Genomes and Genes
Gene Symbol: FHIT
Description: fragile histidine triad
Alias: AP3Aase, FRA3B, bis(5'-adenosyl)-triphosphatase, AP3A hydrolase, diadenosine 5',5'''-P1,P3-triphosphate hydrolase, dinucleosidetriphosphatase
Publications375 found, 100 shown here
- Identification of novel candidate genes for type 2 diabetes from a genome-wide association scan in the Old Order Amish: evidence for replication from diabetes-related quantitative traits and from independent populationsEvadnie Rampersaud
Division of Endocrinology, Diabetes and Nutrition, University of Maryland School of Medicine, 660 West Redwood St, Room 494, Baltimore, MD 21201, USA
Diabetes 56:3053-62. 2007..We sought to identify type 2 diabetes susceptibility genes through a genome-wide association scan (GWAS) in the Amish...
- Identification of unstable sequences within the common fragile site at 3p14.2: implications for the mechanism of deletions within fragile histidine triad gene/common fragile site at 3p14.2 in tumorsShantel Corbin
Section of Hematology Oncology, and the Cancer Research Center, The University of Chicago, Illinois 60637, USA
Cancer Res 62:3477-84. 2002The FRA3B, at 3p14.2, lies within the fragile histidine triad (FHIT) gene and is the most highly expressed of the common fragile sites observed when DNA replication is perturbed by aphidicolin...
- Contig array CGH at 3p14.2 points to the FRA3B/FHIT common fragile region as the target gene in diffuse large B-cell lymphomaYoshihiro Kameoka
Division of Molecular Medicine, Aichi Cancer Center Research Institute, Aichi, Japan
Oncogene 23:9148-54. 2004..All of the deleted regions were located within the fragile histidine triad (FHIT) gene, and the most frequent region of loss was mapped to 0...
- The FHIT gene, spanning the chromosome 3p14.2 fragile site and renal carcinoma-associated t(3;8) breakpoint, is abnormal in digestive tract cancersM Ohta
Kimmel Cancer Center, Jefferson Medical College, Philadelphia, Pennsylvania, USA
Cell 84:587-97. 1996A 200-300 kb region of chromosome 3p14.2, including the fragile site locus FRA3B, is homozygously deleted in multiple tumor-derived cell lines...
- The FHIT gene 3p14.2 is abnormal in lung cancerG Sozzi
Kimmel Cancer Center, Jefferson Medical College, Philadelphia, Pennsylvania 19107, USA
Cell 85:17-26. 1996To determine the role of the FHIT gene, which encompasses the fragile site at 3p14...
- Direct cloning of DNA sequences from the common fragile site region at chromosome band 3p14.2F V Rassool
Section of HematologysolidusOncology, The University of Chicago, Chicago, Illinois, 60637, USA
Genomics 35:109-17. 1996..2, a common fragile site (FRA3B)...
- Fhit, a putative tumor suppressor in humans, is a dinucleoside 5',5"'-P1,P3-triphosphate hydrolaseL D Barnes
Department of Biochemistry, University of Texas Health Science Center, San Antonio 78284 7760, USA
Biochemistry 35:11529-35. 1996..histidines are required for full activity, and the central histidine of the triad is absolutely essential for Ap3A hydrolase activity...
- FRA3B extends over a broad region and contains a spontaneous HPV16 integration site: direct evidence for the coincidence of viral integration sites and fragile sitesC M Wilke
Department of Pediatrics, University of Michigan, Ann Arbor 48109, USA
Hum Mol Genet 5:187-95. 1996The common fragile site at 3p14.2 (FRA3B) is the most sensitive site on normal human chromosomes for the formation of gaps and breaks when DNA replication is perturbed by aphidicolin or folate stress...
- Structure and expression of the human FHIT gene in normal and tumor cellsT Druck
Department of Microbiology, Kimmel Cancer Center, Jefferson Medical College, Philadelphia, Pennsylvania 19107, USA
Cancer Res 57:504-12. 1997..2, the FRA3B common fragile region, and homozygous deletions in various cancer-derived cell lines...
- FHIT gene therapy prevents tumor development in Fhit-deficient miceK R Dumon
Kimmel Cancer Center, Jefferson Medical College, 233 South 10th Street, Philadelphia, PA 19107, USA
Proc Natl Acad Sci U S A 98:3346-51. 2001The tumor suppressor gene FHIT spans a common fragile site and is highly susceptible to environmental carcinogens. FHIT inactivation and loss of expression is found in a large fraction of premaligant and malignant lesions...
- Altered expression of the fragile histidine triad gene in primary gastric adenocarcinomasS H Lee
Department of Biochemistry, College of Medicine, Soonchunhyang University, Cheon An 330 090, Korea
Biochem Biophys Res Commun 284:850-5. 2001Genomic alterations and abnormal expression of the fragile histidine triad (FHIT) gene in gastric carcinomas were examined to determine whether the FHIT gene is actually a frequent target for alteration during gastric carcinogenesis...
- The tumor spectrum in FHIT-deficient miceN Zanesi
Department of Microbiology and Immunology, Kimmel Cancer Center, Jefferson Medical College, Philadelphia, PA 19107, USA
Proc Natl Acad Sci U S A 98:10250-5. 2001Mice carrying one inactivated Fhit allele (Fhit +/- mice) are highly susceptible to tumor induction by N-nitrosomethylbenzylamine, with 100% of Fhit +/- mice exhibiting tumors of the forestomach/squamocolumnar junction vs...
- FRA3B and other common fragile sites: the weakest linksK Huebner
Kimmel Cancer Center, Jefferson Medical College, Philadelphia, Pennsylvania 19107, USA
Nat Rev Cancer 1:214-21. 2001..The product of the fragile histidine triad (FHIT) gene, which encompasses this fragile site, is partially or entirely lost in most human cancers, indicating that it ..
- Loss of fragile histidine triad (FHIT) expression and microsatellite instability in periocular sebaceous gland carcinoma in patients with Muir-Torre syndromeLeonard M Holbach
Department of Ophthalmology and Eye Hospital, University Erlangen Nurnberg, Germany
Am J Ophthalmol 134:147-8. 2002..To report fragile histidine triad expression and microsatellite instability in periocular sebaceous gland carcinoma...
- [Loss of fragile histidine triad expression and metastasis in breast cancer]Po Zhao
Department of Pathology, General Hospital of People s Liberation Army, Beijing 100853, P R China
Ai Zheng 21:668-70. 2002Fragile histidine triad(FHIT), a tumor suppressor candidate gene, encompasses FRA3B, a common region with the highest fragility in the human genome, and is altered in a large number of human cancers, particularly those of epithelial cell ..
- Evidence that instability within the FRA3B region extends four megabasesNicole A Becker
Department of Experimental Pathology, Mayo Foundation, Rochester, Minnesota, MN 55905, USA
Oncogene 21:8713-22. 2002b>FRA3B is the most frequently expressed common fragile site localized within human chromosomal band 3p14.2, which is frequently deleted in many different cancers, including cervical cancer...
- Designed FHIT alleles establish that Fhit-induced apoptosis in cancer cells is limited by substrate bindingFrancesco Trapasso
Genetics and Molecular Biology Program, Kimmel Cancer Center, Philadelphia, PA 19107, USA
Proc Natl Acad Sci U S A 100:1592-7. 2003The FHIT gene is inactivated early in the development of many human tumors, and Fhit-deficient mice have increased cancer incidence. Viral reexpression of Fhit kills Fhit-deficient cells by induction of apoptosis...
