Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2007-4-10
pubmed:abstractText
Cancer dormancy delineates a situation in which residual tumor cells persist in a patient with no apparent clinical symptoms. Although the precise mechanisms underlying cancer dormancy have not been explained, experimental models have provided some insights into the factors that might be involved in the induction and maintenance of a tumor dormant state. The authors of the present chapter studied a murine B cell lymphoma that can be made dormant when interacting with antibodies directed against the idiotype on its immunoglobulin Ig receptor. This experimental model of antibody-induced dormancy enabled the isolation and characterization of dormant lymphoma cells. The results indicated that anti-Ig antibodies activate growth-inhibiting signals that induced cycle arrest and apoptosis. This process appeared to be balanced by the growth of the tumor cells such that the tumor did not expand. In contrast, antibodies against HER-2expressed on prostate adenocarcinoma (PAC) cells were not growth inhibitory. However, an immunotoxin (IT) prepared by conjugating HER-2 to the A-chain of ricin (RTA) was internalized by PAC cells, followed by induction of cycle arrest and apoptotic death. Infusion of HER-2-specific IT into PAC-bearing immunodeficient mice did not eradicate the tumor but retained it dormant over an extended period of time. Hence, certain aspects of signaling receptors expressed on cancer can be manipulated by antibodies to induce and maintain a tumor dormant state.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0065-230X
pubmed:author
pubmed:issnType
Print
pubmed:volume
97
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
189-202
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:17419946-Adenocarcinoma, pubmed-meshheading:17419946-Animals, pubmed-meshheading:17419946-Antibodies, Anti-Idiotypic, pubmed-meshheading:17419946-Apoptosis, pubmed-meshheading:17419946-Breast Neoplasms, pubmed-meshheading:17419946-Cell Cycle, pubmed-meshheading:17419946-Disease Progression, pubmed-meshheading:17419946-Female, pubmed-meshheading:17419946-Humans, pubmed-meshheading:17419946-Immunologic Surveillance, pubmed-meshheading:17419946-Immunotherapy, pubmed-meshheading:17419946-Immunotoxins, pubmed-meshheading:17419946-Lymphoma, B-Cell, pubmed-meshheading:17419946-Male, pubmed-meshheading:17419946-Mice, pubmed-meshheading:17419946-Mice, Inbred BALB C, pubmed-meshheading:17419946-Mice, SCID, pubmed-meshheading:17419946-Models, Biological, pubmed-meshheading:17419946-Neoplasm, Residual, pubmed-meshheading:17419946-Prostatic Neoplasms, pubmed-meshheading:17419946-Receptor, erbB-2, pubmed-meshheading:17419946-Receptors, Antigen, B-Cell, pubmed-meshheading:17419946-Ricin
pubmed:year
2007
pubmed:articleTitle
Cancer dormancy: lessons from a B cell lymphoma and adenocarcinoma of the prostate.
pubmed:affiliation
Lautenberg Center for General and Tumor Immunology, Hebrew University of Jerusalem, Jerusalem 91120, Israel.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't