Claudio J. Conti

ORCID: 0000-0003-4753-0722
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About
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Research Areas
  • Cancer-related Molecular Pathways
  • Skin and Cellular Biology Research
  • Cancer Cells and Metastasis
  • Ubiquitin and proteasome pathways
  • Cancer and Skin Lesions
  • Estrogen and related hormone effects
  • Prostate Cancer Treatment and Research
  • Cancer Genomics and Diagnostics
  • Hair Growth and Disorders
  • Wnt/β-catenin signaling in development and cancer
  • Skin Protection and Aging
  • Nonmelanoma Skin Cancer Studies
  • Virus-based gene therapy research
  • Growth Hormone and Insulin-like Growth Factors
  • Microtubule and mitosis dynamics
  • Carcinogens and Genotoxicity Assessment
  • Cancer, Hypoxia, and Metabolism
  • Reproductive Biology and Fertility
  • Cancer Risks and Factors
  • PI3K/AKT/mTOR signaling in cancer
  • Epigenetics and DNA Methylation
  • Cell Adhesion Molecules Research
  • Angiogenesis and VEGF in Cancer
  • Melanoma and MAPK Pathways
  • Wound Healing and Treatments

Universidad Carlos III de Madrid
2013-2022

Hospital Universitario Fundación Jiménez Díaz
2014-2020

Texas A&M Health Science Center
2013-2019

The University of Texas MD Anderson Cancer Center
2002-2015

National Taiwan University
2014

Marche Polytechnic University
2014

The University of Texas Health Science Center at Houston
1997-2011

Harvard University
1999

Massachusetts General Hospital
1999

Central University of Venezuela
1997

Nuclear accumulation of p53 protein has been shown to be strongly associated with missense mutations. Studies nuclear in prostate carcinoma cells have date confined material from primary tumors.We studied the specimens obtained and metastatic sites carcinoma. By examining this as a function stage, histologic grade, androgen responsiveness tumor, we hoped determine role mutation progression carcinoma.The cell nuclei was determined by immunohistochemical methods using polyclonal antibody human...

10.1093/jnci/85.20.1657 article EN JNCI Journal of the National Cancer Institute 1993-10-20

Epidemiological and dietary studies suggest that nonsteroidal anti-inflammatory drugs (NSAIDs) reduce the risk of colon cancer, possibly through a mechanism involving inhibition cyclooxygenase (COX)-2, which is overexpressed in premalignant adenomatous polyps cancer. Because ultraviolet light (UV) can induce COX-2 nonspecific NSAIDs decrease UV-induced skin we evaluated ability two compounds, celecoxib (a specific inhibitor) indomethacin NSAID), to block tumor development SKH:HR-1-hrBr...

10.1002/(sici)1098-2744(199908)25:4<231::aid-mc1>3.0.co;2-f article EN Molecular Carcinogenesis 1999-08-01

Transgenic mice expressing human insulin-like growth factor 1 (IGF-1) in basal epithelial cells of prostate have been characterized. Transgene expression led to activation the IGF-1 receptor and spontaneous tumorigenesis epithelium. Hyperplasia was evident these by 2–3 months age. Atypical hyperplasias prostatic intraepithelial neoplasia were 6–7 Well differentiated adenocarcinomas appeared 6 or older. Less tumors, diagnosed as small cell carcinomas, also observed two older mice. Both lobes...

10.1073/pnas.97.7.3455 article EN Proceedings of the National Academy of Sciences 2000-03-28

p21 WAF1/Cip1 is one of the best characterized downstream targets p53, and growth suppressing function this cyclin-dependent kinase inhibitor well established. However, whether exerts a tumor-suppressing its own remains to be We report here that, similarly loss disruption gene results in markedly increased susceptibility chemically induced skin carcinoma formation, whereas number papillomas reduced. Previous evidence indicates that malignant versus benign keratinocyte tumor formation likely...

10.1073/pnas.96.16.9089 article EN Proceedings of the National Academy of Sciences 1999-08-03

To study the involvement of cyclin D1 in epithelial growth and differentiation its putative role as an oncogene skin, transgenic mice were developed carrying human gene driven by a bovine keratin 5 promoter. As expected, all squamous epithelia including oral mucosa, trachea, vaginal epithelium, compartment thymus expressed aberrant levels D1. The rate epidermal proliferation increased dramatically mice, which also showed basal cell hyperplasia. However, was unaffected, shown normal arrest...

