Results 81 to 90 of about 117,801 (299)

Analysis of chromosomal radiosensitivity of healthy BRCA2 mutation carriers and non-carriers in BRCA families with the G2 micronucleus assay [PDF]

, 2017
Breast cancer risk drastically increases in individuals with a heterozygous germline BRCA1 or BRCA2 mutation, while it is estimated to equal the population risk for relatives without the familial mutation (non-carriers).
Baert, Annelot, Claes, Kathleen, De Leeneer, Kim, De Nobele, Sylvia, Depuydt, Julie, Malfait, Fransiska, Perletti, Gianpaolo, Poppe, Bruce, Van Damme, Tim, Van Maerken, Tom, Vral, Anne   +10 more
core   +1 more source

Individual and family characteristics associated with BRCA1/2 genetic testing in high‐risk families [PDF]

, 2012
Background Little is known about family members' interrelated decisions to seek genetic testing for breast cancer susceptibility. Methods The specific aims of this cross‐sectional, descriptive, cohort study were (i) to examine whether individual and
Katapodi, Maria C., Liu, Guipeng, Merajver, Sofia D., Milliron, Kara J., Northouse, Laurel L.   +4 more
core   +1 more source

Tumor mutational burden as a determinant of metastatic dissemination patterns

Molecular Oncology, EarlyView.
This study performed a comprehensive analysis of genomic data to elucidate whether metastasis in certain organs share genetic characteristics regardless of cancer type. No robust mutational patterns were identified across different metastatic locations and cancer types.
Eduardo Candeal, Andrea Moreno‐Manuel, Miguel Salvadó‐Pertierra, Cristina Santos‐Vivas, Rebeca Sanz‐Pamplona   +4 more
wiley   +1 more source

Prevalence of Germline Mutations in Genes Engaged in DNA Damage Repair by Homologous Recombination in Patients with Triple-Negative and Hereditary Non-Triple-Negative Breast Cancers.

PLoS ONE, 2015
PurposeThis study sought to assess the prevalence of common germline mutations in several genes engaged in the repair of DNA double-strand break by homologous recombination in patients with triple-negative breast cancers and hereditary non-triple ...
Pawel Domagala, Anna Jakubowska, Katarzyna Jaworska-Bieniek, Katarzyna Kaczmarek, Katarzyna Durda, Agnieszka Kurlapska, Cezary Cybulski, Jan Lubinski   +7 more
doaj   +1 more source

BRIP-1 germline mutation and its role in colon cancer: presentation of two case reports and review of literature. [PDF]

, 2019
BackgroundHereditary colon cancer is characterized by the inheritance of an abnormal gene mutation which predisposes to malignancy. Recent advances in genomic medicine have identified mutations in "novel" genes as conferring an increased risk of ...
Ali, Mir, Chaudhary, Uzair, Delozier, Celia Dawn   +2 more
core  

Frequency of the IVS10-6T→G variant in Australian multiple-case breast cancer families [PDF]

, 2004
BACKGROUND: Germline mutations in the genes BRCA1 and BRCA2 account for only a proportion of hereditary breast cancer, suggesting that additional genes contribute to hereditary breast cancer.
Geoffrey J Lindeman, Melody Hiew, Jane E Visvader, Jennifer Leary, Michael Field, Clara L Gaff, RJ McKinlay Gardner, Kevin Trainor, Glenice Cheetham, Graeme Suthers, Judy Kirk, D Ford, AC Antoniou, KK Khanna, Y Shiloh, D Cortez, M Gatei, K Savitsky, RA Gatti, M Swift, M Swift, P Athma, HM Inskip, N Janin, B Geoffroy-Perez, JH Olsen, I Vorechovsky, MG FitzGerald, J Chen, G Chenevix-Trench, H Lei, CI Szabo, A Broeks, JL Bernstein, National Health and Medical Research Council, DA Berry, OT Johannsson, JE Armes, G Chenevix-Trench, T Dörk, A Broeks, N Foray, SS Sommer   +42 more
core   +2 more sources

TRAIL‐PEG‐Apt‐PLGA nanosystem as an aptamer‐targeted drug delivery system potential for triple‐negative breast cancer therapy using in vivo mouse model

Molecular Oncology, EarlyView.
Aptamers are used both therapeutically and as targeting agents in cancer treatment. We developed an aptamer‐targeted PLGA–TRAIL nanosystem that exhibited superior therapeutic efficacy in NOD/SCID breast cancer models. This nanosystem represents a novel biotechnological drug candidate for suppressing resistance development in breast cancer.
Gulen Melike Demirbolat, Aslihan Kucuk, Omer Erdogan, Samed Ozer, Bensu Kozan, Tugba Cuceli, Erkan Gumus, Evrim Cevik, Ozge Cevik   +8 more
wiley   +1 more source

