Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1998-3-2
pubmed:databankReference
pubmed:abstractText
Loss of heterozygosity (LOH) at chromosome 10q23-q25 is frequent in small cell lung cancer (SCLC), indicating the presence of putative tumor suppressor genes. PTEN/ MMAC1, a newly cloned candidate tumor suppressor gene at 10q23, was mutated in multiple human cancers. We investigated whether mutations of PTEN/MMAC1 play an important role in SCLC tumorigenesis. We examined 16 SCLC cell lines for PTEN/MMAC1 mRNA expression by reverse-transcriptase polymerase chain reaction (RT-PCR) and potential mutations by sequencing analysis of the PTEN/MMAC1 coding region. No mutation was observed in PTEN/MMAC1 cDNAs in 15 cell lines expressing PTEN/MMAC1. One SCLC cell line, DMS79, did not have detectable PTEN/ MMAC1 expression. Importantly, we identified a novel homologue of PTEN/MMAC1, termed PTH2, localized to chromosome 9p21-q13 and containing only ten amino acid substitutions compared with the PTEN/MMAC1 coding region. However, because the putative initiation codon for PTEN/MMAC1 gene was changed to arginine in PTH2, the translational initiation site of PTH2 is very likely to differ from that of the PTEN/MMAC1. PTH2 was expressed in two normal lung tissues and two normal colon tissues, but in only four of 16 SCLC cell lines. A missense mutation in PTH2 was identified in a SCLC cell line that did not express PTEN/MMAC1 mRNA. Our data suggest that inactivation of PTEN/ MMAC1 is a rare event in SCLC tumorigenesis. However, the PTEN/MMAC1 homologue PTH2 may play a role in SCLC tumorigenesis.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0950-9232
pubmed:author
pubmed:issnType
Print
pubmed:day
8
pubmed:volume
16
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
89-93
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:9467947-Amino Acid Sequence, pubmed-meshheading:9467947-Base Sequence, pubmed-meshheading:9467947-Carcinoma, Small Cell, pubmed-meshheading:9467947-Chromosome Mapping, pubmed-meshheading:9467947-Chromosomes, Human, Pair 9, pubmed-meshheading:9467947-DNA, Complementary, pubmed-meshheading:9467947-Genes, Tumor Suppressor, pubmed-meshheading:9467947-Humans, pubmed-meshheading:9467947-Lung Neoplasms, pubmed-meshheading:9467947-Molecular Sequence Data, pubmed-meshheading:9467947-PTEN Phosphohydrolase, pubmed-meshheading:9467947-Phosphoric Monoester Hydrolases, pubmed-meshheading:9467947-Polymerase Chain Reaction, pubmed-meshheading:9467947-Protein Tyrosine Phosphatases, pubmed-meshheading:9467947-Proteins, pubmed-meshheading:9467947-Sequence Homology, Amino Acid, pubmed-meshheading:9467947-Tumor Cells, Cultured, pubmed-meshheading:9467947-Tumor Suppressor Proteins
pubmed:year
1998
pubmed:articleTitle
Alterations of PTEN/MMAC1, a candidate tumor suppressor gene, and its homologue, PTH2, in small cell lung cancer cell lines.
pubmed:affiliation
Department of Thoracic/Head and Neck Medical Oncology, The University of Texas M.D. Anderson Cancer Center, Houston 77030, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.