- Cancer and the FRA3B/FHIT fragile locus: it's a HITK Huebner
Kimmel Cancer Institute, Jefferson Medical College, Philadelphia, PA 19107, USA
Br J Cancer 88:1501-6. 2003The FHIT gene encompassing the most active common human chromosomal fragile region, FRA3B, was discovered in 1996 and proposed as a tumour suppressor gene for important human cancers...
- Effect of FHIT gene replacement on growth, cell cycle and apoptosis in pancreatic cancer cellsVelliyur K Gopalakrishnan
Department of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE 68198, USA
Pancreatology 3:293-302. 2003The human FHIT gene is altered or lost in many cancers and FHIT has been shown to be a tumor suppressor. However, the mechanism of tumor suppression by the FHIT gene remains unclear...
- Fhit is a physiological target of the protein kinase SrcYuri Pekarsky
Kimmel Cancer Center, Thomas Jefferson University, 233 South 10th Street, Philadelphia, PA 19107, USA
Proc Natl Acad Sci U S A 101:3775-9. 2004The FHIT gene is a tumor suppressor that is frequently inactivated by genomic alterations at chromosomal region 3p14.2...
- Hypermethylation of the 5' CpG island of the FHIT gene is associated with hyperdiploid and translocation-negative subtypes of pediatric leukemiaShichun Zheng
Laboratory for Molecular Epidemiology, Department of Epidemiology and Biostatistics, University of California at San Francisco, San Francisco, CA 94143 0560, USA
Cancer Res 64:2000-6. 2004The human FHIT (fragile histidine triad) gene is a putative tumor suppressor gene located at chromosome region 3p14.2...
- The apoptotic pathway triggered by the Fhit protein in lung cancer cell lines is not affected by Bcl-2 or Bcl-x(L) overexpressionLuca Roz
Department of Experimental Oncology, Istituto Nazionale Tumori, Via Venezian 1, Milan 20133, Italy
Oncogene 23:9102-10. 2004The expression of the tumour suppressor protein fragile histidine triad (Fhit) is often impaired in many human cancers and its restoration in Fhit-negative cancer cell lines suppresses tumorigenicity and induces apoptosis...
- Fhit modulation of the Akt-survivin pathway in lung cancer cells: Fhit-tyrosine 114 (Y114) is essentialS Semba
Comprehensive Cancer Center and Department of Molecular Virology, Immunology, and Medical Genetics, The Ohio State University, Columbus, 43210, USA
Oncogene 25:2860-72. 2006The Fhit tumor suppressor binds and hydrolyses diadenosine polyphosphates and the Fhit-substrate complex has been proposed as a proapoptotic effector, as determined by infection of susceptible cancer cells with adenoviruses carrying wild-..
- FHIT-proteasome degradation caused by mitogenic stimulation of the EGF receptor family in cancer cellsFrancesca Bianchi
Molecular Biology Unit, Department of Experimental Oncology, Istituto Nazionale Tumori, Via Venezian 1, 20133 Milan, Italy
Proc Natl Acad Sci U S A 103:18981-6. 2006The tumor suppressor gene FHIT is inactivated by genetic and epigenetic changes in the majority of common human cancers...
- Fhit expression protects against HER2-driven breast tumor development: unraveling the molecular interconnectionsFrancesca Bianchi
Fondazione IRCCS Istituto Nazionale Tumori, Milan, Italy
Cell Cycle 6:643-6. 2007The tumor suppressor gene FHIT is inactivated by genetic and epigenetic changes, i.e., loss of heterozygosity or promoter hypermethylation, in common human cancers...
- Fhit interaction with ferredoxin reductase triggers generation of reactive oxygen species and apoptosis of cancer cellsFrancesco Trapasso
Ohio State University, Comprehensive Cancer Center, Columbus, Ohio 43210, USA
J Biol Chem 283:13736-44. 2008b>Fhit protein is lost in most cancers, its restoration suppresses tumorigenicity, and virus-mediated FHIT gene therapy induces apoptosis and suppresses tumors in preclinical models...
- Investigation of mutations and expression of the FHIT gene in Turkish patients with brain metastases derived from non-small cell lung cancerAhmet Bekar
Department of Neurosurgery, Faculty of Medicine, Uludag University, Bursa, Turkey
Tumori 93:604-7. 2007..Although it has been determined that there is a relationship between the FHIT gene and several primary tumors, its role in the initiation and progression of brain tumors has not yet been ..
- Intramitochondrial calcium regulation by the FHIT gene product sensitizes to apoptosisAlessandro Rimessi
Department of Experimental and Diagnostic Medicine, Interdisciplinary Center for the Study of Inflammation, Emilia Romagna Laboratory BioPharmaNet Laboratory, University of Ferrara, 44100 Ferrara, Italy
Proc Natl Acad Sci U S A 106:12753-8. 2009Despite the growing interest in the Fhit tumor suppressor protein, frequently deleted in human cancers, the mechanism of its powerful proapoptotic activity has remained elusive...
- Pathology and biology associated with the fragile FHIT gene and gene productJoshua C Saldivar
Integrated Biomedical Science Graduate Program, Ohio State University Medical Center, Columbus, Ohio, USA
J Cell Biochem 109:858-65. 2010..scientific publications after the discovery of the first gene at a chromosome fragile site, the FHIT gene at FRA3B, there are still questions to pursue concerning the selective advantage conferred to cells by loss of expression ..
- Association of the promoter methylation and protein expression of Fragile Histidine Triad (FHIT) gene with the progression of differentiated thyroid carcinomaDe Tao Yin
Department of General Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, P R China
Int J Clin Exp Pathol 3:482-91. 2010The role of aberrant methylation of fragile histidine triad (FHIT) promoters in the differentiated thyroid carcinoma (DTC) is not yet clear...
- Homozygous deletion but not mutation of exons 5 and 8 of the fragile histidine triad (FHIT) gene is associated with features of differentiated thyroid carcinomaDe Tao Yin
Department of General Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China
Ann Clin Lab Sci 40:267-72. 2010The fragile histidine triad (FHIT) gene encompasses the most common human fragile site, FRA3B at 3p14.2, a region that is involved in homozygous deletions in a variety of human tumors...
- Restoration of fragile histidine triad (FHIT) expression inhibits cell growth and induces apoptosis in cutaneous T-cell lymphoma cell lineXiangfeng Song
Department of Immunology, Xinxiang Medical University, Xingxiang, China
Cancer Invest 28:1019-23. 2010To investigate the effects of fragile histidine triad (FHIT) restoration on cell proliferation and apoptosis in human cutaneous T-cell lymphoma cell line, Hut-78, in vitro and in nude mouse...
- Cell-type-specific replication initiation programs set fragility of the FRA3B fragile siteAnne Letessier
Institut Curie, Centre de Recherche, 26 Rue d Ulm, 75248 Paris, France
Nature 470:120-3. 2011..Here we show, in contrast to this view, that the fragility of FRA3B--the most active common fragile site in human lymphocytes--does not rely on fork slowing or stalling but on a ..
- microRNA-143 protects cells from DNA damage-induced killing by downregulating FHIT expressionYu Xiang Lin
Department of Medical Molecular Biology, Beijing Institute of Biotechnology, China
Cancer Biother Radiopharm 26:365-72. 2011..Recent studies suggest roles of miRNAs in carcinogenesis. Fragile histidine triad (FHIT) gene deletion, methylation, and reduced Fhit protein expression occur in about 70% of human epithelial tumors and ..