10.1073/pnas.93.15.7634 article EN Proceedings of the National Academy of Sciences 1996-07-23

Using a transgenic mouse model expressing the E2F1 gene under control of keratin 5 (K5) promoter, we previously demonstrated that increased activity can promote tumorigenesis by cooperating with either v-Ha-ras transgene to induce benign skin papillomas or p53 deficiency spontaneous carcinomas. We now report as K5 mice age, they are predisposed develop tumors in variety K5-expressing tissues, including skin, vagina, forestomach, and odontogenic epithelium. On other hand, found be resistant...

10.1128/mcb.19.9.6408 article EN Molecular and Cellular Biology 1999-09-01

No AccessJournal of UrologyClinical Urology: Original Article1 Feb 1997Expression BCL-2 Oncoprotein and P53 Protein Accumulation in Bone Marrow Metastases Androgen Independent Prostate Cancer Timothy J. McDonnel, Nora M. Navone, Patricia Troncoso, Louis L. Pisters, Claudio Conti, Andrew C. von Eschenbach, Shawn Brisbay, Christopher Logothetis McDonnelTimothy McDonnel , NavoneNora Navone TroncosoPatricia Troncoso PistersLouis Pisters ContiClaudio Conti EschenbachAndrew Eschenbach BrisbayShawn...

10.1016/s0022-5347(01)65204-2 article EN The Journal of Urology 1997-02-01

Loss of heterozygosity in human chromosome 7q was studied to determine the location a putative tumor suppressor gene. Twenty-six 31 cases presented loss at one or more loci on 7q. Eighty-three percent (in 11 informative cases) detected by using (C-A)n microsatellite repeat marker D7S522 7q31.1-7q31.2. These results suggest that gene relevant development breast cancer is present 7q31.1-7q31.2 region, confirming our previous evidence for this and frequent deletions long arm primary cancers.

10.1073/pnas.91.25.12155 article EN Proceedings of the National Academy of Sciences 1994-12-06

The proto-oncogene c-myc encodes a transcription factor that is implicated in the regulation of cellular proliferation, differentiation, and apoptosis has also been found to be deregulated several forms human experimental tumors.We have shown forced expression epithelial tissues transgenic mice (K5-Myc) resulted keratinocyte hyperproliferation development spontaneous tumors skin oral cavity.Although number genes involved cancer are regulated by c-myc, actual mechanisms leading Myc-induced...

10.1128/mcb.24.17.7538-7547.2004 article EN Molecular and Cellular Biology 2004-08-16

Abstract Using a direct cytogenetic technique, we identified nonrandom trisomy of chromosome 6 in 12 aneuploid mouse skin papillomas and 10 11 squamous cell carcinomas induced by chemical carcinogenesis. The second most common abnormality observed was 7 found dysplastic carcinomas. two trisomies were the only abnormalities all several Mutation at codon 61 Ha‐ ras gene, which resides on 7, also feature tumors sampled. Extensive homology exists between human recently suggested as primary event...

10.1002/mc.2940020104 article EN Molecular Carcinogenesis 1989-01-01

Cyclooxygenase-2 (COX-2) overexpression is an established factor linking chronic inflammation with metaplastic and neoplastic change in various tissues. We generated transgenic mice (BK5.COX-2) which elevation of COX-2 its effectors trigger a metaplasia-dysplasia sequence exocrine pancreas. Histologic evaluation revealed pancreatitis-like state characterized by acinar-to-ductal metaplasia well-vascularized fibroinflammatory stroma that develops 3 months. By 6 to 8 months, strongly dysplastic...

10.1593/neo.08330 article EN cc-by-nc-nd Neoplasia 2008-08-01

Journal Article Aneuploidy, an early event in mouse skin tumor development Get access Claudio J. Conti, Conti 1 To whom reprint requests should be sent Search for other works by this author on: Oxford Academic PubMed Google Scholar M. Aldaz, Aldaz John O'Connell, O'Connell Andres J.P. Klein-Szanto, Klein-Szanto 2Fox Chase Cancer Center, Department of Pathology, 7701 Burholme AvenuePhiladelphia, PA 19111, USA Thomas Slaga Carcinogenesis, Volume 7, Issue 11, November 1986, Pages 1845–1848,...

10.1093/carcin/7.11.1845 article EN Carcinogenesis 1986-01-01

Recessive dystrophic epidermolysis bullosa (RDEB), Kindler syndrome (KS) and xeroderma pigmentosum complementation group C (XPC) are three cancer‐prone genodermatoses whose causal genetic mutations cannot fully explain, on their own, the array of associated phenotypic manifestations. Recent evidence highlights role stromal microenvironment in pathology these disorders. To investigate, by means comparative gene expression analysis, played dermal fibroblasts pathogenesis RDEB, KS XPC. We...

10.1111/bjd.17698 article EN cc-by-nc British Journal of Dermatology 2019-01-29
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