Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of mouse control cell line and a cell line surviving exposure to tumor-specific CTL (cytolytic T lymphocyte)


ABSTRACT: The CMS4 sarcoma, kindly provided by A. DeLeo (University of Pittsburgh, Pittsburgh, PA), is a solid tumor of BALB/c (H-2d) origin, which grows aggressively in naive, syngeneic hosts following a s.c. transplant. Although the parental tumor cell line forms few metastatic foci in the lungs following i.v. administration, a highly metastatic subline, termed CMS4-met, was established from lung digests of those mice as described (Ryan MH, Bristol JA, McDuffie E, Abrams SI. Regression of extensive pulmonary metastases in mice by adoptive transfer of antigen-specific CD8(+) CTL reactive against tumor cells expressing a naturally occurring rejection epitope. J Immunol 2001;167:4286-92).
In this experiment we compare the gene expression profiles between a control cell line and a cell line surviving exposure to tumor-specific CTL (cytolytic T lymphocyte). CMS4-met cells were injected iv. to the mouse tails. Three days later, either saline or tumor-specific CTL were injected iv into mouse tails. Single cell suspensions were made from mouse lungs and put in culture. Tumor cells were recovered from cultures. Tumor cells established from mice receiving saline were termed CMS4-met.cntl. Tumor cells established from mice receiving CTL were termed CMS4-met.sel. The gene expression profiles of these two tumor cell lines were then compared to CMS4-met.

ORGANISM(S): Mus musculus

SUBMITTER: Kebin Liu 

PROVIDER: E-MEXP-287 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Immune selection and emergence of aggressive tumor variants as negative consequences of Fas-mediated cytotoxicity and altered IFN-gamma-regulated gene expression.

Liu Kebin K   Caldwell Sheila A SA   Abrams Scott I SI  

Cancer research 20050501 10


Antitumor responses can be induced in patients via active or adoptive immunotherapy, yet complete tumor eradication occurs infrequently. This paradox in tumor immunology led us to address two questions: (a) Does an antitumor response, which is intended to destroy the aberrant target population, also at the same time select for aggressive tumor variants (ATV) in vivo? (b) If this process does occur, what is the contribution of the perforin- or Fas-mediated effector mechanism in the immune selecti  ...[more]

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