- FHIT promotes the apoptosis of QBC939 by reducing the expression of cyclin D1Qiang Huang
Department of General Surgery, Affiliated Provincial Hospital of Anhui Medical University, Hefei, China
Hepatogastroenterology 58:713-8. 2011The fragile histidine triad (FHIT) gene is a candidate tumor suppressor gene. Recent studies have found that FHIT protein is lost in digestive system neoplasms...
- Genome wide study of maternal and parent-of-origin effects on the etiology of orofacial cleftsMin Shi
Biostatistics Branch, NIEHS NIH, Durham, North Carolina, USA
Am J Med Genet A 158:784-94. 2012..Thus, the most promising SNPs identified by this study may still be worth further investigation...
- Expression of Ki-67, galectin-3, fragile histidine triad, and parafibromin in malignant and benign parathyroid tumorsOu Wang
Key laboratory of Endocrine, Ministry of Health, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing 100730, China
Chin Med J (Engl) 125:2895-901. 2012..Our study aimed to investigate the differential expression of Ki-67, galectin-3, fragile histidine triad (FHIT) gene, and parafibromin in PC, parathyroid adenoma (PA), parathyroid hyperplasia (PH), and normal parathyroid (NP) ..
- Initiation of genome instability and preneoplastic processes through loss of Fhit expressionJoshua C Saldivar
Biomedical Sciences Graduate Program, Ohio State University, Columbus, Ohio, United States of America
PLoS Genet 8:e1003077. 2012..A frequent, perhaps earliest, genetic alteration in preneoplasias is deletion within the fragile FRA3B/FHIT locus, leading to loss of Fhit protein expression...
- Recurrent loss of the FHIT gene and its impact on lymphatic metastasis in early oral squamous cell carcinomaYoung Hoon Joo
Department of Otorhinolaryngology, Head and Neck Surgery, College of Medicine, Catholic University of Korea, Seoul, Korea
Acta Otolaryngol 133:992-9. 2013Our findings show that copy number loss of FHIT is associated with lymph node metastasis (LNM) and suggest that the down-regulation of Fhit indicates poor prognosis in early oral squamous cell carcinoma (OSCC).
- Reduced FHIT expression is associated with tumor progression in sporadic colon adenocarcinomaSanja Kapitanovic
Laboratory for Personalized Medicine, Ruđer Bošković Institute, Bijenicka c 54, 10000 Zagreb, Croatia Electronic address
Exp Mol Pathol 96:92-7. 2014Tumor supressor gene FHIT was identified at chromosome 3p14.2 spanning the FRA3B fragile site and is very often inactivated in different types of cancer...
- Genetic, biochemical, and crystallographic characterization of Fhit-substrate complexes as the active signaling form of FhitH C Pace
Kimmel Cancer Institute, Thomas Jefferson University, Philadelphia, PA 19107, USA
Proc Natl Acad Sci U S A 95:5484-9. 1998Alterations in the FHIT gene at 3p14.2 occur as early and frequent events in the development of several common human cancers...
- Molecular analysis of the FHIT gene in human prostate cancerA Latil
Laboratoire d oncogénétique, Centre Rene Huguenin, St Cloud, France
Oncogene 16:1863-8. 1998A variety of studies suggest that the FHIT gene, which encompasses the fragile site at 3p14.2, is a candidate tumor suppressor gene in several forms of human cancer...
- Distribution of Fhit protein in rat tissues and its intracellular localizationF Golebiowski
Department of Molecular Medicine, Medical University of Gdansk, Poland
Mol Cell Biochem 226:49-55. 2001..The way in which Fhit exerts its tumor suppressor activity and the relationship of the Ap3A hydrolase activity to tumor suppression are not known...
- Down-regulation of fragile histidine triad expression in prostate carcinomaRebecca L Fouts
Department of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, Indiana, USA
Cancer 97:1447-52. 2003..The gene encompasses the common human chromosomal fragile site, the FRA3B locus at chromosome 3p14.2, and is expressed in most normal adult tissues and tumor cell lines...
- Loss of FHIT protein expression is a marker of adverse evolution in good prognosis localized breast cancerChristophe Ginestier
Département d Oncologie Moléculaire, Institut Paoli Calmettes and U119 Inserm, IFR57, Marseille, France
Int J Cancer 107:854-62. 2003The FHIT tumor suppressor gene, which encompasses the fragile site FRA3B at 3p14.2, is altered frequently in many types of human cancers...
- Fragile site orthologs FHIT/FRA3B and Fhit/Fra14A2: evolutionarily conserved but highly recombinogenicAyumi Matsuyama
Kimmel Cancer Center, Thomas Jefferson University, 233 South 10th Street, Philadelphia, PA 19107, USA
Proc Natl Acad Sci U S A 100:14988-93. 2003..b>FRA3B, located at chromosome region 3p14...
- Dose-dependent effect of FHIT-inducible expression in Calu-1 lung cancer cell lineAndrea Cavazzoni
Department of Experimental Medicine, University of Parma, Via Volturno 39, Parma 43100, Italy
Oncogene 23:8439-46. 2004Abnormalities in the expression of the tumour suppressor fragile histidine triad (FHIT) gene have been reported in a variety of human tumours, including lung cancer and restoration of its expression in cancer cell lines resulted in the ..
- Phosphorylation of the human Fhit tumor suppressor on tyrosine 114 in Escherichia coli and unexpected steady state kinetics of the phosphorylated formsPreston N Garrison
Department of Biochemistry, University of Texas Health Science Center, San Antonio, Texas 78229 3900, USA
Biochemistry 44:6286-92. 2005The human tumor suppressor Fhit is a homodimeric histidine triad (HIT) protein of 147 amino acids which has Ap(3)A hydrolase activity...
- Increased sensitivity to cisplatin in non-small cell lung cancer cell lines after FHIT gene transferF Andriani
Department of Experimental Oncology, Istituto Nazionale Tumori, Milan, Italy
Neoplasia 8:9-17. 2006To evaluate the relevance of fragile histidine triad (FHIT) status in relation to drug treatment, we analyzed the sensitivity of the Fhit-negative non-small cell lung cancer (NSCLC) cell line NCI-H460 to different drugs, after treatment ..
- Preclinical assessment of FHIT gene replacement therapy in human leukemia using a chimeric adenovirus, Ad5/F35Flavia Pichiorri
Ohio State University Comprehensive Cancer Center, Columbus, Ohio 43210, USA
Clin Cancer Res 12:3494-501. 2006Expression of the FHIT protein is lost or reduced in most solid tumors and a significant fraction of hematopoietic malignancies...
- Association between germline variation in the FHIT gene and prostate cancer in Caucasians and African AmericansAlbert M Levin
Departments of Human Genetics, University of Michigan Medical School, Ann Arbor, Michigan, USA
Cancer Epidemiol Biomarkers Prev 16:1294-7. 2007..Encompassing the most active fragile site in the human genome, FRA3B, FHIT has become the model fragile site-associated tumor suppressor gene...
- Correlation of intracellular diadenosine triphosphate (Ap3A) with apoptosis in Fhit-positive HEK293 cellsDavid I Fisher
Cell Regulation and Signalling Group, School of Biological Sciences, University of Liverpool, Liverpool L69 7ZB, UK
Cancer Lett 259:186-91. 2008The pro-apoptotic Fhit tumor suppressor protein binds and hydrolyses diadenosine triphosphate (Ap3A) and diadenosine tetraphosphate (Ap4A) in vitro...
