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Hodis, Eran

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Hodis

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Eran

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Hodis, Eran
Author's Publications: search.filters.isAuthorOfPublication.c287be7f-d2bb-46b7-92ea-b3b143628d9d

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    The genomic landscape and evolution of endometrial carcinoma progression and abdominopelvic metastasis
    (2016) Gibson, William; Hoivik, Erling A.; Halle, Mari K.; Taylor-Weiner, Amaro; Cherniack, Andrew D.; Berg, Anna; Holst, Frederik; Zack, Travis Ian; Werner, Henrica M. J.; Staby, Kjersti M.; Rosenberg, Mara; Stefansson, Ingunn M.; Kusonmano, Kanthida; Chevalier, Aaron; Mauland, Karen K.; Trovik, Jone; Krakstad, Camilla; Giannakis, Marios; Hodis, Eran; Woie, Kathrine; Bjorge, Line; Vintermyr, Olav K.; Wala, Jeremiah; Lawrence, Michael; Getz, Gad; Carter, Scott; Beroukhim, Rameen; Salvesen, Helga B.
    Recent studies have detailed the genomic landscape of primary endometrial cancers, but their evolution into metastases has not been characterized. We performed whole-exome sequencing of 98 tumor biopsies including complex atypical hyperplasias, primary tumors, and paired abdominopelvic metastases to survey the evolutionary landscape of endometrial cancer. We expanded and reanalyzed TCGA-data, identifying novel recurrent alterations in primary tumors, including mutations in the estrogen receptor cofactor NRIP1 in 12% of patients. We found that likely driver events tended to be shared by primary and metastatic tissue-samples, with notable exceptions such as ARID1A mutations. Phylogenetic analyses indicated that the sampled metastases typically arose from a common ancestral subclone that was not detected in the primary tumor biopsy. These data demonstrate extensive genetic heterogeneity within endometrial cancers and relative homogeneity across metastatic sites.
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    Melanoma genome sequencing reveals frequent PREX2 mutations
    (2012) Berger, Michael F.; Hodis, Eran; Heffernan, Timothy P.; Deribe, Yonathan Lissanu; Lawrence, Michael S.; Protopopov, Alexei; Ivanova, Elena; Watson, Ian; Nickerson, Elizabeth; Ghosh, Papia; Zhang, Hailei; Zeid, Rhamy; Ren, Xiaojia; Cibulskis, Kristian; Sivachenko, Andrey Y.; Wagle, Nikhil; Sucker, Antje; Sougnez, Carrie; Onofrio, Roberto; Ambrogio, Lauren; Auclair, Daniel; Fennell, Timothy; Carter, Scott L.; Drier, Yotam; Stojanov, Petar; Singer, Meredith A.; Voet, Douglas; Jing, Rui; Saksena, Gordon; Barretina, Jordi; Ramos, Alex H.; Pugh, Trevor J.; Stransky, Nicolas; Parkin, Melissa Ann; Winckler, Wendy; Mahan, Scott; Ardlie, Kristin; Baldwin, Jennifer; Wargo, Jennifer Ann; Schadendorf, Dirk; Meyerson, Matthew; Gabriel, Stacey B.; Golub, Todd; Wagner, Stephan N.; Lander, Eric; Getz, Gad; Chin, Lynda; Garraway, Levi
    Melanoma is notable for its metastatic propensity, lethality in the advanced setting, and association with ultraviolet (UV) exposure early in life1. To obtain a comprehensive genomic view of melanoma, we sequenced the genomes of 25 metastatic melanomas and matched germline DNA. A wide range of point mutation rates was observed: lowest in melanomas whose primaries arose on non-UV exposed hairless skin of the extremities (3 and 14 per Mb genome), intermediate in those originating from hair-bearing skin of the trunk (range = 5 to 55 per Mb), and highest in a patient with a documented history of chronic sun exposure (111 per Mb). Analysis of whole-genome sequence data identified PREX2 - a PTEN-interacting protein and negative regulator of PTEN in breast cancer2 - as a significantly mutated gene with a mutation frequency of approximately 14% in an independent extension cohort of 107 human melanomas. PREX2 mutations are biologically relevant, as ectopic expression of mutant PREX2 accelerated tumor formation of immortalized human melanocytes in vivo. Thus, whole-genome sequencing of human melanoma tumors revealed genomic evidence of UV pathogenesis and discovered a new recurrently mutated gene in melanoma.