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  • 1
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    p53 status and the efficacy of cancer therapy in vivo (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-11-04
    Description: The therapeutic responsiveness of genetically defined tumors expressing or devoid of the p53 tumor suppressor gene was compared in immunocompromised mice. Tumors expressing the p53 gene contained a high proportion of apoptotic cells and typically regressed after treatment with gamma radiation or adriamycin. In contrast, p53-deficient tumors treated with the same regimens continued to enlarge and contained few apoptotic cells. Acquired mutations in p53 were associated with both treatment resistance and relapse in p53-expressing tumors. These results establish that defects in apoptosis, here caused by the inactivation of p53, can produce treatment-resistant tumors and suggest that p53 status may be an important determinant of tumor response to therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lowe, S W -- Bodis, S -- McClatchey, A -- Remington, L -- Ruley, H E -- Fisher, D E -- Housman, D E -- Jacks, T -- 5R27CA17575/CA/NCI NIH HHS/ -- CA14051/CA/NCI NIH HHS/ -- R01CA40602/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1994 Nov 4;266(5186):807-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Cancer Research, Massachusetts Institute of Technology, Cambridge 02139.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7973635" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Doxorubicin/*therapeutic use ; Drug Resistance ; Fibrosarcoma/drug therapy/*genetics/radiotherapy/*therapy ; *Gamma Rays ; *Genes, p53/genetics ; Immunocompromised Host ; Mice ; Mice, Nude ; Mutation ; Neoplasm Recurrence, Local ; Neoplasm Transplantation ; Radiation Tolerance
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    The melanoma revolution: from UV carcinogenesis to a new era in therapeutics (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-11-22
    Description: Melanoma, the deadliest form of skin cancer, is an aggressive disease that is rising in incidence. Although melanoma is a historically treatment-resistant malignancy, in recent years unprecedented breakthroughs in targeted therapies and immunotherapies have revolutionized the standard of care for patients with advanced disease. Here, we provide an overview of recent developments in our understanding of melanoma risk factors, genomics, and molecular pathogenesis and how these insights have driven advances in melanoma treatment. In addition, we review benefits and limitations of current therapies and look ahead to continued progress in melanoma prevention and therapy. Remarkable achievements in the field have already produced a paradigm shift in melanoma treatment: Metastatic melanoma, once considered incurable, can now be treated with potentially curative rather than palliative intent.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4701046/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4701046/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lo, Jennifer A -- Fisher, David E -- P01 CA163222/CA/NCI NIH HHS/ -- P01CA163222/CA/NCI NIH HHS/ -- R01 AR043369/AR/NIAMS NIH HHS/ -- R01 CA150226/CA/NCI NIH HHS/ -- R01AR043369/AR/NIAMS NIH HHS/ -- R01CA150226/CA/NCI NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- T32GM007753/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2014 Nov 21;346(6212):945-9. doi: 10.1126/science.1253735.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cutaneous Biology Research Center, Department of Dermatology and MGH Cancer Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA. ; Cutaneous Biology Research Center, Department of Dermatology and MGH Cancer Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA. dfisher3@partners.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25414302" target="_blank"〉PubMed〈/a〉
    Keywords: Carcinogenesis/genetics/*pathology ; Drug Approval ; Epigenesis, Genetic ; Humans ; Immunotherapy ; Melanocytes/*pathology ; Melanoma/*drug therapy/genetics/pathology ; *Molecular Targeted Therapy ; Mutation ; Neoplasms, Radiation-Induced/drug therapy/genetics/pathology ; Skin Neoplasms/*drug therapy/genetics/pathology ; Sunlight ; Ultraviolet Rays/adverse effects
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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