- Correlation of fragile histidine triad (Fhit) protein structural features with effector interactions and biological functionsFlavia Pichiorri
Department of Molecular Virology, Immunology and Medical Genetics, Ohio State University and Comprehensive Cancer Center, Columbus, Ohio 43210, USA
J Biol Chem 284:1040-9. 2009We have previously shown that Fhit tumor suppressor protein interacts with Hsp60 chaperone machinery and ferredoxin reductase (Fdxr) protein...
- Association of FHIT (fragile histidine triad), a candidate tumour suppressor gene, with the ubiquitin-conjugating enzyme hUBC9Y Shi
Department of Biological and Medical Research MBC 03, King Faisal Specialist Hospital and Research Center, P O Box 3354, Riyadh 11211, Saudi Arabia
Biochem J 352:443-8. 2000b>FHIT (fragile histidine triad), a candidate tumour suppressor gene, has recently been identified at chromosomal region 3p14.2, and deletions of the gene have been reported in many types of human cancer...
- Synergistic tumor suppression by coexpression of FHIT and p53 coincides with FHIT-mediated MDM2 inactivation and p53 stabilization in human non-small cell lung cancer cellsMasahiko Nishizaki
Department of Thoracic and Cardiovascular Surgery, University of Texas M D Anderson Cancer Center, Houston, Texas 77030, USA
Cancer Res 64:5745-52. 2004Aberrations of the tumor suppressor genes FHIT and p53 are frequently associated with a wide range of human cancers, including lung cancer...
- Reduced Fhit expression is associated with mismatch repair deficiency in human advanced colorectal carcinomaH Andachi
Second Department of Internal Medicine, Faculty of Medicine, Tottori University, Yonago 683 8504, Japan
Br J Cancer 87:441-5. 2002The Fragile Histidine Triad gene, encompassing the FRA3B fragile site at chromosome 3p14.2, is a candidate tumour suppressor gene involved in multiple tumour types including colorectal carcinomas...
- Genetic analysis of lung tumours of non-smoking subjects: p53 gene mutations are constantly associated with loss of heterozygosity at the FHIT locusA Marchetti
Department of Oncology, University of Pisa, Italy
Br J Cancer 78:73-8. 1998..We have examined the status of p53 and K-ras genes and the presence of loss of heterozygosity (LOH) at the FHIT locus in a series of 35 lung adenocarcinomas that developed in subjects who had never smoked...
- Use of monoclonal antibodies in the functional characterization of the Saccharomyces cerevisiae Sep1 proteinA Holler
Institute of General Microbiology, University of Bern, Switzerland
Eur J Biochem 231:329-36. 1995..The implications of these data for the interpretation of proteins which promote homologous pairing of DNA are discussed, in particular in light of the reannealing activity of the p53 human tumor-suppressor protein...
- Cancer prevention and therapy in a preclinical mouse model: impact of FHIT virusesHideshi Ishii
Center for Molecular Medicine, Jichi Medical School, Tochigi 329 0498, Japan
Curr Gene Ther 4:53-63. 2004..identified by positional cloning of the chromosome region spanning the carcinogen-sensitive, common fragile site, FRA3B at 3p14.2...
- p53 tumor suppressor protein and H-RAS oncogene in maxillofacial tumors: immunohistochemical and genetic investigation, induction chemotherapy response and prognosis evaluationT Cutilli
Maxillofacial Institute Surgical Department, University of L Aquila, Italy
J Chemother 10:411-7. 1998..However, the cases studied confirm that, in regard to p53, there is a certain degree of correlation between absence of mutations and sensitivity to neoadjuvant chemotherapy...
- High-risk human papillomavirus, tumor suppressor protein p53 and mitomycin-C in invasive squamous cell carcinoma cervixS Rajaram
Department of Obstetrics and Gynaecology, Guru Teg Bahadur Hospital, University College of Medical Sciences, Delhi 110 095, India
Indian J Cancer 43:156-62. 2006..Clinical data relating to human papillomavirus (HPV) infection and p53 status in cervical cancer has been sparse and confusing...
- Common fragile sites, extremely large genes, neural development and cancerDavid I Smith
Co head of the Ovarian Cancer Program, Mayo Clinic Cancer Center, Mayo Clinic College of Medicine, Division of Experimental Pathology, Department of Laboratory Medicine and Pathology, Rochester, MN 55905, USA
Cancer Lett 232:48-57. 2006..The first CFS to be cloned and characterized was FRA3B, the most active CFS in the human genome. Instability within this region extends for over 4...
- Structure of the Wilms tumor suppressor protein zinc finger domain bound to DNARaphael Stoll
Department of Molecular Biology and Skaggs Institute for Chemical Biology, The Scripps Research Institute, La Jolla, CA 92037, USA
J Mol Biol 372:1227-45. 2007..The mutations are of two types, and either destabilize the zinc finger structure or replace key base contact residues...
- RNA interference-mediated silencing of the p53 tumor-suppressor protein drastically increases apoptosis after inhibition of endogenous fatty acid metabolism in breast cancer cellsJavier A Menendez
Department of Medicine, Evanston Northwestern Healthcare Research Institute, Evanston, IL 60201, USA
Int J Mol Med 15:33-40. 2005....
- Study of FHIT and WWOX expression in mucoepidermoid carcinoma and adenoid cystic carcinoma of salivary glandNazmiye Dincer
Hacettepe University, Faculty of Medicine, Department of Pathology, Ankara, Turkey
Oral Oncol 46:195-9. 2010..FHIT and WWOX are tumor suppressor genes that encompass the FRA3B and FRA16D fragile sites at chromosomes 3p14.2 and 16q23.3, respectively...
- Molecular analysis of the fragile histidine triad (FHIT) tumor suppressor gene in vesical tumors of cattle with chronic enzootic hematuria (CEH)E Guidi
Department of Genetics and Microbiology A Buzzati Traverso, University of Pavia, Pavia, Italy
Cytogenet Genome Res 120:173-7. 2008..gene is a tumor suppressor gene known to be inactivated in many tumors including bladder tumors and is spanning FRA3B, a very active common fragile site in the human genome...
- Hepatitis C virus core protein inhibits tumor suppressor protein promyelocytic leukemia function in human hepatoma cellsKerstin Herzer
I Medical Department, Johannes Gutenberg Universitat, Mainz, Germany
Cancer Res 65:10830-7. 2005..Taken together, our results suggest a potential mechanism for HCV-associated development of hepatocellular carcinoma through HCV core-mediated inactivation of the PML tumor suppressor pathway...
- Protein phosphatase type 1-dependent dephosphorylation of the retinoblastoma tumor suppressor protein in ultraviolet-irradiated human skin and keratinocytesM J Edwards
University of Wales Institute Cardiff, School of Applied Sciences, Llandaff Campus, Western Avenue, Cardiff, U K
J Invest Dermatol 115:88-94. 2000....
- Loss of FHIT expression in transitional cell carcinoma of the urinary bladderR Baffa
Department of Urology, Kimmel Cancer Center, Jefferson Medical College of Thomas Jefferson University, Philadelphia, Pennsylvania, USA
Am J Pathol 156:419-24. 2000..We recently cloned the tumor suppressor gene FHIT (fragile histidine triad) at 3p14...
