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Carlo M. Croce

Researcher at Ohio State University

Publications -  1156
Citations -  199822

Carlo M. Croce is an academic researcher from Ohio State University. The author has contributed to research in topics: microRNA & Cancer. The author has an hindex of 198, co-authored 1135 publications receiving 189007 citations. Previous affiliations of Carlo M. Croce include University of Nebraska Medical Center & University of California, Los Angeles.

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Journal ArticleDOI

The High Mobility Group A proteins contribute to thyroid cell transformation by regulating miR-603 and miR-10b expression.

TL;DR: Analysis of the miRNA expression profile of v‐ras‐Ki oncogene‐transformed thyroid cells expressing or not HMGA1 proteins shows that, among the miRNAs regulated by cell transformation, there are miR‐10b, miR•21, miB‐125b,miR‐125 b, mi R‐221 and miR •222 that are positively regulated byHMGA1 expression, andMiR‐34a and miG‐603 that are
Journal Article

Genetic approaches to the study of the molecular basis of human cancer.

Carlo M. Croce
- 15 Sep 1991 - 
TL;DR: A potential candidate involved in the 3p deletion characteristic of lung cancer has been identified and it will indicate that transmembrane protein tyrosine phosphatase may represent a class of tumor suppressors.
Book ChapterDOI

The role of deletions at the FRA3B/FHIT locus in carcinogenesis.

TL;DR: Analysis of the approximately 300-kb DNA sequence encompassing FHIT exon 5 in the FRA3B epicenter has provided clues to the mechanism of repair of the fragile site double strand breaks and suggests that the FHit gene is a tumor suppressor gene whose inactivation may drive clonal expansion of preneoplastic and neoplastic cells.
Journal Article

Characterization of the Human Homologue of RAD54: A Gene Located on Chromosome 1p32 at a Region of High Loss of Heterozygosity in Breast Tumors

TL;DR: The complete cDNA sequence and the characterization of the genomic locus coding for the human homologue of the yeast RAD54 gene (hRAD54) are described and, although the gene region appears to be deleted in several tumors, at present no coding sequence mutations are found.