High Levels of Expression of p27KIP1 and Cyclin E in Invasive Primary Malignant Melanomas
Cancer cells have abnormal cell cycle regulation which favors accelerated proliferation, chromosomal instability, and resistance to the senescence response. Although the p16INK4a locus is the most prominent susceptibility locus for familial melanomas, the low frequency of p16 mutations in sporadic m...
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Published in | Journal of investigative dermatology Vol. 113; no. 6; pp. 1039 - 1046 |
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Main Authors | , , , , , , , , , , |
Format | Journal Article Conference Proceeding |
Language | English |
Published |
Danvers, MA
Elsevier Inc
01.12.1999
Nature Publishing |
Subjects | |
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Abstract | Cancer cells have abnormal cell cycle regulation which favors accelerated proliferation, chromosomal instability, and resistance to the senescence response. Although the p16INK4a locus is the most prominent susceptibility locus for familial melanomas, the low frequency of p16 mutations in sporadic melanomas suggests additional alterations in other cell cycle regulatory genes. Here we used primary melanoma tumors to reveal early cell cycle alterations that could be masked in advanced metastatic lesions due to their inherently high genetic instability. Unexpectedly, the cyclin-dependent kinase inhibitors p27KIP1 and/or p21Waf-1/SDI-1 were found to be expressed in 13 of 18 (72%) of the primary melanomas with a Breslow thickness greater than 0.076 mm. In general, p27 and/or p21 staining in the primary tumors correlated with low Ki-67 index. Importantly, most of the p21- and p27-positive tumors expressed high levels of cyclin D1 and cyclin E. In proliferating cells p27 is predominantly associated with cyclin D-CDK4 complexes, but does not inhibit the kinase activity, whereas in quiescent cells p27 is found associated with inactive CDK2 complexes. p27 was also expressed at high levels in proliferating primary melanomas in culture, and found to be associated with active cyclin E–CDK2 complexes containing high levels of cyclin E. It is thus likely that accumulation of cyclin E overcomes the potent inhibitory activity of p27 and p21 in CDK2 complexes. Of the primary melanomas with no indication of invasiveness, only three of 15 (20%) were positive for p27 and/or p21. We propose that high levels of p27 and p21 may confer upon melanoma tumors their characteristic resistance to conventional therapies. In turn, high levels of cyclins E and D1 may contribute to unlimited proliferation in primary melanomas that express the tumor suppressor p16INK4.J Invest Dermatol 113:1039–1046 1999 |
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AbstractList | Cancer cells have abnormal cell cycle regulation which favors accelerated proliferation, chromosomal instability, and resistance to the senescence response. Although the p16INK4a locus is the most prominent susceptibility locus for familial melanomas, the low frequency of p16 mutations in sporadic melanomas suggests additional alterations in other cell cycle regulatory genes. Here we used primary melanoma tumors to reveal early cell cycle alterations that could be masked in advanced metastatic lesions due to their inherently high genetic instability. Unexpectedly, the cyclin-dependent kinase inhibitors p27KIP1 and/or p21Waf-1/SDI-1 were found to be expressed in 13 of 18 (72%) of the primary melanomas with a Breslow thickness greater than 0.076 mm. In general, p27 and/or p21 staining in the primary tumors correlated with low Ki-67 index. Importantly, most of the p21- and p27-positive tumors expressed high levels of cyclin D1 and cyclin E. In proliferating cells p27 is predominantly associated with cyclin D-CDK4 complexes, but does not inhibit the kinase activity, whereas in quiescent cells p27 is found associated with inactive CDK2 complexes. p27 was also expressed at high levels in proliferating primary melanomas in culture, and found to be associated with active cyclin E–CDK2 complexes containing high levels of cyclin E. It is thus likely that accumulation of cyclin E overcomes the potent inhibitory activity of p27 and p21 in CDK2 complexes. Of the primary melanomas with no indication of invasiveness, only three of 15 (20%) were positive for p27 and/or p21. We propose that high levels of p27 and p21 may confer upon melanoma tumors their characteristic resistance to conventional therapies. In turn, high levels of cyclins E and D1 may contribute to unlimited proliferation in primary melanomas that express the tumor suppressor p16INK4.J Invest Dermatol 113:1039–1046 1999 |
Author | Bales, Elise S. Bandyopadhyay, Debdutta Conrad, Nicole Medrano, Estela E. Dietrich, Cheryl Xu, Weidong Leiss, Paula Didenko, Vladimir Pereira-Smith, Olivia Orengo, Ida Schwahn, Denise J. |
Author_xml | – sequence: 1 givenname: Elise S. surname: Bales fullname: Bales, Elise S. organization: Huffington Center on Aging, Houston, Texas, U.S.A – sequence: 2 givenname: Cheryl surname: Dietrich fullname: Dietrich, Cheryl organization: Huffington Center on Aging, Houston, Texas, U.S.A – sequence: 3 givenname: Debdutta surname: Bandyopadhyay fullname: Bandyopadhyay, Debdutta organization: Huffington Center on Aging, Houston, Texas, U.S.A – sequence: 4 givenname: Denise J. surname: Schwahn fullname: Schwahn, Denise J. organization: Huffington Center on Aging, Houston, Texas, U.S.A – sequence: 5 givenname: Weidong surname: Xu fullname: Xu, Weidong organization: Huffington Center on Aging, Houston, Texas, U.S.A – sequence: 6 givenname: Vladimir surname: Didenko fullname: Didenko, Vladimir organization: Department of Neurosurgery, Baylor College of Medicine and Department of Dermatology, Houston, Texas, U.S.A – sequence: 7 givenname: Paula surname: Leiss fullname: Leiss, Paula organization: Department of Dermatology, Houston, Texas, U.S.A – sequence: 8 givenname: Nicole surname: Conrad fullname: Conrad, Nicole organization: Department of Dermatology, Houston, Texas, U.S.A – sequence: 9 givenname: Olivia surname: Pereira-Smith fullname: Pereira-Smith, Olivia organization: Huffington Center on Aging, Houston, Texas, U.S.A – sequence: 10 givenname: Ida surname: Orengo fullname: Orengo, Ida organization: Department of Dermatology, Houston, Texas, U.S.A – sequence: 11 givenname: Estela E. surname: Medrano fullname: Medrano, Estela E. email: medrano@bcm.tmc.edu organization: Huffington Center on Aging, Houston, Texas, U.S.A |
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Keywords | Human Skin disease Enzyme Kinase Transferases Malignant melanoma Enzyme inhibitor Malignant tumor Metastasis Cyclin D1 Carcinogenesis |
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SubjectTerms | Biological and medical sciences CDC2-CDC28 Kinases Cell Cycle Proteins Cyclin D1 - analysis Cyclin E - analysis Cyclin-Dependent Kinase 2 Cyclin-Dependent Kinase Inhibitor p27 Cyclin-Dependent Kinases - analysis Dermatology Humans Immunohistochemistry Medical sciences Melanoma - chemistry Microfilament Proteins - analysis Microtubule-Associated Proteins - analysis Muscle Proteins Protein-Serine-Threonine Kinases - analysis Tumor Suppressor Proteins Tumors of the skin and soft tissue. Premalignant lesions |
Title | High Levels of Expression of p27KIP1 and Cyclin E in Invasive Primary Malignant Melanomas |
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