- FHIT (fragile histidine triad) gene analysis in cervical intraepithelial neoplasiaF S Liu
Division of Gynecologic Oncology, Taichung Veterans General Hospital, Taichung, Taiwan, Republic of China
Gynecol Oncol 82:283-90. 2001Recently a candidate tumor suppressor gene, FHIT (fragile histidine triad), was identified at chromosome 3p14.2. Abnormality of this gene has been observed in a variety of human tumors...
- An FHIT tumor suppressor gene?M M Le Beau
Section of Hematology Oncology, University of Chicago, Illinois 60637, USA
Genes Chromosomes Cancer 21:281-9. 1998The FRA3B at 3p14.2 is the most common of the constitutive aphidicolin-inducible fragile sites. Using independent approaches, four groups of investigators have cloned and characterized this fragile site...
- Analysis of the tumour suppressor genes, FHIT and WT-1, and the tumour rejection genes, BAGE, GAGE-1/2, HAGE, MAGE-1, and MAGE-3, in benign and malignant neoplasms of the salivary glandsH Nagel
Department of Cytopathology, Georg August University of Gottingen, Robert Koch Straszligbeta e 40, D 37075 Gottingen, Germany
Mol Pathol 56:226-31. 2003..This study aimed to analyse the expression of putative tumour suppressor genes, FHIT and WT-1, and tumour rejection genes, BAGE, GAGE-1/2, MAGE-1, MAGE-3, and HAGE (which are reported to be important ..
- Expression of Fhit, cell adhesion molecules and matrix metalloproteinases in atypical adenomatous hyperplasia and pulmonary adenocarcinomaKeith M Kerr
Department of Pathology, Aberdeen University Medical School, Aberdeen, UK
J Pathol 203:638-44. 2004..We examined the expression of the putative tumour suppressor gene product Fhit, cell adhesion molecules CD44v6, E-cadherin and beta-catenin, and matrix metalloproteinase 2 and its inhibitor, ..
- High-affinity binding of tumor-suppressor protein p53 and HMGB1 to hemicatenated DNA loopsMichal Stros
Laboratory of Analysis of Chromosomal Proteins, Academy of Sciences of the Czech Republic, Institute of Biophysics, 612 65 Brno, Czech Republic
Biochemistry 43:7215-25. 2004..Only the full-length p53 can form stable ternary complexes with hcDNA and HMGB1. The possible biological relevance of p53 and HMGB1 binding to hemicatenanes is discussed...
- Alterations of the Fhit gene in hepatocellular carcinomas induced by N-nitrosodiethylamine in ratsToshifumi Tsujiuchi
Department of Oncological Pathology, Cancer Center, Nara Medical University, Kashihara, Nara, Japan
Mol Carcinog 34:19-24. 2002The present study was conducted to assess whether Fhit gene alterations are a feature of hepatocellular carcinomas (HCCs) induced by N-nitrosodiethylamine (DEN) in male Fischer 344 rats...
- Alterations of the fragile histidine triad gene in hepatitis C virus-associated hepatocellular carcinomaAbdel Rahman N Zekri
Virology and Immunology Unit, Cairo University, Cairo, Egypt
J Gastroenterol Hepatol 20:87-94. 2005..to address whether homozygous deletion (HZD) or transcriptional alterations of the fragile histidine triad (FHIT) gene play a role in the development and progression of hepatitis C virus-associated hepatocellular carcinoma (HCC).
- Loss of FHIT expression in breast cancer is correlated with poor prognostic markersBanu Arun
Division of Hematology, The University of Texas M D Anderson Cancer Center, 1515 Holcombe Boulevard 424, Houston, TX 77030, USA
Cancer Epidemiol Biomarkers Prev 14:1681-5. 2005The fragile histidine triad (FHIT) gene is a putative tumor suppressor gene that is thought to be involved in the carcinogenesis of breast cancer...
- [Expression of nuclear factor-kappa-B/P65 and fragile histidine triad in colorectal carcinoma and clinical significance thereof]Yang Lu
Department of Pathology, General Hospital of Chinese People s Liberation Army, Beijing 100853, China
Zhonghua Yi Xue Za Zhi 88:610-4. 2008To investigate the expression of nuclear factor-kappa-B (NF-KB)/P65 and fragile histidine triad (FHIT) in colorectal carcinoma and clinical significance thereof.
- Abnormalities of fragile histidine triad genomic and complementary DNAs in cervical cancer: association with human papillomavirus typeC Y Muller
Department of Obstetrics and Gynecology, Hamon Center for Therapeutic Oncology Research, The University of Texas Southwestern Medical Center, Dallas 75235 9032, USA
J Natl Cancer Inst 90:433-9. 1998Chromosome 3p14.2 contains FRA3B, the most active chromosome breakage site in the human genome. The fragile histidine triad (FHIT) gene, a putative tumor suppressor gene, overlaps FRA3B...
- [Abnormal expression of fragile histidine triad (FHIT) and Mut S homolog 2 (MSH2) proteins in human sporadic colorectal carcinoma and their clinical significance]Cheng Cai Yao
Department of Oncology, Zhongnan Hospital, Wuhan University, Wuhan, Hubei, 430071, PR China
Ai Zheng 23:310-6. 2004Frequent loss of fragile histidine triad (FHIT) expression in human gastrointestinal tract carcinomas has been reported; however, there were divergent opinions regarding FHIT expression in colorectal carcinoma...
- Comparative genomic mapping of the bovine Fragile Histidine Triad (FHIT) tumour suppressor gene: characterization of a 2 Mb BAC contig covering the locus, complete annotation of the gene, analysis of cDNA and of physiological expression profilesCristina Uboldi
Department of Genetics and Microbiology A, Buzzati Traverso, University of Pavia, Italy
BMC Genomics 7:123. 2006..FHIT is frequently hit by deletions caused by fragility at FRA3B, the most active of human common fragile sites, where FHIT lays...
- Protein expression profiling identifies cyclophilin A as a molecular target in Fhit-mediated tumor suppressionShuho Semba
Comprehensive Cancer Center and Department of Molecular Virology, Immunology, and Medical Genetics, Ohio State University, Room 455C, Wiseman Hall, 410 West 12th Avenue, Columbus, 43210, USA
Mol Cancer Res 4:529-38. 2006Loss of fragile histidine triad (Fhit) expression is often associated with human malignancies, and Fhit functions as a tumor suppressor in controlling cell growth and apoptosis, although specific signal pathways are still undefined...
- Genetic deletions in sputum as diagnostic markers for early detection of stage I non-small cell lung cancerRuiYun Li
Department of Surgery, The University of Maryland School of Medicine, 10 South Pine Street, Baltimore, MD 21201, USA
Clin Cancer Res 13:482-7. 2007..The aim of this study was to determine whether the genetic changes can be used as markers in sputum specimen for the early detection of lung cancer...
- Allelic imbalance and abnormal expression of FHIT in endemic nasopharyngeal carcinoma: association with clinicopathological featuresYan Fei Deng
Department of Otolaryngology, Zhongshan Hospital, Xiamen University, 209 Hubin South Road, Xiamen, Fujian, 361004, People s Republic of China
Eur Arch Otorhinolaryngol 267:1933-41. 2010The FHIT gene is involved in the pathogenesis of many cancers...