Correlation of the differential expression of PIK3R1 and its spliced variant, p55α, in pan‐cancer

Molecular Oncology, EarlyView.
PIK3R1 undergoes alternative splicing to generate the isoforms, p85α and p55α. By combining large patient datasets with laboratory experiments, we show that PIK3R1 spliced variants shape cancer behavior. While tumors lose the protective p85α isoform, p55α is overexpressed, changes linked to poorer survival and more pronounced in African American ...
Ishita Gupta, Yang Song, Madeleine Ndahayo, Anirudh Saxena, Theresa Guo, Dylan Z. Kelley, Jessica Gore, Andrew Hennigan, Alexa Anderson, John C. Papadimitriou, Daria A. Gaykalova   +10 more
wiley   +1 more source

The FANCM:p.Arg658* truncating variant is associated with risk of triple-negative breast cancer. [PDF]

, 2019
Breast cancer is a common disease partially caused by genetic risk factors. Germline pathogenic variants in DNA repair genes BRCA1, BRCA2, PALB2, ATM, and CHEK2 are associated with breast cancer risk.
Aalfs, Cora M, ABCTB Investigators, Adank, Muriel A, Adlard, Julian, Agata, Simona, Agnarsson, Bjarni A, Ahearn, Thomas, Aittomäki, Kristiina, Ambrosone, Christine B, Andrews, Lesley, Anton-Culver, Hoda, Antonenkova, Natalia N, Arndt, Volker, Arnold, Norbert, Aronson, Kristan J, Arun, Banu K, Asseryanis, Ella, Auber, Bernd, Auvinen, Päivi, Azzollini, Jacopo, Balmaña, Judith, Barkardottir, Rosa B, Barnes, Daniel R, Barrowdale, Daniel, Barwell, Julian, Beane Freeman, Laura E, Beauparlant, Charles Joly, Beckmann, Matthias W, Behrens, Sabine, Benitez, Javier, Berger, Raanan, Bermisheva, Marina, Blanco, Amie M, Blomqvist, Carl, Bogdanova, Natalia V, Bogliolo, Massimo, Bojesen, Anders, Bojesen, Stig E, Bolla, Manjeet K, Bonanni, Bernardo, Borg, Ake, Brady, Angela F, Brauch, Hiltrud, Brenner, Hermann, Brüning, Thomas, Burwinkel, Barbara, Buys, Saundra S, Cadoo, Karen, Caldés, Trinidad, Caleca, Laura, Caliebe, Almuth, Caligo, Maria A, Campa, Daniele, Campbell, Ian G, Canzian, Federico, Castelao, Jose E, Catucci, Irene, Chang-Claude, Jenny, Chanock, Stephen J, Claes, Kathleen BM, Clarke, Christine L, Collavoli, Anita, Conner, Thomas A, Cox, David G, Cybulski, Cezary, Czene, Kamila, Daly, Mary B, de la Hoya, Miguel, Dennis, Joe, Devilee, Peter, Diez, Orland, Ding, Yuan Chun, Dite, Gillian S, Ditsch, Nina, Domchek, Susan M, Dorfling, Cecilia M, Dos-Santos-Silva, Isabel, Durda, Katarzyna, Dwek, Miriam, Eccles, Diana M, Ekici, Arif B, Eliassen, A Heather, Ellberg, Carolina, Eriksson, Mikael, Evans, D Gareth, Fasching, Peter A, Figlioli, Gisella, Figueroa, Jonine, Flyger, Henrik, Foulkes, William D, Friebel, Tara M, Friedman, Eitan, Gabrielson, Marike, Gaddam, Pragna, Kiiski, Johanna I, Lasheras, Sandra Viz, Leslie, Goska, Michailidou, Kyriaki, Muranen, Taru A, Pujol, Roser   +99 more
core  

Basroparib inhibits YAP‐driven cancers by stabilizing angiomotin

Molecular Oncology, EarlyView.
Basroparib, a selective tankyrase inhibitor, suppresses Wnt signaling and attenuates YAP‐driven oncogenic programs by stabilizing angiomotin. It promotes AMOT–YAP complex formation, enforces cytoplasmic YAP sequestration, inhibits YAP/TEAD transcription, and sensitizes YAP‐active cancers, including KRAS‐mutant colorectal cancer, to MEK inhibition.
Young‐Ju Kwon, Dong Young Kim, Yuna Kim, Uk‐Il Kim, Jae‐Sung Kim   +4 more
wiley   +1 more source