Showing papers by "Anil Potti published in 2012"

Retraction in part: A genomic approach to identify molecular pathways associated with chemotherapy resistance.

Abstract: Using previously published annotations for chemotherapy sensitivity in the NCI-60 series of cancer cell lines (2), we performed gene set enrichment analysis on predefined groups of sensitive and resistantNCI-60 cell lines for a range of chemotherapies to identify biological pathways associated with resistance. We purposefully used the annotations for sensitivity and resistance published in the Nature Medicine article and applied a complementary computational approach in order to glean biological insight from the differential gene expression. The article upon which our annotations were based has now been retracted (3). After re-examination, the annotations for the cell lines with respect to chemotherapy sensitivity were erroneous. Thus, our manuscript propagates this error and the results in Table 1 and Supplemental Table 1 from our manuscript are invalid.

Retraction: Acharya CR, et al. Gene expression signatures, clinicopathological features, and individualized therapy in breast cancer. JAMA. 2008;299(13):1574-1587

Abstract: To the Editor: We would like to retract the article entitled “Gene Expression Signatures, Clinicopathological Features, and Individualized Therapy in Breast Cancer,” which was published in the April 2, 2008, issue of JAMA. A component of this article reported the use of chemotherapy sensitivity predictions based on an approach described by Potti et al in Nature Medicine in 2006. The Nature Medicine article was recently retracted due to an inability to reproduce the results with the chemotherapy signatures. Because a significant component of this JAMA article was based on the use of chemotherapy signatures reported in the Nature Medicine paper, we have decided to retract the JAMA article. We apologize for any negative impact on scientific research or clinical care caused by the publication of our article in JAMA.

A Pathway-Based Approach to Identify Molecular Biomarkers in Cancer

Abstract: Many examples highlight the power of gene expression profiles, or signatures, to provide an understanding of biological phenotypes. This is best seen in the context of cancer, where expression signatures have tremendous power to identify new cancer subtypes and to predict clinical outcomes. Gene expression profiles have been developed to personalize medicine, accurately predicting disease recurrence and tumor response to therapy. The use of these signatures as surrogate phenotypes allows us to link diverse experimental systems, which dissect the complexity of biological systems, with the in vivo setting in a way that was not previously feasible. Taken together, these new genomic tools provide the opportunity to develop rational strategies for treating the individual cancer patient.

Retraction: Characterizing the Clinical Relevance of an Embryonic Stem Cell Phenotype in Lung Adenocarcinoma

Abstract: Purpose: Cancer cells possess traits reminiscent of those ascribed to normal stem cells. It is unclear whether these phenotypic similarities are the result of a common biological phenotype, such as regulatory pathways. Experimental Design: Lung cancer cell lines with corresponding gene expression data and genes associated with an embryonic stem cell identity were used to develop a signature of embryonic stemness (ES) activity specific to lung adenocarcinoma. Biological characteristics were elucidated as a function of cancer biology/oncogenic pathway dysregulation. The ES signature was applied to three independent early-stage (I-IIIa) lung adenocarcinoma data sets with clinically annotated gene expression data. The relationship between the ES phenotype and cisplatin (current standard of care) sensitivity was evaluated. Results: Pathway analysis identified specific regulatory networks [Ras ( P = 0.0005), Myc ( P = 0.0224), wound healing ( P P P n = 82; P = 0.0001), National Cancer Institute Director9s Challenge Consortium ( n = 442; P = 0.0002), and Duke ( n = 45; P = 0.06)]. The ES signature was not prognostic in prostate, breast, or ovarian adenocarcinomas. Lung tumors ( n = 569) and adenocarcinoma cell lines ( n = 31) expressing the ES phenotype were more likely to be resistant to cisplatin ( P P = 0.006, respectively). Conclusions: Lung adenocarcinomas that share a common gene expression pattern with normal human embryonic stem cells were associated with decreased survival, increased biological complexity, and increased likelihood of resistance to cisplatin. This indicates the aggressiveness of these tumors. (Clin Cancer Res 2009;15(24):7553–61)