- Direct interaction of the beta-domain of VHL tumor suppressor protein with the regulatory domain of atypical PKC isotypesH Okuda
Department of Urology, Kochi Medical School, Kochi, 783 8505, Japan
Biochem Biophys Res Commun 263:491-7. 1999..Since aPKC isotypes have been implicated in the regulation of cell growth and apoptosis, these results suggest that aPKC isotypes are potential direct target of the VHL beta-domain...
- The FHIT gene in oral squamous cell carcinoma: allelic imbalance is frequent but cDNA aberrations are uncommonS Pateromichelakis
Department of Oral and Maxillofacial Surgery Molecular Oncology, Guy s, King s and St Thomas School of Dentistry, Caldecot Road, London, UK
Oral Oncol 36:180-8. 2000The FHIT (fragile histidine triad) gene at chromosome 3p14.2 spans the FRA3B fragile site and encodes for a diadenosine triphosphate hydrolase-type protein...
- Multiple regions with allelic loss at chromosome 3 in superficial multifocal bladder tumorsJ Louhelainen
ICRF Cancer Medicine Research Unit, Cancer Research Building, St James s University Hospital, Leeds LS9 7TF, UK
Int J Oncol 18:203-10. 2001..The majority (4/5) of the patients had LOH at or close to the fragile histidine triad (FHIT) gene (3p14.2; D3S1300), which is a candidate tumor suppressor gene for many cancer types...
- Structural and biosensor analyses of a synthetic biotinylated peptide probe for the isolation of adenomatous polyposis coli tumor suppressor protein complexesJ D Wade
Howard Florey Institute, University of Melbourne, Victoria, Australia
J Pept Res 58:204-12. 2001....
- Hsp90 chaperones wild-type p53 tumor suppressor proteinDawid Walerych
International Institute of Molecular and Cell Biology in Warsaw, 02 109 Warsaw, Poland
J Biol Chem 279:48836-45. 2004..In summary, the results presented in this article state that chaperone activity of Hsp90 is important for the transcriptional activity of genotypically wild-type p53...
- Lung cancer susceptibility in Fhit-deficient mice is increased by Vhl haploinsufficiencyNicola Zanesi
Comprehensive Cancer Center, Ohio State University, Columbus, Ohio 43210, USA
Cancer Res 65:6576-82. 2005The FHIT gene plays important roles in cancer development, including lung cancers, in which the Fhit protein is frequently lost...
- Influence of FHIT on benzo[a]pyrene-induced tumors and alopecia in mice: chemoprevention by budesonide and N-acetylcysteineRoumen Balansky
Department of Health Sciences, University of Genoa, Via A Pastore 1, I 16132 Genoa, Italy
Proc Natl Acad Sci U S A 103:7823-8. 2006The FHIT gene has many hallmarks of a tumor-suppressor gene and is involved in a large variety of cancers...
- A novel approach to simultaneously scan genes at fragile sitesPascale Willem
Department of Hematology and Molecular Medicine University of the Witwatersrand and the National Health Laboratory Services, Wits Medical School, 8 York road, 2193 Parktown, South Africa
BMC Cancer 6:205. 2006..The two most commonly expressed fragile sites FRA3B and FRA16D host the histidine triad (FHIT) and WW domain containing oxidoreductase (WWOX) genes respectively...
- Aberrations of the FHIT gene and Fhit protein in canine lymphoma cell linesHiroko Hiraoka
Laboratory of Veterinary Internal Medicine, Faculty of Agriculture, Yamaguchi University, Yamaguchi, Japan
J Vet Med Sci 71:769-77. 2009The fragile histidine triad (FHIT) gene is a tumor-associated gene, and aberrant FHIT gene and protein expression have been described in many types of human tumors...
- Adenosine monophosphoramidase activity of Hint and Hnt1 supports function of Kin28, Ccl1, and Tfb3Pawel Bieganowski
Structural Biology and Bioinformatics Program, Kimmel Cancer Center, Philadelphia, Pennsylvania 19107, USA
J Biol Chem 277:10852-60. 2002..hydrolases and nucleotide transferases consists of a branch of proteins related to Hint and Aprataxin, a branch of Fhit-related hydrolases, and a branch of galactose-1-phosphate uridylyltransferase (GalT)-related transferases...
- FHIT mRNA expression in thymomaH Sasaki
Department of Surgery II, Nagoya City University Medical School, Nagoya, Japan
Eur J Surg Oncol 29:904-7. 2003The FHIT gene is located at 3p14.2 a region frequently lost in multiple tumour types. Loss of FHIT expression has been found to occur frequently in multiple tumour types...
- The murine Fhit gene is highly similar to its human orthologue and maps to a common fragile site regionT W Glover
Department of Pediatrics and Human Genetics, University of Michigan, Ann Arbor 48109, USA
Cancer Res 58:3409-14. 1998..exhibits both genomic deletions and aberrant transcripts in a variety of tumors and spans the common fragile site FRA3B. This fragile site extends over a broad region of several hundred kb within the FHIT gene and may account for its ..
- Aberrant transcripts of the FHIT gene are expressed in normal and leukaemic haemopoietic cellsM Carapeti
Department of Haematology, Imperial College School of Medicine, Hammersmith Hospital, London, UK
Br J Cancer 78:601-5. 1998Deletions and apparent transcriptional abnormalities of the FHIT gene at 3p14.2 have recently been reported in a wide variety of solid tumours...
- p53 and FHIT mutations and microsatellite alterations in malignancy-associated pleural effusionJin Hwa Lee
Department of Internal Medicine, Medical Research Center, Ewha Womans University Mokdong Hospital, 911 1 Mokdong Yangcheon gu, Seoul 158 710, South Korea
Lung Cancer 44:33-42. 2004..whether the genetic analysis of pleural fluid can be used to diagnose malignant effusion, we investigated p53 and FHIT mutations and microsatellite alterations (MA) in the pleural fluid of 40 patients with pleural effusion associated ..
- Chromosomal fragile sites FRA3B and FRA16D show correlated expression and association with failure of apoptosis in lymphocytes from patients with thyroid cancerIsabella Sbrana
Department of Human and Environmental Sciences, University of Pisa, Pisa, Italy
Genes Chromosomes Cancer 45:429-36. 2006..This appears to be the case for FRA3B and FRA16D, localized in two tumor-suppressor genes (FHIT and WWOX, respectively) that are altered by deletions or ..
- DNA methylation and loss of protein expression in esophageal squamous cell carcinogenesis of high-risk areaX Q Guo
Department of Endoscopy, The 4th Affiliated Hospital, Hebei Medical University, China
J Exp Clin Cancer Res 26:587-94. 2007..The purpose of this study was to investigate aberrant promoter methylation of the p16 and FHIT genes in tissues and plasma and loss of protein expression in esophageal precancerous conditions (EPC) and ..
- A hybrid machine learning-based method for classifying the Cushing's Syndrome with comorbid adrenocortical lesionsJack Y Yang
Department of Radiology, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
BMC Genomics 9:S23. 2008..as hTERT, PCNA and Ki-67 can be considered as cancer markers, while another set of antigens such as P27KIP1 and FHIT are possible markers for normal tissue...
- SAMY LEWIZ HABIB; Fiscal Year: 2016....
- JOSEPH STEVEN LIPSICK; Fiscal Year: 2016..A better understanding of the precise structures that mediate this interaction may lead to the development of new small molecules that will be useful in the treatment of breast cancers with increased levels of B-Myb. ..
- Regulation of tumorigenic spliced isoforms in cancerAixa Tapia Santos; Fiscal Year: 2010..abstract_text> ..
