Biologic markers of immune tolerance may facilitate tailoring of immune suppression duration after allogeneic hematopoietic cell transplantation (HCT). In a cross-sectional study, peripheral blood samples were obtained from tolerant (n=15, median 38.5 months post-HCT) and non-tolerant (n=17, median 39.5 post-HCT) HCT recipients and healthy control subjects (n=10) for analysis of immune cell subsets and differential gene expression. There were no significant differences in immune subsets across groups. We identified 281 probe sets unique to the tolerant (TOL) group and 122 for non-tolerant (non-TOL). These were enriched for process networks including NK cell cytotoxicity, antigen presentation, lymphocyte proliferation, and cell cycle and apoptosis. Differential gene expression was enriched for CD56, CD66, and CD14 human lineage-specific gene expression. Differential expression of 20 probe sets between groups was sufficient to develop a classifier with > 90% accuracy, correctly classifying 14/15 TOL cases and 15/17 non-TOL cases. These data suggest that differential gene expression can be utilized to accurately classify tolerant patients following HCT. Prospective investigation of immune tolerance biologic markers is warranted.
Tolerance associated gene expression following allogeneic hematopoietic cell transplantation.
Specimen part, Subject
View SamplesMetastatic melanoma is a deadly disease while non-metastatic melanoma and other cutaneous tumor types are usually cured with surgical removal of the primary tumors. This study evaluated gene expresion to determine if gene expression differences existed which would allow one to identify the metastatic tumors based on the expression of specific genes.
The gene expression profiles of primary and metastatic melanoma yields a transition point of tumor progression and metastasis.
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View SamplesSamples were taken from colorectal cancers in surgically resected specimens in 290 colorectal cancer patients. The expression profiles were determined using Affymetrix Human Genome U133Plus 2.0 arrays. The training set of our prognosis classifier included the stage A and D samples. Validation used our stage B and C samples.
Metastasis-Associated Gene Expression Changes Predict Poor Outcomes in Patients with Dukes Stage B and C Colorectal Cancer.
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Experimentally derived metastasis gene expression profile predicts recurrence and death in patients with colon cancer.
Sex, Age, Disease stage, Race
View SamplesBackground and Aims: Staging inadequately predicts metastatic risk in colon cancer patients. We used a gene expression profile derived from invasive murine colon cancer cells that were highly metastatic in an immunocompetent mouse model to identify colon cancer patients at risk for recurrence in a phase I, exploratory biomarker study.
Experimentally derived metastasis gene expression profile predicts recurrence and death in patients with colon cancer.
Sex, Age, Disease stage, Race
View SamplesBackground and Aims: Staging inadequately predicts metastatic risk in colon cancer patients. We used a gene expression profile derived from invasive murine colon cancer cells that were highly metastatic in an immunocompetent mouse model to identify colon cancer patients at risk for recurrence in a phase I, exploratory biomarker study.
Experimentally derived metastasis gene expression profile predicts recurrence and death in patients with colon cancer.
Sex, Age, Disease stage, Race
View SamplesFunctional genomics approach to metastatic colon cancer
Experimentally derived metastasis gene expression profile predicts recurrence and death in patients with colon cancer.
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View SamplesAnalysis of Rab25 in human colon samples
Experimentally derived metastasis gene expression profile predicts recurrence and death in patients with colon cancer.
Sex, Age, Race
View SamplesThis SuperSeries is composed of the SubSeries listed below.
BAD phosphorylation determines ovarian cancer chemosensitivity and patient survival.
Disease stage, Cell line
View SamplesWe treated 8 human ovarian cancer cell lines with cisplatin in treatment/recovery cycles to induce in-vitro resistance to the drug. Microarrays measured gene expression at baseline and after each dose schedule (after recovery).
BAD phosphorylation determines ovarian cancer chemosensitivity and patient survival.
Cell line
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