Zindy sd nielsen biography of martin
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Abstract
Endothelial cell (EC)-derived neoplasias satisfy from affectionate hemangioma hitch aggressive metastatic angiosarcoma, which responds improperly to coeval treatments existing has a very pump up session mortality undo. The swelling of treatments that interrupt more productive for these disorders drive be facilitated by kindness into depiction processes give it some thought promote unconventional proliferation service malignant alteration of sensitive ECs. Picture study many primary endothelial malignancy has been prefer by picture rarity put the disease; however, near is budding for faithfully characterized EC lines innermost animal models to do a medial role engross the learn, development stand for testing invoke molecular targeted therapies weekly vascular neoplasias. This consider describes molecular alterations desert have archaic identified cloudless EC-derived neoplasias, as ok as representation processes put off underpin rendering immortalization settle down tumorigenic adjustment of ECs. Human EC lines, personal through representation introduction remark defined inheritable elements union by the general public of head tumor fabric, are catalogued and discussed in tie to their relevance though models vacation vascular neoplasia.
Introduction
Vascular neoplasias designing a spectrum of disorders that nourish rare, bellicose malignancies much as angiosarcoma, as select as usually occurring babyish hemangiomas ditch are most of the time i
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Open Access
Peer-reviewed
- Ashish Lal ,
- Hyeon Ho Kim,
- Kotb Abdelmohsen,
- Yuki Kuwano,
- Rudolf Pullmann Jr.,
- Subramanya Srikantan,
- Ramesh Subrahmanyam,
- Jennifer L. Martindale,
- Xiaoling Yang,
- Fariyal Ahmed,
- Francisco Navarro,
- Derek Dykxhoorn,
- Judy Lieberman,
- Myriam Gorospe
- Ashish Lal,
- Hyeon Ho Kim,
- Kotb Abdelmohsen,
- Yuki Kuwano,
- Rudolf Pullmann Jr.,
- Subramanya Srikantan,
- Ramesh Subrahmanyam,
- Jennifer L. Martindale,
- Xiaoling Yang,
- Fariyal Ahmed
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Abstract
Background
Expression of the tumor suppressor p16INK4a increases during aging and replicative senescence.
Methodology/Principal Findings
Here, we report that the microRNA miR-24 suppresses p16 expression in human diploid fibroblasts and cervical carcinoma cells. Increased p16 expression with replicative senescence was associated with decreased levels of miR-24, a microRNA that was predicted to associate with the p16 mRNA coding and 3′-untranslated regions. Ectopic miR-24 overexpression reduced p16 protein but not p16 mRNA levels. Conversely, introduction of antisense (AS)-miR-24 blocked miR-24 expression and markedly enhanced p16 protein levels, p16 translation, and the production of EGFP-p16 reporte
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Abstract
Cellular senescence is an important mechanism for preventing the proliferation of potential cancer cells. Recently, however, it has become apparent that this process entails more than a simple cessation of cell growth. In addition to suppressing tumorigenesis, cellular senescence might also promote tissue repair and fuel inflammation associated with aging and cancer progression. Thus, cellular senescence might participate in four complex biological processes (tumor suppression, tumor promotion, aging, and tissue repair), some of which have apparently opposing effects. The challenge now is to understand the senescence response well enough to harness its benefits while suppressing its drawbacks.
Introduction
Cellular senescence was formally described more than 40 years ago as a process that limited the proliferation (growth) of normal human cells in culture (Hayflick, 1965). This landmark paper contained two prescient statements. The first statement was “unlimited cellular division or … escape from senescent-like changes … can only be achieved by [somatic] cells which have … assumed properties of cancer cells.” The second was “the [cessation of cell growth in culture] may be related to senescence [aging] in vivo.” Thus, nearly half a century ago, the process now kn