A5000634626- Cancer-related Molecular Pathways
- Epigenetics and DNA Methylation
- Ubiquitin and proteasome pathways
- Cancer Research and Treatments
- Telomeres, Telomerase, and Senescence
- Microtubule and mitosis dynamics
- Ocular Oncology and Treatments
- Melanoma and MAPK Pathways
- Advanced Breast Cancer Therapies
- Genomics and Chromatin Dynamics
- interferon and immune responses
- RNA modifications and cancer
- Virus-based gene therapy research
- Cancer Cells and Metastasis
- Cancer Genomics and Diagnostics
- Cancer, Hypoxia, and Metabolism
- Retinoids in leukemia and cellular processes
- Cancer-related molecular mechanisms research
- Autophagy in Disease and Therapy
- PI3K/AKT/mTOR signaling in cancer
- CRISPR and Genetic Engineering
- Cell Adhesion Molecules Research
- Hedgehog Signaling Pathway Studies
- Lung Cancer Treatments and Mutations
- melanin and skin pigmentation
Tufts University
2015-2024
Tufts Medical Center
2009-2023
Molecular Oncology (United States)
2009-2023
The Graduate Center, CUNY
2021
Institut thématique Génétique, génomique et bioinformatique
2013
Boston University
2013
Ariadne Diagnostics (United States)
2013
Harvard University
1997-2006
University of Virginia
2005
Howard Hughes Medical Institute
2005
The 11-4 p53 cDNA clone failed to transform primary rat fibroblasts when cotransfected with the ras oncogene. Two linker insertion mutations at amino acid 158 or 215 (of 390 acids) activated this for transformation ras. These mutant cDNAs produced a protein that lacked an epitope, recognized by monoclonal antibody PAb246 (localized acids 88 110 in protein) and preferentially bound heat shock protein, hsc70. In cells transformed genomic plus ras, two populations of proteins were detected,...
Previous experiments have brought into question which amino acid sequence of the p53 oncogene product should be considered wild type and whether normal protein is capable cooperating with ras to transform cells in culture. To address these questions, a series cDNA-genomic hybrid clones been compared for ability cooperate transformation assays. From experiments, it has become clear that alanine at position 135, either genomic clone or cDNA clone, failed produce cooperated transformed cells....
The cyclin D1 (PRAD1, CCND1) gene is affected by translocations and amplification in the genomes of a number human tumors, suggesting that these changes confer growth advantage on developing tumor cell clones. We show here cultured cells, cDNA clone can contribute to transformation complementing defective adenovirus E1A oncogene. In such this candidate oncogene indeed functions like an oncogene, similar role progression vivo.
Cyclin D1 plays an important role in the development of breast cancer and is required for normal cell proliferation differentiation associated with pregnancy. We show that ectopic expression cyclin can stimulate transcriptional activity estrogen receptor absence estradiol this be inhibited by 4-hydroxytamoxifen ICI 182,780. form a specific complex receptor. Stimulation independent cyclin-dependent kinase 4 activation. may manifest its oncogenic potential part through binding to activation
The 11-4 p53 cDNA clone failed to transform primary rat fibroblasts when cotransfected with the ras oncogene. Two linker insertion mutations at amino acid 158 or 215 (of 390 acids) activated this for transformation ras. These mutant cDNAs produced a protein that lacked an epitope, recognized by monoclonal antibody PAb246 (localized acids 88 110 in protein) and preferentially bound heat shock protein, hsc70. In cells transformed genomic plus ras, two populations of proteins were detected,...
In mammals, hair cell loss causes irreversible hearing and balance impairment because cells are terminally differentiated do not regenerate spontaneously. By profiling gene expression in developing mouse vestibular organs, we identified the retinoblastoma protein (pRb) as a candidate regulator of cycle exit cells. Differentiated functional with targeted deletion Rb1 undergo mitosis, divide, cycle, yet continue to become highly functional. Moreover, acute postnatal caused reentry....
A rabbit antiserum was prepared against the C-terminal peptide of 21 amino acids from human heat shock protein hsp70. These antibodies were shown to be specific for this highly inducible (72 kilodaltons [kDa] in rat cells), and a moderately inducible, constitutively expressed protein, hsc70 (74 kDa). In six independently derived cell lines transformed by murine cDNA-genomic hybrid clone p53 plus an activated Ha-ras gene, elevated levels detected immunoprecipitation using murine-specific...
The molecular basis for the inverse relationship between differentiation and tumorigenesis is unknown. function of runx2, a master regulator osteoblast belonging to runt family tumor suppressor genes, consistently disrupted in osteosarcoma cell lines. Ectopic expression runx2 induces p27KIP1, thereby inhibiting activity S-phase cyclin complexes leading dephosphorylation retinoblastoma protein (pRb) G1 cycle arrest. Runx2 physically interacts with hypophosphorylated form pRb, known...
In this study, we show that NANOG, a master transcription factor, regulates S-phase entry in human embryonic stem cells (hESCs) via transcriptional regulation of cell cycle regulatory components. Chromatin immunoprecipitation combined with reporter-based transfection assays the C-terminal region NANOG binds to regions CDK6 and CDC25A genes under normal physiological conditions. Decreased expression hESCs suggest both are involved regulation. The effects overexpression on mitigated by...
Abstract Although BRCA1 function is essential for maintaining genomic integrity in all cell types, it unclear why increased risk of cancer individuals harbouring deleterious mutations restricted to only a select few tissues. Here we show that human mammary epithelial cells (HMECs) from -mutation carriers ( mut/+ ) exhibit instability and rapid telomere erosion the absence tumour-suppressor loss. Furthermore, uncover novel form haploinsufficiency-induced senescence (HIS) specific cells, which...