<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>94(1)</volume><submitter>Puisieux A</submitter><pubmed_abstract>A major obstacle to the expansion of abnormal cells with significant proliferative potential is the induction of programmed cell death. Consequently, oncogene-driven hyperproliferation must be associated with apoptosis inhibition to allow malignant outgrowth. The oncogenic cooperation of N-Myc and Twist-1 in the development of neuroblastoma, the most common and deadly solid tumour of childhood, perfectly illustrates such a process. N-Myc promotes cell proliferation, whereas Twist-1 counteracts its pro-apoptotic properties by knocking-down the ARF/p53 pathway. On the basis of numerous recent studies reporting its overexpression in a variety of human cancers, we discuss in this review the role of Twist-1 as a potent inhibitor of the cell safety programs engaged in response to an abnormal mit</pubmed_abstract><journal>British journal of cancer</journal><pagination>13-7</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC2361066</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>A twist for survival and cancer progression.</pubmed_title><pmcid>PMC2361066</pmcid><pubmed_authors>Ansieau S</pubmed_authors><pubmed_authors>Puisieux A</pubmed_authors><pubmed_authors>Valsesia-Wittmann S</pubmed_authors></additional><is_claimable>false</is_claimable><name>A twist for survival and cancer progression.</name><description>A major obstacle to the expansion of abnormal cells with significant proliferative potential is the induction of programmed cell death. Consequently, oncogene-driven hyperproliferation must be associated with apoptosis inhibition to allow malignant outgrowth. The oncogenic cooperation of N-Myc and Twist-1 in the development of neuroblastoma, the most common and deadly solid tumour of childhood, perfectly illustrates such a process. N-Myc promotes cell proliferation, whereas Twist-1 counteracts its pro-apoptotic properties by knocking-down the ARF/p53 pathway. On the basis of numerous recent studies reporting its overexpression in a variety of human cancers, we discuss in this review the role of Twist-1 as a potent inhibitor of the cell safety programs engaged in response to an abnormal mit</description><dates><release>2006-01-01T00:00:00Z</release><publication>2006 Jan</publication><modification>2025-04-18T15:08:57.156Z</modification><creation>2019-03-27T02:44:55Z</creation></dates><accession>S-EPMC2361066</accession><cross_references><pubmed>16306876</pubmed><doi>10.1038/sj.bjc.6602876</doi></cross_references></HashMap>