations must be expanded. Current CI5 data indicate a rise in PCa ASIR in several populous Asian countries. If these rates continue to rise, it is uncertain whether there will be sufficient resources in place, in terms of trained personnel and infrastructure for medical treatment and continuum of care, to handle the increase in PCa patient volume. The recommendation by some experts to initiate PSA screening in Asian nations could compound a resource shortfall. Obtaining accurate estimates of PCa incidence in these countries is critically important for preparing for a potential shift in the public health burden posed by this disease.
  Journal of Carcinogenesis 01/2012; 11:7.
• Article: Oncogenic activation in prostate cancer progression and metastasis: Molecular insights and future challenges.

  Subhamoy Dasgupta, Srinivasa Srinidhi, Jamboor K Vishwanatha
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  ABSTRACT: Prostate cancer is a leading cause of death among men in the United States, and currently early diagnosis and appropriate treatment remain key approaches for patient care. Molecularly prostate cancer cells carry multiple perturbations that generate malignant phenotype capable of uncontrolled growth, survival, and invasion-metastasis to other organs. These alterations are acquired both by genetic and epigenetic changes in tumor cells resulting in the activation of growth factor receptors, signaling proteins, kinases, transcription factors and coregulators, and multiple proteases required for the progression of the disease. Recent advances provide novel insights into the molecular functions of these oncogenic activators, implicating potential therapeutic targeting opportunities for the treatment of prostate cancer.
  Journal of Carcinogenesis 01/2012; 11:4.
• Article: CyclinD1 protein plays different roles in modulating chemoresponses in MCF7 and MDA-MB231 cells.

  Yuan Sun, Dianzhong Luo, D Joshua Liao
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  ABSTRACT: CyclinD1 is an essential sensor and activator of cell cycle initiation and progression; overexpression of cyclinD1 is linked to various human cancers, including breast cancer. The elevated cyclinD1 in some types of cancers is believed to be associated with tumor progression and response to systemic treatments. In this study, we anticipate to address the questions in human breast cancer; the function of cyclinD1 in mediating chemoresponses; and the signaling pathway cooperating with cyclinD1 to interfere with the drug functions. Using the cell clones, concurrent ectopic expression of the wild-type or K112E-mutated human cyclinD1 protein in the MCF7 and MDA-MB231 (MB231) breast cancer cells to study the function of cyclinD1 in responses to the chemotherapeutic treatments. Three drugs, cisplatin (CDDP), 5-fluorouracil (5-FU), and Gemzar were used in this study; the 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay, cell cycle and cell death analysis, clonogenic survival assay, acridine orange (AO)/ethidium bromide (EB) staining, and Western blot assay were conducted to evaluate the drugs' effects in the cell clones. The cell clones expressing the D1 protein in MCF7 and MB231 cells result in distinct effects on the responses to chemotherapeutic treatments. Particularly with Gemzar, ectopic expression of cyclinD1 protein in MCF7 cells results in a potentiated effect, which is CDK4 kinase activity dependent, whereas in MB231 cells, an opposite effect was observed. Moreover, our results suggested that the distinct chemosensitivities among those cell clones were not resulted from accelerated cell cycle, cell proliferation driven by the cyclinD1CDK4/6-Rb-E2F signaling chain, rather, they were results of the cell cycle-independent functions led by cyclinD1 alone or in complex with CDK4. Our results suggest that the functions of cyclinD1 protein in modulating chemoresponses in the MCF7 and MB231 cells are independent to its function as cell cycle initiator through activation of CDK4/6. Furthermore, the signals modulated by cyclinD1 upon treatment are determined by the drug and the cellular network.
  Journal of Carcinogenesis 01/2012; 11:12.
• Article: Advances in bronchoscopy for lung cancer.

  Samjot Singh Dhillon, Elisabeth U Dexter
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  ABSTRACT: Bronchoscopic techniques have seen significant advances in the last decade. The development and refinement of different types of endobronchial ultrasound and navigation systems have led to improved diagnostic yield and lung cancer staging capabilities. The complication rate of these minimally invasive procedures is extremely low as compared to traditional transthoracic needle biopsy and surgical sampling. These advances augment the safe array of methods utilized in the work up and management algorithms of lung cancer.
  Journal of Carcinogenesis 01/2012; 11:19.
• Article: Breast cancer disparities: Frontline strategies, proceedings of the 7(th) annual texas conference on health disparities.

  Marilyne Kpetemey, Meghana V Kashyap, Lee Gibbs, Jamboor K Vishwanatha
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  ABSTRACT: There are striking disparities in health status, access to health care, and risk factors among racial and ethnic minorities and the general population in Texas. The disparities are multifactorial comprising genetic, sociocultural, and environmental variables. The Texas Center for Health Disparities (TCHD), a NIMHD Center of Excellence (COE), aims to prevent, reduce, and eliminate health disparities in the communities through research, education, and community-based programs. As part of the center's outreach activities, an annual conference is organized to build awareness and knowledge on health disparities. The overall theme for the 2012 conference was "Battling Breast Cancer Disparities: Frontline Strategies". The scientific program consisted of three sessions: "Breakthroughs in Breast Cancer", "Triple Negative Breast Cancer," and "Hormone Resistant Breast Cancer" featuring different aspects of bench-research from molecular biology, proteomics, and genetics to the clinical aspects such as detection, diagnosis, and finally to community-based approaches. This article summarizes the proceedings of the meeting providing salient strategies and best practices presented by the speakers.
  Journal of Carcinogenesis 01/2012; 11:16.