Integrative Clinical Genomics of Advanced Prostate Cancer

Robinson, Dan R.; Allen, Eliezer M. Van; Wu, Yi-Mi; Schultz, Nikolaus; Lonigro, Robert J.; Mosquera, Juan-Miguel; Montgomery, Bruce; Taplin, Mary‐Ellen; Pritchard, Colin C.; Attard, Gerhardt; Beltran, Himisha; Abida, Wassim; Bradley, Robert K.; Vinson, Jake; Cao, Xuhong; Vats, Pankaj; Kunju, Lakshmi P.; Hussain, Maha; Feng, Felix Y.; Tomlins, Scott A.; Cooney, Kathleen A.; Smith, David C.; Brennan, Christine; Siddiqui, Javed; Mehra, Rohit; Chen, Yu; Rathkopf, Dana E.; Morris, Michael J.; Solomon, Stephen B.; Durack, Jeremy C.; Reuter, Victor E.; Gopalan, Anuradha; Gao, Jianjiong; Loda, Massimo; Lis, Rosina T.; Bowden, Michaela; Balk, Steve; Gaviola, Glenn C.; Sougnez, Carrie; Gupta, Manaswi; Yu, Evan Y.; Mostaghel, Elahe A.; Cheng, Heather H.; Mulcahy, Hyojeong; True, Lawrence D.; Plymate, Stephen R.; Dvinge, Heidi; Ferraldeschi, Roberta; Flohr, Penny; Miranda, Susana; Zafeiriou, Zafeiris; Tunariu, Nina; Mateo, Joaquín; Pérez-López, Raquel; Demichelis, Francesca; Robinson, Brian D.; Schiffman, Marc; Nanus, David M.; Tagawa, Scott T.; Sigaras, Alexandros; Eng, Kenneth; Elemento, Olivier; Sboner, Andrea; Heath, Elisabeth I.; Scher, Howard I.; Pienta, Kenneth J.; Kantoff, Philip W.; Bono, Johann S. de; Rubin, Mark A.; Nelson, Peter S.; Garraway, Levi A.; Sawyers, Charles L.; Chinnaiyan, Arul M.

doi:10.1016/j.cell.2015.06.053

Cited by 556 publications

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“…The 2016 WHO blue book states that the grade groups should be reported in conjunction with the 2014 modified ISUP Gleason scores. [34][35][36][37]. Only a few abnormalities in specific genes are highly recurrent, but alterations in certain signalling pathways predominate, such as PI3K/PTEN/AKT, cell cycle regulation, and chromatin regulation [34].…”

Section: Immunophenotypementioning

confidence: 99%

“…In primary clinically localized prostate cancer, there are relatively few recurrent nonsynonymous point mutations, including mutations in the SPOP (11%) and FOXA1 (3%) genes [37]. In comparison, in castration-resistant metastatic prostate cancer, there are increased alteration rates in many genes and pathways, including abnormalities in androgen receptor (AR) signalling (usually due to AR gene amplification or mutation), DNA repair, and PI3K pathways, as well as mutations or deletions in the TP53, RB1, KMT2C, and KMT2D genes [36,37]. This landscape of somatic genetic abnormalities in adenocarcinoma of the prostate is discussed in depth in a genetic profile section, and a model for molecular classification of prostate cancer is shown.…”

Section: Immunophenotypementioning

confidence: 99%

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The 2016 WHO Classification of Tumours of the Urinary System and Male Genital Organs—Part B: Prostate and Bladder Tumours

et al. 2016

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It has been 12 yr since the publication of the last World Health Organization (WHO) classification of tumours of the prostate and bladder. During this time, significant new knowledge has been generated about the pathology and genetics of these tumours. Intraductal carcinoma of the prostate is a newly recognized entity in the 2016 WHO classification. In most cases, it represents intraductal spread of aggressive prostatic carcinoma and should be separated from high-grade prostatic intraepithelial neoplasia. New acinar adenocarcinoma variants are microcystic adenocarcinoma and pleomorphic giant cell adenocarcinoma. Modifications to the Gleason grading system are incorporated into the 2016 WHO section on grading of prostate cancer, and it is recommended that the percentage of pattern 4 should be reported for Gleason score 7. The new WHO classification further recommends the recently developed prostate cancer grade grouping with five grade groups. For bladder cancer, the 2016 WHO classification continues to recommend the 1997 International Society of Urological Pathology grading classification. Newly described or better defined noninvasive urothelial lesions include urothelial dysplasia and urothelial proliferation of uncertain malignant potential, which is frequently identified in patients with a prior history of urothelial carcinoma. Invasive urothelial carcinoma with divergent differentiation refers to tumours with some percentage of "usual type" urothelial carcinoma combined with other morphologies. Pathologists should mention the percentage of divergent histologies in the pathology report. PATIENT SUMMARY Intraductal carcinoma of the prostate is a newly recognized entity in the 2016 World Health Organization classification. Better defined noninvasive urothelial lesions include urothelial dysplasia and urothelial proliferation of uncertain malignant potential. v a i l a b l e a t w w w . s c i e n c e d i r e c t . c o m j AbstractIt has been 12 yr since the publication of the last World Health Organization (WHO) classification of tumours of the prostate and bladder. During this time, significant new knowledge has been generated about the pathology and genetics of these tumours.

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Section: Immunophenotypementioning

confidence: 99%

Section: Immunophenotypementioning

confidence: 99%

The 2016 WHO Classification of Tumours of the Urinary System and Male Genital Organs—Part B: Prostate and Bladder Tumours

et al. 2016

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“…Additionally, they observed alterations in FANCA, CDK12, RAD51B, and RAD51C, all of which are known to be involved in DNA repair [5]. Of the aforementioned genes, BRCA1 and BRCA2 have been the most widely studied.…”

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confidence: 99%

“…The frequency of BRCA2 germline mutations is reported at 1.2% in an unselected cohort of all stages prostate cancer patients aged ≤65 [8] and 5.3% in metastatic CRPC [5]. The reported prevalence of somatic BRCA2 mutations in metastatic CRPC is higher, between 11% and 13% [5,6]. BRCA mutations appear to be a poor prognostic factor associated with more advanced disease at presentation [9].…”

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confidence: 99%