Authors’ reply to Weiner et al. DOI Creative Commons
Vidya Veldore,

Hitesh M. Goswami,

Kshitij D. Rishi

et al.

Cancer Research Statistics and Treatment, Journal Year: 2024, Volume and Issue: 7(1), P. 132 - 133

Published: Jan. 1, 2024

We appreciate the critical review of our research,[1] and interest shown by Weiner et al.[2] acknowledge that frequencies homologous recombinant repair (HRR) mutations observed in cohort were high, probably due to fact study comprised patients with at least one HRR mutation. Our aimed assess highlight frequency variants cancers beyond breast, ovarian, prostate cancers. India ranks third cancer incidence worldwide, major types are lung, colorectal, as per Global Cancer Observatory (GLOBOCAN) 2020 data.[3] As today, clinical trials database includes 160 studies exploring possible therapeutic options various a recombination deficiency (HRD) phenotype, including advanced solid tumors (27 trials), ovarian (57 breast gastrointestinal tract (11 (8 pancreatic (7 endometrial fallopian tube (5 miscellaneous (12 trials).[4] was derived from an initial pan-cancer 1749 patients, who had undergone comprehensive genomic profiling.[1] After eliminating 1090 (62.3%) without variants, 659 (37.7%) gene included study. The relative prevalence across intriguing, identifying targetable biomarkers rare those where there is paucity actionable targets, will be valuable providing for these patients. These findings could provide leads designing trials, wherein we explore efficacy novel targeted molecules reduced toxicities, which may help further improving quality life survival basis advancing HRD phenotype/HRR biomarker/genomic signature towards becoming tumor-agnostic signature. While it known non-BRCA not invariably associated phenotype,[5] presence suggests possibility phenotype consequent sensitivity poly (ADP-ribose) polymerase inhibitors (PARPi)[6] platinum-based therapy. opportunity therapy would targets. Furthermore, currently limited data do allow leverage group good/poor responders PARPi prospectively; however, agree identify populations benefit It interesting take this forward independent future. thank insightful comments, excellent description study, emphasizing its importance scenarios. Financial support sponsorship supported internal funding 4baseCare Onco Solutions Pvt. Ltd., Bengaluru, India. Conflicts There no conflicts interest.

Language: Английский

Authors’ reply to Weiner et al. DOI Creative Commons
Vidya Veldore,

Hitesh M. Goswami,

Kshitij D. Rishi

et al.

Cancer Research Statistics and Treatment, Journal Year: 2024, Volume and Issue: 7(1), P. 132 - 133

Published: Jan. 1, 2024

We appreciate the critical review of our research,[1] and interest shown by Weiner et al.[2] acknowledge that frequencies homologous recombinant repair (HRR) mutations observed in cohort were high, probably due to fact study comprised patients with at least one HRR mutation. Our aimed assess highlight frequency variants cancers beyond breast, ovarian, prostate cancers. India ranks third cancer incidence worldwide, major types are lung, colorectal, as per Global Cancer Observatory (GLOBOCAN) 2020 data.[3] As today, clinical trials database includes 160 studies exploring possible therapeutic options various a recombination deficiency (HRD) phenotype, including advanced solid tumors (27 trials), ovarian (57 breast gastrointestinal tract (11 (8 pancreatic (7 endometrial fallopian tube (5 miscellaneous (12 trials).[4] was derived from an initial pan-cancer 1749 patients, who had undergone comprehensive genomic profiling.[1] After eliminating 1090 (62.3%) without variants, 659 (37.7%) gene included study. The relative prevalence across intriguing, identifying targetable biomarkers rare those where there is paucity actionable targets, will be valuable providing for these patients. These findings could provide leads designing trials, wherein we explore efficacy novel targeted molecules reduced toxicities, which may help further improving quality life survival basis advancing HRD phenotype/HRR biomarker/genomic signature towards becoming tumor-agnostic signature. While it known non-BRCA not invariably associated phenotype,[5] presence suggests possibility phenotype consequent sensitivity poly (ADP-ribose) polymerase inhibitors (PARPi)[6] platinum-based therapy. opportunity therapy would targets. Furthermore, currently limited data do allow leverage group good/poor responders PARPi prospectively; however, agree identify populations benefit It interesting take this forward independent future. thank insightful comments, excellent description study, emphasizing its importance scenarios. Financial support sponsorship supported internal funding 4baseCare Onco Solutions Pvt. Ltd., Bengaluru, India. Conflicts There no conflicts interest.

Language: Английский

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