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Alberg A.J.,Medical University of South Carolina | Brock M.V.,Johns Hopkins University | Ford J.G.,Brooklyn Hospital Center | Samet J.M.,University of Southern California | Spivack S.D.,Yeshiva University
Chest | Year: 2013

Background: Ever since a lung cancer epidemic emerged in the mid-1900s, the epidemiology of lung cancer has been intensively investigated to characterize its causes and patterns of occurrence. This report summarizes the key findings of this research. Methods: A detailed literature search provided the basis for a narrative review, identifying and summarizing key reports on population patterns and factors that affect lung cancer risk. Results: Established environmental risk factors for lung cancer include smoking cigarettes and other tobacco products and exposure to secondhand tobacco smoke, occupational lung carcinogens, radiation, and indoor and outdoor air pollution. Cigarette smoking is the predominant cause of lung cancer and the leading worldwide cause of cancer death. Smoking prevalence in developing nations has increased, starting new lung cancer epidemics in these nations. A positive family history and acquired lung disease are examples of host factors that are clinically useful risk indicators. Risk prediction models based on lung cancer risk factors have been developed, but further refinement is needed to provide clinically useful risk stratification. Promising biomarkers of lung cancer risk and early detection have been identified, but none are ready for broad clinical application. Conclusions: Almost all lung cancer deaths are caused by cigarette smoking, underscoring the need for ongoing efforts at tobacco control throughout the world. Further research is needed into the reasons underlying lung cancer disparities, the causes of lung cancer in never smokers, the potential role of HIV in lung carcinogenesis, and the development of biomarkers. Copyright © by the American College of Chest Physicians 2013.

Freed J.,Brooklyn Hospital Center | Kelly K.M.,Columbia University
Pediatric Drugs | Year: 2010

Hodgkin lymphoma is one of the few cancers that affect both adults and children. Cure rates for Hodgkin lymphoma remain among the best for pediatric cancers. However, cure is often associated with significant delayed effects of therapy, including an elevated risk for second malignancies, cardiotoxicity, pulmonary toxicity, and gonadal and non-gonadal endocrine dysfunction. Therefore, the aim of current treatment strategies is to further improve outcomes while minimizing therapy-related complications.At diagnosis, patients are classified into risk groups based on disease stage, and the presence of clinical, biologic, and serologic risk factors. In general, the most recent trials have intensified therapy in those patients with high-risk disease to improve disease control, and have limited therapy in those patients with low-risk disease to avoid secondary effects. In low-risk patients, multiple studies have been conducted to investigate limiting either radiation therapy or chemotherapy to prevent long-term side effects without affecting the excellent cure rate. In intermediate- and high-risk patients, many studies have examined intensifying therapy to improve event-free survival rates. In addition, response assessment by fluorine-18-2-fluoro-2-deoxy-D-glucosepositron emission tomography (FDG-PET) may be particularly important in pediatric Hodgkin lymphoma; it may allow modification of treatment to maximize treatment efficacy and minimize late effects of chemotherapy and radiation therapy. Despite the improvements in treatment for all stages of Hodgkin lymphoma, there is still a subgroup of patients who do not enter remission with initial therapy or relapse after initial response to therapy. Unfortunately, standard-dose salvage chemotherapy for relapsed disease has disappointing results in terms of overall survival since patients have typically already received intensive therapy. While there is no standard of care in terms of salvage chemotherapy, high-dose chemotherapy with autologous stem cell transplant (ASCT) rescue has become the standard of care for the majority of children with relapsed Hodgkin lymphoma. The use of allogeneic transplantation is controversial in relapsed or refractory Hodgkin lymphoma; because of the high transplant-related mortality, allogeneic transplant has not been associated with improved overall survival over ASCT.As more has been learned about the biologic mechanisms involved in Hodgkin lymphoma, biologically-based therapies are being investigated for use in this disease, both at initial diagnosis and relapse. Both immunotherapy and small molecules are being studied as possible therapeutic agents in Hodgkin lymphoma. Unfortunately, the vast majority of investigations of novel agents have occurred exclusively in adult patients. However, since pediatric Hodgkin lymphoma and adult Hodgkin lymphoma are similar, these results may potentially be extrapolated to pediatric Hodgkin lymphoma. © 2010 Adis Data Information BV. All rights reserved.