- Mechanism of Dnmt1 Up-regulation by Fhit LossCHARLES M BRENNER; Fiscal Year: 2012..Whereas the FHIT gene has been defined as a gene that causes programmed cell death when reintroduced to cancer cells, normal ..
- Role of MDM2 in Cell Proliferation and TumorigenesisZhi Xiong Jim Xiao; Fiscal Year: 2010..Information obtained from this study would further our understanding of human carcinogenesis and help identify therapeutic drug targets for cancer prevention and treatment. ..
- EARLY DETECTION OF URINARY BLADDER CANCERBogdan Czerniak; Fiscal Year: 2009..e. the forerunner genes and Aurora-A with its partners, appear to be universally involved in human carcinogenesis the completion of this project will have major relevance for early detection of other common human cancers. ..
- Cell-cell adhesion and signal transductionValeri Vasioukhin; Fiscal Year: 2012..This knowledge is necessary for development of novel targeted therapies for treatment of skin cancer. ..
- Haojie Huang; Fiscal Year: 2016..Findings from this study will not only enhance our understanding of age-related prostate cancinogenesis, but could also provide new molecular targets to devise strategies for prostate cancer prevention and therapy. ..
- Peiqing Sun; Fiscal Year: 2016..Results from these studies will define the signal transduction pathway mediating the senescence response and tumor suppression, and may lead to the development of novel cancer therapies targeting the senescence pathway. ..
- Amato J Giaccia; Fiscal Year: 2014..By identifying and characterizing the genes repressed by p53 and HIF through JARID1B during hypoxia, our studies should clarify some of the complex regulatory mechanisms activated in the hypoxic microenvironment. ..
- Paul M Lieberman; Fiscal Year: 2016..The proposed studies should further our understanding of EBV latent cycle gene regulation and host-virus interactions. ..
- Chemical Modulators for p53 Functions in Transcriptional RegulationSYED S MUJTABA; Fiscal Year: 2012..The newly developed CBP BRD SMIs will be also used as innovative tools to dissect molecular interactions of p53, which could open new avenues for therapeutic development. ..
- p53 Acetylation as a Mechanism in Chemoprevention by AspirinJAYARAMA B GUNAJE; Fiscal Year: 2010..These studies will provide a novel mechanism by which aspirin may exert anticancer effects in DNA damaged cells via acetylation of p53, induction of Bax and inhibition of p21. ..
- TERMINAL DIFFERENTIATION OF THE RENAL EPITHELIUMSamir S El-Dahr; Fiscal Year: 2012....
- Gary L Firestone; Fiscal Year: 2015..Our proposed studies will establish the preclinical foundation that is needed to eventually develop novel and low cost I3C-based therapeutic strategies for human skin cancers. ..
- Carol Prives; Fiscal Year: 2014..Further, Nup98 has been found in chromosomal translocations with a large number of partners in some leukemias and its deregulation in that regard may inform how it functions as a tumor suppressor. ..
- JEFF JOSEPH SEKELSKY; Fiscal Year: 2015..abstract_text> ..
- Regulation of p53 Transcription by Viral Oncoproteins &Covalent ModificationsCheng Ming Chiang; Fiscal Year: 2012....
- Polyoma Virus Disrupts ARF Signaling to p53Michael Fried; Fiscal Year: 2011..Our goal is to determine the molecular mechanisms underlying ARF signaling to p53, which is dysfunctional in a number of human cancers. ..
- p53-Regulation in Liver RegenerationMICHELLE ANN BARTON; Fiscal Year: 2012..How p53 functions in normal cells and during regeneration is essentially unknown. ..
- CELL CYCLE CHECKPOINT CONTROL IN RESPONSE TO DNA DAMAGENancy C Walworth; Fiscal Year: 2011..Our studies make use of the excellent genetics of this organism to elucidate mechanisms that are universally important for governing cell division in the face of DNA damage. ..
- Alcohol and PAH-induced carcinogenesisJagat J Mukherjee; Fiscal Year: 2013..Data obtained from these studies will help assessing the associated health risk presented by alcohol in presence of tobacco smoke constituents and will be useful to develop therapeutic strategies in the prevention of cancer. ..
- Transcriptional regulation of apoptosisJames J Manfredi; Fiscal Year: 2013....
- Kelly L Jordan-Sciutto; Fiscal Year: 2015..Given its potentially unique function and regulation in post-mitotic neurons, we believe E2F1 may serve as a target to prevent neuronal loss in HIV associated dementia. ..
- Merav Socolovsky; Fiscal Year: 2014..1 at gene promoters. This work has the potential to uncover fundamental mechanisms of Rb and PU.1 regulation of cell cycle and differentiation, relevant to leukemia and to anemia. ..
- FHIT Gene Therapy in Cancer Prevention and TreatmentCarlo M Croce; Fiscal Year: 2011b>FHIT Gene Therapy in Cancer Prevention and Treatment. We have developed murine upper digestive tract cancer models induced by oral /V-nitrosomethylbenzylamine(NMBA) or 4-nitroquinoline 1-oxide (NQO) treatment...
- Reactivation of the p53-mediated pro-Apoptotic Pathway Using Stapled PeptidesFederico Bernal; Fiscal Year: 2009..Bernal's development as an independent investigator in the field of cancer chemical biology. ..
- Transcriptional dynamics and cellular function of p53 pulsesJeremy Purvis; Fiscal Year: 2012..Understanding this relationship will guide the design of therapeutic methods that alter p53 dynamics in order to rescue its proper function in stemming tumor development. ..
- Functional analysis of a putative ATM/ATR substrate RFWD3Yi Wang; Fiscal Year: 2012..Uncovering new positive regulator of p53 and understand its function will potentially advance our knowledge of cancer development and treatment. ..
- Mechanisms of Mitotic RecombinationJEFF JOSEPH SEKELSKY; Fiscal Year: 2010..These studies will enhance our understanding of mechanisms of mitotic crossing over and the role that the important tumor suppressor protein BLM plays in preventing mitotic crossing over. ..
- The Function of RASSF1A in T CellsJOANNE PRATT; Fiscal Year: 2009..Understanding the role of RASSF1A in cell function is critical to predict possible outcomes of expression/re-expression of this protein. ..
- TONY R HUNTER; Fiscal Year: 2016..abstract_text> ..
- DNA Recombinational Repair: Role of the p53 Tumor Suppressor ProteinSimon N Powell; Fiscal Year: 2010....
- RNA localization and tumor suppression by APCStavroula Mili; Fiscal Year: 2010..This work will explore a novel APC role and its connection to tumor progression, and could thus provide valuable information towards prevention or treatment of colorectal cancers. ..
- Cell Polarity in Self-renewal and Differentiation of Stem/Progenitor CellsValeri Vasioukhin; Fiscal Year: 2012..Knowledge obtained during this study will help to develop new therapies for treatment of tissue injury, degenerative diseases and cancer. ..
- Xiaohua Wu; Fiscal Year: 2014..These studies will shed light on how BRCA1 is involved in the prevention of breast cancer and will help to open new avenues for developing therapeutic strategies for breast cancer prevention and treatment. ..
- A Functional Census of p53 Cancer and Suppressor MutantsRichard H Lathrop; Fiscal Year: 2013..About 250,000 US deaths yearly are due to tumors with full length but mutated and inactive p53. The long-term goal of this research, a drug that reactivates mutant p53, could prevent or delay these deaths. ..
