George Calin

Dr. George Calin

Department of Translational Molecular Pathology, Center for RNA Interference and Non-coding RNAs, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA
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Research Focus & Metrics

Academic Career Length

33Years (1994-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 November 2006 in Nature Reviews Cancer
Verified
Journal Article
Closed access
PDF file
George CalinGeorge Calin
George Calin
CCCarlo M. Croce
Carlo M. Croce

3 February 2006 in Proceedings of the National Academy of Sciences
Verified
Journal Article
Closed access
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Stefano VoliniaStefano Volinia
Stefano Volinia
George CalinGeorge Calin
George Calin
CLChang-Gong Liu
Chang-Gong Liu
Stefan AmbsStefan Ambs
Stefan Ambs
Amelia CimminoAmelia Cimmino
Amelia Cimmino
CCCarlo Crocecarlo
Carlo Crocecarlo
Small noncoding microRNAs (miRNAs) can contribute to cancer development and progression and are differentially expressed in normal tissues and cancers. From a large-scale miRnome analysis on 540 samples including lung, breast, stomach, prostate, colon, and pancreatic tumors, we identified a solid cancer miRNA signature composed by a large portion of overexpressed miRNAs. Among these miRNAs are some with well characterized cancer association, such as miR-17-5p , miR-20a , miR-21 , miR-92 , miR-106a , and miR-155 . The predicted targets for the differentially expressed miRNAs are significantly enriched for protein-coding tumor suppressors and oncogenes ( P < 0.0001). A number of the predicted targets, including the tumor suppressors RB1 (Retinoblastoma 1) and TGFBR2 (transforming growth factor, beta receptor II) genes were confirmed experimentally. Our results indicate that miRNAs are extensively involved in cancer pathogenesis of solid tumors and support their function as either dominant or recessive cancer genes.

14 November 2002 in Proceedings of the National Academy of Sciences
Verified
Journal Article
Closed access
PDF file
George CalinGeorge Calin
George Calin
CDCalin Dan Dumitru
Calin Dan Dumitru
MSMasayoshi Shimizu
Masayoshi Shimizu
RBRoberta Bichi
Roberta Bichi
SZSimona Zupo
Simona Zupo
CCCarlo M. Croce
Carlo M. Croce
Micro-RNAs ( miR genes) are a large family of highly conserved noncoding genes thought to be involved in temporal and tissue-specific gene regulation. MiRs are transcribed as short hairpin precursors (≈70 nt) and are processed into active 21- to 22-nt RNAs by Dicer, a ribonuclease that recognizes target mRNAs via base-pairing interactions. Here we show that miR15 and miR16 are located at chromosome 13q14, a region deleted in more than half of B cell chronic lymphocytic leukemias (B-CLL). Detailed deletion and expression analysis shows that miR15 and miR16 are located within a 30-kb region of loss in CLL, and that both genes are deleted or down-regulated in the majority (≈68%) of CLL cases.

15 August 2005 in Cancer Research
Verified
Journal Article
Closed access
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Marilena IorioMarilena Iorio
Marilena Iorio
MFManuela Ferracin
Manuela Ferracin
CLChang-Gong Liu
Chang-Gong Liu
Angelo VeroneseAngelo Veronese
Angelo Veronese
Riccardo SpizzoRiccardo Spizzo
Riccardo Spizzo
CCCarlo M. Croce
Carlo M. Croce
MicroRNAs (miRNAs) are a class of small noncoding RNAs that control gene expression by targeting mRNAs and triggering either translation repression or RNA degradation. Their aberrant expression may be involved in human diseases, including cancer. Indeed, miRNA aberrant expression has been previously found in human chronic lymphocytic leukemias, where miRNA signatures were associated with specific clinicobiological features. Here, we show that, compared with normal breast tissue, miRNAs are also aberrantly expressed in human breast cancer. The overall miRNA expression could clearly separate normal versus cancer tissues, with the most significantly deregulated miRNAs being mir-125b, mir-145, mir-21, and mir-155. Results were confirmed by microarray and Northern blot analyses. We could identify miRNAs whose expression was correlated with specific breast cancer biopathologic features, such as estrogen and progesterone receptor expression, tumor stage, vascular invasion, or proliferation index.

15 September 2005 in Proceedings of the National Academy of Sciences
Verified
Journal Article
Open access
PDF file
Amelia CimminoAmelia Cimmino
Amelia Cimmino
George CalinGeorge Calin
George Calin
MFMuller Fabbri
Muller Fabbri
Marilena IorioMarilena Iorio
Marilena Iorio
MFManuela Ferracin
Manuela Ferracin
CCCarlo Crocecarlo
Carlo Crocecarlo
Chronic lymphocytic leukemia (CLL) is the most common human leukemia and is characterized by predominantly nondividing malignant B cells overexpressing the antiapoptotic B cell lymphoma 2 (Bcl2) protein. miR-15a and miR-16-1 are deleted or down-regulated in the majority of CLLs. Here, we demonstrate that miR-15a and miR-16-1 expression is inversely correlated to Bcl2 expression in CLL and that both microRNAs negatively regulate Bcl2 at a posttranscriptional level. BCL2 repression by these microRNAs induces apoptopsis in a leukemic cell line model. Therefore, miR-15 and miR-16 are natural antisense Bcl2 interactors that could be used for therapy of Bcl2-overexpressing tumors.

1 March 2006 in Cancer Cell
Verified
Journal Article
Closed access
NYNozomu Yanaihara
Nozomu Yanaihara
NCNatasha J. Caplen
Natasha J. Caplen
EBElise Bowman
Elise Bowman
MSMasahiro Seike
Masahiro Seike
KKKensuke Kumamoto
Kensuke Kumamoto
CHCurtis C. Harris
Curtis C. Harris