We have developed an in vitro system of cancer cell redirection that employs the 1:50 ratio of cancer cells to normal cells. Using our in vitro system of cancer cell redirection we investigated the genetic profiles of erbB2-overexpressing mammary tumor-derived cells as they undergo the redirection phenomenon.
RNA Expression Profiling Reveals Differentially Regulated Growth Factor and Receptor Expression in Redirected Cancer Cells.
Specimen part
View SamplesWhen using cell lines to study cancer, phenotypic similarity to the original tumor is paramount. Yet, little has been done to characterize how closely Merkel cell carcinoma (MCC) cell lines model native tumors. To determine their similarity to MCC tumor samples, we characterized MCC cell lines via gene expression microarrays. Using whole transcriptome gene expression signatures and a computational bioinformatic approach, we identified significant differences between variant cell lines (UISO, MCC13, and MCC26) and fresh frozen MCC tumors. Conversely, the classic WaGa and Mkl-1 cell lines more closely represented the global transcriptome of MCC tumors. When compared to publicly available cancer lines, WaGa and Mkl-1 cells were similar to other neuroendocrine tumors, but the variant cell lines were not. WaGa and Mkl-1 cells grown as xenografts in mice had histological and immunophenotypical features consistent with MCC, while UISO xenograft tumors were atypical for MCC. Spectral karyotyping and short tandem repeat analysis of the UISO cells matched the original cell line's description, ruling out contamination. Our results validate the use of transcriptome analysis to assess the cancer cell line representativeness and indicate that UISO, MCC13, and MCC26 cell lines are not representative of MCC tumors, whereas WaGa and Mkl-1 more closely model MCC.
Assessment of cancer cell line representativeness using microarrays for Merkel cell carcinoma.
Specimen part, Disease, Cell line
View SamplesThe purpose of this study was to treat cutaneous melanoma metastases with topical DPCP, and then to comprehensively study the induced immune responses associated with tumor regression.
Molecular Profiling of Immune Activation Associated with Regression of Melanoma Metastases Induced by Diphencyprone.
Specimen part, Disease, Treatment, Subject, Time
View SamplesSpecific mutations in the XPD subunit of transcription factor IIH result in combined xeroderma pigmentosum (XP)/Cockayne syndrome (CS), a severe DNA repair disorder characterized at the cellular level by a transcriptional arrest following UV irradiation. This transcriptional arrest has always been thought to be the result of faulty transcription-coupled repair. In the present study, we investigate the transcriptional dysregulation that follows UV irradiation in XP-D/CS compared with “pure” XP-D cells or WT cells. We also study how this process is affected by the inhibition of the histone deacetylase Sirt1.
Sirt1 suppresses RNA synthesis after UV irradiation in combined xeroderma pigmentosum group D/Cockayne syndrome (XP-D/CS) cells.
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Daytime variation of perioperative myocardial injury in cardiac surgery and its prevention by Rev-Erbα antagonism: a single-centre propensity-matched cohort study and a randomised study.
Specimen part
View SamplesNuclear receptor Reverb alpha is a component of circadian rythm which could be evolved in cardioprotection strategy. We test if pharmacological modulation of these target could be suitable for cardioprotection after ischemia reperfusion injury
Daytime variation of perioperative myocardial injury in cardiac surgery and its prevention by Rev-Erbα antagonism: a single-centre propensity-matched cohort study and a randomised study.
Specimen part
View SamplesDuring malaria infection is observed a robust immune response culminating on release of inflammatory mediators. This exacerbated immune response is involved in malaria symptoms and mortality. There are evidences that this response is mediated by innate immunity where pattern recognition receptors have a key role. We used microarrays to elucidate some pro-inflammatory genes that are differential expressed during P. chabaudi infection, a malarial murine model
Daily Rhythms of TNFα Expression and Food Intake Regulate Synchrony of Plasmodium Stages with the Host Circadian Cycle.
Sex, Age, Specimen part
View SamplesGene expression profile in CS1AN deficient and CSBwt restored cell lines after 24 hours of UV or alphe-amanitin treatment (only for restored). The comaprison of expression profile between 0 and 24 hours revealed
Regulatory interplay of Cockayne syndrome B ATPase and stress-response gene ATF3 following genotoxic stress.
Specimen part, Treatment
View SamplesThe goal of this experiment was to compare gene expression after t-RA treatment in cells with or without the presence of the PolyADP ribose Glycohydrolase protein (PARG)
Poly (ADP-ribose) glycohydrolase regulates retinoic acid receptor-mediated gene expression.
Cell line
View SamplesThe identification of subtype-specific translocations has revolutionized diagnostics of sarcoma and provided new insight into oncogenesis. We used RNA-Seq to investigate samples diagnosed as small round cell tumors of bone, possibly Ewing sarcoma, but lacking the canonical EWSR1-ETS translocation. A new fusion was observed between the BCL6 co-repressor (BCOR) and the testis specific cyclin B3 (CCNB3) genes on chromosome X. RNA-Seq results were confirmed by RT-PCR and cloning the tumor-specific genomic translocation breakpoints. 24 BCOR-CCNB3-positive tumors were identified among a series of 594 sarcomas. Gene profiling experiments indicate that BCOR-CCNB3-positive cases are biologically distinct from other sarcomas, particularly Ewings sarcoma. Finally, we show that CCNB3 immunohistochemistry is a powerful diagnostic marker for this group of sarcoma and that over-expression of BCOR-CCNB3 or of a truncated CCNB3 activates S-phase in NIH3T3 cells. Thus the intrachromosomal X fusion described here represents a new subtype of bone sarcoma caused by a novel gene fusion mechanism.
A new subtype of bone sarcoma defined by BCOR-CCNB3 gene fusion.
Sex, Age, Specimen part
View Samples