- Sheng Hong Chen; Fiscal Year: 2015..The proposed study will provide new insights into the mechanisms by which a cel makes the choice to recover, die or senesce and will be important in helping design efficient and selective cancer therapeutics. ..
- Da Qing Yang; Fiscal Year: 2014..Findings from this project will provide new insights into the functional link between suppression of cap- dependent translation and p53 induction and may lead to new therapeutic agents against cancer. ..
- Bin Wang; Fiscal Year: 2016..It will provide novel targets for cancer treatment. ..
- Role of Estrogen Receptor alpha-p53 Interaction in Resistance to Tamoxifen TherapSwati Kulkarni; Fiscal Year: 2010..Thus, results from the proposed study could impact the development of individualized therapy for breast cancer patients. ..
- Carl G Maki; Fiscal Year: 2014....
- FHIT GENE ALTERATIONS IN CERVICAL CANCER PATHOGENESISKATHLEEN CHO; Fiscal Year: 2000..Two-color fluorescence in situ hybridization will be used to identify HPV integration in the FRA3B/FHIT locus in primary tumors and cell lines...
- Juanita L Merchant; Fiscal Year: 2014..Collectively, these studies will establish a link between ZBP-89 and pATMS1981, in the biosynthesis and function of 5HT in response to luminal butyrate. ..
- Role of the Tail Domain in Vinculin FunctionSharon L Campbell; Fiscal Year: 2010..Results obtained from these studies may aid in developing novel therapeutic approaches for counteracting aberrant vinculin activity in human disease. ..
- Samir S El-Dahr; Fiscal Year: 2014..We propose that replacement of the endogenous p53 gene with a non-phosphorytable version of p53 (p53S/A23) rescues HNF1[unreadable] expression and terminal differentiation in salt-stressed BdkrB2-/- embryos. ..
- Mechanism of Renal Cell Injury in DiabetesGoutam Ghosh Choudhury; Fiscal Year: 2013....
- Pradeep P A Mammen; Fiscal Year: 2016..Thus, the proposed NIH R01 Research Grant Application is relevant to and in keeping with the missions of both the NIH and NHBLI. ..
- MICHAEL A O'REILLY; Fiscal Year: 2014....
- RANDAL SCOT TIBBETTS; Fiscal Year: 2016....
- Ian G Macara; Fiscal Year: 2014..Finally, we discovered that in HeLa cells, which express the E7 oncoprotein, RB is not detectably methylated. We will address the underlying mechanism that blocks RB methylation in these cells. ..
- Mechanism of PCNA PolyubiquitinationCHRISTOPHER EDWARD BERNDSEN; Fiscal Year: 2010..The functions of HLTF and SHPRH are likely linked to their role in polyubiquitination of PCNA and the initiation of error-free DNA damage tolerance. ..
- Targeting the ARF/CtBP Axis in Pancreatic CancerSteven R Grossman; Fiscal Year: 2010....
- Exercise Regulation of Glucose Metabolism in Skeletal MuscleLaurie J Goodyear; Fiscal Year: 2012..g. LKB1, SNARK, TRB3) that are likely to be important in mediating the beneficial effects of exercise and their elucidation could lead to the development of novel therapeutic options for individuals with type 2 diabetes. ..
- Role of p53 family in neuropathogenesis in AIDSBassel E Sawaya; Fiscal Year: 2012..The results of these studies will highlight the pathways used by Tat to cause damage to neurons and lead to new avenues for the development of safe and effective therapeutic approaches to inhibit neurodegeneration seen in AIDS patients. ..
- RECEPTOR-TARGETED COPPER RADIOPHARMACEUTICALS FOR CANCER IMAGING AND THERAPYCarolyn J Anderson; Fiscal Year: 2012..abstract_text> ..
- Fhit as modulator of Chk1 termination and response to DNA-damaging agentsJOSHUA SALDIVAR; Fiscal Year: 2012..Interestingly, FHIT, a replicative stress target, is frequently altered in several types of cancer, alterations resulting in the loss ..
- REDOX REGULATION OF TUMOR SUPPRESSION BY MNSODDaret K St Clair; Fiscal Year: 2012....
- Mechansims of Lung Carcinogenesis Induced by Asbestos and Cigarette SmokeDeborah E Sullivan; Fiscal Year: 2012..The focus of this proposal is upon the molecular mechanisms through which cigarette smoke amplifies lung carcinogenesis associated with inhaled asbestos. ..
- Caveolin 1: a novel modulator of the PP2A/ATM/p53 pathwayFerruccio Galbiati; Fiscal Year: 2013....
- Development of Small Molecule Crm-1 Inhibitor for Pancreatic Cancer TherapyRamzi M Mohammad; Fiscal Year: 2013..Our newly developed KPT-SINE's are highly specific, orally active drugs with excellent pharmacokinetic parameters and hold promise against deadly pancreatic cancer. ..
- Regulation of Skeletal Muscle LKB1WILLIAM WINDER; Fiscal Year: 2010..The proposed studies will provide additional rationale for convincing a predominantly sedentary population of the importance of regular exercise in combating inactivity-related diseases. ..
- Carol Prives; Fiscal Year: 2016..We will elucidate the mechanism by which MdmX increases Mdm2 and Wip1 expression, via increasing p53 binding to their promoters. Finally we will validate our findings in cells from MdmX null mice. ..
- CHROMOSOME BREAKPOINTS, RENAL & SMALL CELL LUNG CANCERDavid Smith; Fiscal Year: 2000DESCRIPTION (Adapted from the Investigator's Abstract): FRA3B, at chromosomal band 3p14.2, is the most active common fragile site in the human genome...
- EFFECTS OF BENZO[A]PYRENE IN TRANSGENIC MODEL OF CERVICAELLEN RORKE; Fiscal Year: 2002..Use of our novel transgenic model provides an innovative approach for addressing these questions. ..
- Human Neurotropic JC Virus and CNS DiseasesKamel Khalili; Fiscal Year: 2006..abstract_text> ..
- GASTRIC CANCER INDUCED BY H PYLORI IN P27 DEFICIENT MICESteven Moss; Fiscal Year: 2009..We propose to evaluate a new mouse model of H. pylori-induced gastric cancer that we have developed, in order to address these important questions. ..
- DEPENDENCE OF P53 ON THIOL MAINTENANCE PROTEINSGary Merrill; Fiscal Year: 2001..Equally important, the experiments test a general approach for deriving oxidation-resistant proteins using yeast. ..
- Alteration of Rb in HTLV-1 transformed cellsFatah Kashanchi; Fiscal Year: 2005..abstract_text> ..
- EXPRESSION OF MATRIX METALLOPROTEINASE AND P53Yubo Sun; Fiscal Year: 2004..Once the molecular mechanism addressed in this proposal is clearly defined, it may be possible to exploit the information gained for the development of an effective strategy for RA treatment. ..
- 12th International p53 WorkshopCarol Prives; Fiscal Year: 2006..This support will be crucial for a key mission of the Workshop, which is to support the science and training of future US leaders in the p53 and cancer research communities. ..
- Study of a FACTp140-SSRP1-associated p53 KinaseHua Lu; Fiscal Year: 2006..This investigation has important implications for anti-cancer drug development. ..
- A High-Throughput Assay for DNA Repair Activity in the Presence of AberrantBRCA1JAMES MATTHEW FORD; Fiscal Year: 2010..g. repair-deficient cancers, degenerative diseases, and various sclerotic diseases), and may generate tools for basic science research. ..