Linked Life Data

10754491

Source:http://linkedlifedata.com/resource/pubmed/id/10754491

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2000-4-27
pubmed:abstractText
We have examined whether the extended life span of cells induced by Bcl-2 in T(1) ductal breast carcinomas might favor the acquisition and accumulation of genetic alterations that induce lymph node metastases. We analyzed the expression of c-Myc, c-erbB-2 and epidermal growth factor receptor by immuno-histochemistry in a group of 142 T(1) (<2 cm) ductal breast carcinomas embedded in paraffin, previously studied for p53 mutation and Bcl-2 over-expression. We also measured the apoptotic status and estimated the excess risk (pOR) for lymph node metastasis according to the number of accumulated oncogene alterations and Bcl-2 and p53 expression. The linear relationship between number of oncogene alterations and presence of lymph node metastasis was statistically significant in Bcl-2-positive tumors (trend test, p = 0.03), p53-mutated tumors (trend test, p = 0.08) and tumors with loss of apoptosis (trend test, p = 0.08). Very large associations (pOR > 12) between the number of oncogene alterations and lymph node metastasis were observed among Bcl-2-positive tumors that showed increased loss of apoptosis (trend test, p = 0.03). Furthermore, in p53-negative tumors, a strong linear association was found between the number of oncogene alterations and risk of lymph node metastasis among Bcl-2-positive tumors (trend test, p = 0.03). In human T(1) ductal breast carcinoma, over-expression of Bcl-2 along with loss of apoptosis might render breast cancer cells susceptible to the acquisition of additional genetic lesions related to disease progression among p53-negative tumors. Thus, in breast cancer, there are at least 2 pathways to progression: Bcl-2- and p53-dependent mechanisms.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0020-7136
pubmed:author
pubmed:copyrightInfo
Copyright 2000 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:day
20
pubmed:volume
89
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
142-7
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:10754491-Antibodies, Monoclonal, pubmed-meshheading:10754491-Apoptosis, pubmed-meshheading:10754491-Breast Neoplasms, pubmed-meshheading:10754491-Carcinoma, Ductal, Breast, pubmed-meshheading:10754491-Female, pubmed-meshheading:10754491-Gene Expression Regulation, Neoplastic, pubmed-meshheading:10754491-Genes, bcl-2, pubmed-meshheading:10754491-Humans, pubmed-meshheading:10754491-In Situ Nick-End Labeling, pubmed-meshheading:10754491-Linear Models, pubmed-meshheading:10754491-Lymphatic Metastasis, pubmed-meshheading:10754491-Proto-Oncogene Proteins c-bcl-2, pubmed-meshheading:10754491-Proto-Oncogene Proteins c-myc, pubmed-meshheading:10754491-Receptor, Epidermal Growth Factor, pubmed-meshheading:10754491-Receptor, erbB-2, pubmed-meshheading:10754491-Receptors, Estrogen, pubmed-meshheading:10754491-Receptors, Progesterone
pubmed:year
2000
pubmed:articleTitle
Bcl-2 with loss of apoptosis allows accumulation of genetic alterations: a pathway to metastatic progression in human breast cancer.
pubmed:affiliation
Departament i Càncer Metàstasis, Institut de Recerca Oncològica, Hospital Duran i Reynals, Ciutat Sanitaria i Universitaria de Bellvitge, Barcelona, Spain. asierra@iro.es
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't