Mutation of FOXL2 in granulosa-cell tumors of the ovary.
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Ryan D. Morin | A. deFazio | D. Bowtell | M. Marra | M. Hirst | Yongjun Zhao | Thomas Zeng | R. Varhol | A. Mes-Masson | R. Morin | S. Shah | S. Aparicio | G. Turashvili | D. Huntsman | M. Köbel | J. Senz | B. Clarke | Kimberly C. Wiegand | G. Leung | Abdalnasser Zayed | Erika Mehl | S. Kalloger | Mark G. F. Sun | Ryan Giuliany | E. Yorida | Steven P. Jones | K. Swenerton | Dianne Miller | P. Clement | Colleen A Crane | J. Madore | D. Provencher | P. Leung | J. Khattra | J. Glover | B. Vanderhyden | Chengquan Zhao | C. Parkinson | M. Jimenez-Linan | J. Brenton | N. Boyd | C. Gilks | Samuel Aparicio | J. Glover | D. Bowtell | Sohrab P. Shah | D. Miller | Sohrab P. Shah | P. B. Clement | Niki Boyd
[1] J. Fletcher,et al. Ovarian granulosa-stromal cell tumors are characterized by trisomy 12. , 1991, The American journal of pathology.
[2] T. Löning,et al. p53 mutations in ovarian tumors, detected by temperature‐gradient gel electrophoresis, direct sequencing and immunohistochemistry , 1995, International journal of cancer.
[3] L. Twiggs,et al. Mitotic count, nuclear atypia, and immunohistochemical determination of Ki-67, c-myc, p21-ras, c-erbB2, and p53 expression in granulosa cell tumors of the ovary: mitotic count and Ki-67 are indicators of poor prognosis. , 1996, Gynecologic oncology.
[4] Fu‐shing Liu,et al. Overexpression of p53 is not a feature of ovarian granulosa cell tumors. , 1996, Gynecologic oncology.
[5] H. Brunner,et al. Analysis of mutations in genes of the follicle-stimulating hormone receptor signaling pathway in ovarian granulosa cell tumors. , 1999, The Journal of clinical endocrinology and metabolism.
[6] K. Devriendt,et al. Spectrum of FOXL2 gene mutations in blepharophimosis-ptosis-epicanthus inversus (BPES) families demonstrates a genotype--phenotype correlation. , 2001, Human molecular genetics.
[7] D. Schlessinger,et al. The putative forkhead transcription factor FOXL2 is mutated in blepharophimosis/ptosis/epicanthus inversus syndrome , 2001, Nature Genetics.
[8] R. Veitia,et al. Evolution and expression of FOXL2 , 2002, Journal of medical genetics.
[9] S. Cannistra,et al. Granulosa cell tumor of the ovary. , 2003, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[10] B. Ellsworth,et al. The gonadotropin releasing hormone (GnRH) receptor activating sequence (GRAS) is a composite regulatory element that interacts with multiple classes of transcription factors including Smads, AP-1 and a forkhead DNA binding protein , 2003, Molecular and Cellular Endocrinology.
[11] J. Vandesompele,et al. The human FOXL2 mutation database , 2004, Human mutation.
[12] S. Chu,et al. Signalling pathways in the molecular pathogenesis of ovarian granulosa cell tumours , 2004, Trends in Endocrinology & Metabolism.
[13] G. Crooks,et al. WebLogo: a sequence logo generator. , 2004, Genome research.
[14] Katrin Anlag,et al. The murine winged-helix transcription factor Foxl2 is required for granulosa cell differentiation and ovary maintenance , 2004, Development.
[15] M. Pisarska,et al. Forkhead l2 is expressed in the ovary and represses the promoter activity of the steroidogenic acute regulatory gene. , 2004, Endocrinology.
[16] G. Churchill,et al. Distal Chr 4 harbors a genetic locus (Gct1) fundamental for spontaneous ovarian granulosa cell tumorigenesis in a mouse model. , 2005, Cancer research.
[17] Mario Cazzola,et al. A gain-of-function mutation of JAK2 in myeloproliferative disorders. , 2005, The New England journal of medicine.
[18] R. Young,et al. Sex cord-stromal tumors of the ovary and testis: their similarities and differences with consideration of selected problems , 2005, Modern Pathology.
[19] R. Veitia,et al. FOXL2 activates P450 aromatase gene transcription: towards a better characterization of the early steps of mammalian ovarian development. , 2006, Journal of molecular endocrinology.
[20] N. Colombo,et al. Management of ovarian stromal cell tumors. , 2007, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[21] J. Diebold,et al. Analysis of selected oncogenes (AKT1, FOS, BCL2L2, TGFbeta) on chromosome 14 in granulosa cell tumors (GCTs): a comprehensive study on 30 GCTs combining comparative genomic hybridization (CGH) and fluorescence-in situ-hybridization (FISH). , 2008, Pathology, research and practice.
[22] Ryan D. Morin,et al. Profiling the HeLa S3 transcriptome using randomly primed cDNA and massively parallel short-read sequencing. , 2008, BioTechniques.
[23] D. Busam,et al. An Integrated Genomic Analysis of Human Glioblastoma Multiforme , 2008, Science.
[24] G. Parmigiani,et al. Integrated analysis of homozygous deletions, focal amplifications, and sequence alterations in breast and colorectal cancers , 2008, Proceedings of the National Academy of Sciences.
[25] Kylie L. Gorringe,et al. No evidence of clonal somatic genetic alterations in cancer-associated fibroblasts from human breast and ovarian carcinomas , 2008, Nature Genetics.
[26] Antony V. Cox,et al. Identification of somatically acquired rearrangements in cancer using genome-wide massively parallel paired-end sequencing , 2008, Nature Genetics.
[27]
R. Durbin,et al.
Mapping Quality Scores Mapping Short Dna Sequencing Reads and Calling Variants Using P ,
2022
.
[28]
Amy E. Hawkins,et al.
DNA sequencing of a cytogenetically normal acute myeloid leukemia genome
,
2008,
Nature.
[29]
Chengquan Zhao,et al.
Identification of the Most Sensitive and Robust Immunohistochemical Markers in Different Categories of Ovarian Sex Cord-stromal Tumors
,
2009,
The American journal of surgical pathology.
[30]
M. Stratton,et al.
The cancer genome
,
2009,
Nature.