hereditary prostate cancer
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2021 ◽  
Vol 159 ◽  
pp. 52-55
Author(s):  
James R. Marthick ◽  
Kelsie Raspin ◽  
Georgea R. Foley ◽  
Nicholas B. Blackburn ◽  
Annette Banks ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
William D. Dupont ◽  
Joan P. Breyer ◽  
Spenser H. Johnson ◽  
W. Dale Plummer ◽  
Jeffrey R. Smith

AbstractThe G84E germline mutation of HOXB13 predisposes to prostate cancer and is clinically tested for familial cancer care. We investigated the HOXB locus to define a potentially broader contribution to prostate cancer heritability. We sought HOXB locus germline variants altering prostate cancer risk in three European-ancestry case–control study populations (combined 7812 cases and 5047 controls): the International Consortium for Prostate Cancer Genetics Study; the Nashville Familial Prostate Cancer Study; and the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Multiple rare genetic variants had concordant and strong risk effects in these study populations and exceeded genome-wide significance. Independent risk signals were best detected by sentinel variants rs559612720 within SKAP1 (OR = 8.1, P = 2E−9) and rs138213197 (G84E) within HOXB13 (OR = 5.6, P = 2E−11), separated by 567 kb. Half of carriers inherited both risk alleles, while others inherited either alone. Under mutual adjustment, the variants separately carried 3.6- and 3.1-fold risk, respectively, while joint inheritance carried 11.3-fold risk. These risks were further accentuated among men meeting criteria for hereditary prostate cancer, and further still for those with early-onset or aggressive disease. Among hereditary prostate cancer cases diagnosed under age 60 and with aggressive disease, joint inheritance carried a risk of OR = 27.7 relative to controls, P = 2E−8. The HOXB sentinel variant pair more fully captured genetic risk for prostate cancer within the study populations than either variant alone.


2021 ◽  
Vol 22 (7) ◽  
pp. 3753
Author(s):  
Maria Teresa Vietri ◽  
Giovanna D’Elia ◽  
Gemma Caliendo ◽  
Marianna Resse ◽  
Amelia Casamassimi ◽  
...  

Prostate cancer (PCa) is globally the second most diagnosed cancer type and the most common cause of cancer-related deaths in men. Family history of PCa, hereditary breast and ovarian cancer (HBOC) and Lynch syndromes (LS), are among the most important risk factors compared to age, race, ethnicity and environmental factors for PCa development. Hereditary prostate cancer (HPCa) has the highest heritability of any major cancer in men. The proportion of PCa attributable to hereditary factors has been estimated in the range of 5–15%. To date, the genes more consistently associated to HPCa susceptibility include mismatch repair (MMR) genes (MLH1, MSH2, MSH6, and PMS2) and homologous recombination genes (BRCA1/2, ATM, PALB2, CHEK2). Additional genes are also recommended to be integrated into specific research, including HOXB13, BRP1 and NSB1. Importantly, BRCA1/BRCA2 and ATM mutated patients potentially benefit from Poly (ADP-ribose) polymerase PARP inhibitors, through a mechanism of synthetic lethality, causing selective tumor cell cytotoxicity in cell lines. Moreover, the detection of germline alterations in MMR genes has therapeutic implications, as it may help to predict immunotherapy benefits. Here, we discuss the current knowledge of the genetic basis for inherited predisposition to PCa, the potential target therapy, and the role of active surveillance as a management strategy for patients with low-risk PCa. Finally, the current PCa guideline recommendations are reviewed.


2020 ◽  
Vol 21 ◽  
pp. S155
Author(s):  
A. Sultanbaev ◽  
A. Nasretdinov ◽  
N. Sultanbaeva ◽  
K. Menshikov ◽  
S. Musin ◽  
...  

2020 ◽  
Author(s):  
Deyana D. Lewis ◽  
Shukmei Wong ◽  
Angela S. Baker ◽  
Joan E. Bailey-Wilson ◽  
John D. Carpten ◽  
...  

2020 ◽  
pp. 283-292
Author(s):  
Veda N. Giri ◽  
Jennifer Beebe-Dimmer ◽  
Kathleen A. Cooney

2019 ◽  
Vol 81 ◽  
pp. 101927
Author(s):  
Isabel Heidegger ◽  
Igor Tsaur ◽  
Hendrik Borgmann ◽  
Christian Surcel ◽  
Alexander Kretschmer ◽  
...  

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