Hayes D.P.,Brooklyn Hospital Center
Biogerontology | Year: 2010

Within the past three to four decades a revolution has occurred in our understanding of vitamin D and its effects. Sundry laboratory and epidemiologic studies have revealed that the active metabolite of vitamin D controls and/or ameliorates various pathologies. As presented here, there is substantive evidence that vitamin D may play a positive and important role in the ageing process. This evidence arises from detailed consideration of various biological mechanisms and processes by which vitamin D operates as well as specific examples of its exerting control/amelioration of various human maladies which contribute to ageing. Arguments are advanced that vitamin D appears to play a major positive role in biogerontology by reducing susceptibility in the elderly to chronic degenerative diseases. It is strongly recommended that the positive role of vitamin D in ageing be taken into account by gerontologists and biogerontology researchers. © 2009 Springer Science+Business Media B.V.

Jain S.,New York University | Singhal S.,Brooklyn Hospital Center | Lee P.,New York University | Xu R.,New York University
American Journal of Translational Research | Year: 2010

Hepatocellular carcinoma (HCC) is the sixth most common malignancy and the third leading cause of cancer deaths worldwide. Proper classification and early identification of HCC and precursor lesions is essential to the successful treatment and survival of HCC patients. Recent molecular genetic, pathologic, and clinical data have led to the stratification of hepatic adenomas into three subgroups: those with mutant TCF1/HNF1 α gene, those with mutant β-catenin, and those without mutations in either of these loci. Hepatic adenomas with β-catenin mutations have a significantly greater risk for malignant transformation in comparison with the other two subgroups. Telangiectatic focal nodular hyperplasia has now been reclassified as telangiectatic adenoma due to the presence of non-random methylation patterns, consistent with the monoclonal origin which is similar to hepatic adenoma and HCC. HCC precursor lesions demonstrate unique molecular alterations of HSP70, CAP2, glypican 3, and glutamine synthetase that have proven useful in the histologic diagnosis of early HCC. Though specific genetic alterations depend on HCC etiology, the main proteins affected include cell membrane receptors (in particular tyrosine kinase receptors) as well as proteins involved in cell signaling (specifically Wnt/beta-catenin, Ras/Raf/MEK/ERK and PI3K/Akt/mTOR pathways), cell cycle regulation (i.e. p53, p16/INK4, cyclin/cdk complex), invasiveness (EMT, TGF-β) and DNA metabolism. Advances in gene expression profiling have provided new insights into the molecular genetics of HCC. HCCs can now be stratified into two clinically relevant groups: Class A, the low survival subclass (overall survival time 30.3± 8.02 months), shows strong expression signatures of cell proliferation and antiapoptosis genes (such as PNCA and cell cycle regulators CDK4, CCNB1, CCNA2, and CKS2) as well as genes involving ubiquitination and sumoylation; Class B, the high survival subclass (overall survival time 83.7 ±10.3 months), does not have the above expression signature. In fact, insights into HCC-specific alterations of signal transduction pathways and protein expression patterns have led to the development of new therapeutic agents with molecular targets such as EGFR, VEGF, or other multikinase inhibitors. In the future, these specific molecular alterations in HCC can potentially serve as diagnostic tools, prognostic markers, and/or therapeutic targets with the potential to alter clinical outcomes.

Wadhera P.,Brooklyn Hospital Center
Nature Reviews Urology | Year: 2013

Intra-acinar and peri-acinar pressures in the prostate might be key factors in the evolution of its zonal morphology and the pathogenesis of BPH and cancer. Herein, I hypothesize that intra-acinar pressures lead to a decrease in apoptosis by distending or stretching acinar epithelium and its surrounding stroma. Increased prostatic smooth muscle content and tone might generate peri-acinar pressures, which could, in the long-term, counteract intra-acinar pressures and decrease epithelial stretch. Thus, it is proposed that BPH (characterized by increased prostatic smooth muscle and, therefore, raised peri-acinar pressures) might decrease the risk of prostate cancer progression by counteracting intra-acinar pressures. In the context of this theory, the transition zone might have evolved as a specialized region within the prostate that can mount a concerted stromal-epithelial response to increased urethral and intra-acinar pressures (BPH), and the urethral angulation, anterior stroma and the prostatic capsule have an adjunctive evolutionary role in this phenomenon. © 2013 Macmillan Publishers Limited. All rights reserved.

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