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Houston, TX, United States

Baylor College of Medicine , located in the Texas Medical Center in Houston, Texas, US, is a health science university. It includes a medical school, Baylor College of Medicine; the Graduate School of Biomedical science; the School of Allied Health science; and the National School of Tropical Medicine. The school, located in the middle of the world's largest medical center, is part owner of Baylor St. Luke's Medical Center, part of the CHI St. Luke's Health system, and has hospital affiliations with: Harris Health System, Texas Children's Hospital, The University of Texas MD Anderson Cancer Center, Memorial Hermann - The Institute for Rehabilitation and Research, Menninger Clinic, the Michael E. DeBakey Veterans Affairs Medical Center and Children's Hospital of San Antonio.The medical school has been consistently considered in the top-tier of programs in the country, and is particularly noted for having the lowest tuition among all private medical schools in the US. Its Graduate School of Biomedical science is among the top 30 graduate schools in the United States. Within the School of Allied Health science, the nurse anesthesia ranks 5th and the physician assistant program ranks 6th. A program in Orthotics and Prosthetics began in 2013, with 18 students in the first class. The National School of Tropical Medicine is the only school in the nation dedicated exclusively to patient care, research, education and policy related to neglected tropical diseases.On June 21, 2010, Dr. Paul Klotman was named as the new President and CEO of the Baylor College of Medicine. In January 2014, the College and CHI St. Luke's became joint owners of Baylor St. Luke's Medical Center. Wikipedia.


Orange J.S.,Baylor College of Medicine
Journal of Allergy and Clinical Immunology | Year: 2013

Natural killer (NK) cells are part of the innate immune defense against infection and cancer and are especially useful in combating certain viral pathogens. The utility of NK cells in human health has been underscored by a growing number of persons who are deficient in NK cells and/or their functions. This can be in the context of a broader genetically defined congenital immunodeficiency, of which there are more than 40 presently known to impair NK cells. However, the abnormality of NK cells in certain cases represents the majority immunologic defect. In aggregate, these conditions are termed NK cell deficiency. Recent advances have added clarity to this diagnosis and identified defects in 3 genes that can cause NK cell deficiency, as well as some of the underlying biology. Appropriate consideration of these diagnoses and patients raises the potential for rational therapeutic options and further innovation. © 2013 American Academy of Allergy, Asthma & Immunology. Source


An unanticipated and tremendous amount of the noncoding sequence of the human genome is transcribed. Long noncoding RNAs (lncRNAs) constitute a significant fraction of non-protein-coding transcripts; however, their functions remain enigmatic. We demonstrate that deletions of a small noncoding differentially methylated region at 16q24.1, including lncRNA genes, cause a lethal lung developmental disorder, alveolar capillary dysplasia with misalignment of pulmonary veins (ACD/MPV), with parent-of-origin effects. We identify overlapping deletions 250 kb upstream of FOXF1 in nine patients with ACD/MPV that arose de novo specifically on the maternally inherited chromosome and delete lung-specific lncRNA genes. These deletions define a distant cis-regulatory region that harbors, besides lncRNA genes, also a differentially methylated CpG island, binds GLI2 depending on the methylation status of this CpG island, and physically interacts with and up-regulates the FOXF1 promoter. We suggest that lung-transcribed 16q24.1 lncRNAs may contribute to long-range regulation of FOXF1 by GLI2 and other transcription factors. Perturbation of lncRNA-mediated chromatin interactions may, in general, be responsible for position effect phenomena and potentially cause many disorders of human development. Source


El-Serag H.B.,Baylor College of Medicine
Gastroenterology | Year: 2012

Most cases of hepatocellular carcinoma (HCC) are associated with cirrhosis related to chronic hepatitis B virus (HBV) or hepatitis C virus (HCV) infection. Changes in the time trends of HCC and most variations in its age-, sex-, and race-specific rates among different regions are likely to be related to differences in hepatitis viruses that are most prevalent in a population, the timing of their spread, and the ages of the individuals the viruses infect. Environmental, host genetic, and viral factors can affect the risk of HCC in individuals with HBV or HCV infection. This review summarizes the risk factors for HCC among HBV- or HCV-infected individuals, based on findings from epidemiologic studies and meta-analyses, as well as determinants of patient outcome and the HCC disease burden, globally and in the United States. © 2012 AGA Institute. Source


Graham D.Y.,Baylor College of Medicine
Gastroenterology | Year: 2015

Helicobacter pylori infection contributes to the development of diverse gastric and extragastric diseases. The infection is necessary but not sufficient for the development of gastric adenocarcinoma. Its eradication would eliminate a major worldwide cause of cancer death, therefore there is much interest in identifying how, if, and when this can be accomplished. There are several mechanisms by which H pylori contributes to the development of gastric cancer. Gastric adenocarcinoma is one of many cancers associated with inflammation, which is induced by H pylori infection, yet the bacteria also cause genetic and epigenetic changes that lead to genetic instability in gastric epithelial cells. H pylori eradication reduces both. However, many factors must be considered in determining whether treating this bacterial infection will prevent cancer or only reduce its risk - these must be considered in designing reliable and effective eradication therapies. Furthermore, H pylori infection has been proposed to provide some benefits, such as reducing the risks of obesity or childhood asthma. When tested, these hypotheses have not been confirmed and are therefore most likely false. © 2015 by the AGA Institute. Source


Mitsiades N.,Baylor College of Medicine
Cancer Research | Year: 2013

Gonadal androgen suppression (castration via orchiectomy or gonadotropin-releasing hormone analogues) suppresses circulating testosterone levels but does not achieve adequate androgen ablation within the prostate cancer microenvironment because it does not address adrenal and intratumoral steroid contributions. These residual extragonadal sources of androgens allow prostate cancer cells to survive, adapt, and evolve into castration-resistant prostate cancer (CRPC). The persistent significance of the androgen receptor (AR) axis in CRPC was recently validated by the clinical efficacy of androgen synthesis inhibitors (abiraterone) and novel, second-generation AR antagonists (enzalutamide). The appreciation that conventional therapeutic approaches achieve a suboptimal ablation of intratumoral androgens and AR axis signaling output opens transformative therapeutic opportunities. A treatment paradigm of comprehensive AR axis targeting at multiple levels (androgen synthesis, metabolism, and action) and at all relevant sites (gonadal, adrenal, intratumoral) simultaneously at the time of initiation of endocrine therapy (instead of the current approach of sequentially adding one agent at a time and only after disease progression) deserves examination in clinical trials to explore whether maximal first-line AR axis suppression via combination therapy can achieve maximal induction of cancer cell apoptosis (before they have the chance to adapt and evolve into CRPC) and thus, improve patient outcomes. © 2013 American Association for Cancer Research. Source

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