![]() Intellia is also providing an update on NTLA-2002, its newest development candidate for the treatment of hereditary angioedema (HAE). Intellia researchers are presenting new data in support of NTLA-5001, the company’s engineered cell therapy candidate for the treatment of acute myeloid leukemia (AML). (NASDAQ: NTLA), a leading genome editing company focused on developing curative therapeutics using CRISPR/Cas9 technology both in vivo and ex vivo, is presenting three oral presentations and two poster presentations at the 23 rd Annual Meeting of the American Society of Gene and Cell Therapy (ASGCT), taking place virtually from May 12-15, 2020. In our hereditary angioedema program, demonstrated durability in reduction of therapeutically relevant marker in non-human primate study for our newest development candidate, NTLA-2002ĬAMBRIDGE, Mass., (GLOBE NEWSWIRE) - Intellia Therapeutics, Inc.Proprietary process supports NTLA-5001 and other potential therapies for solid tumors.Intellia’s CRISPR/Cas9 proprietary process produces multiple, highly efficient sequential edits in T cells that have superior function and minimal translocations, compared to results from standard T cell engineering approaches.Canadian Institutes of Health Research (no. Among germline TP53 mutation carriers, increased residual transcriptional activity is correlated with prolonged lifetime cancer survival and delayed tumor onset, and males are more prone to develop brain and gastric tumors. The retention of mutant p53 transcriptional activity prognosticates superior survival for men with glioma and gastric adenocarcinoma harboring sporadic TP53 mutations. The correlation between mutant p53 residual activity with survival was recapitulated in the dataset of germline TP53 mutation carriers (HR = 3.0, 95% CI, 2.7–3.4, P < 0.001 HR = 2.2, 95% CI, 1.8–2.6, P < 0.001 ), where brain and gastric tumors were more common among males (P < 0.001 and P = 0.001, respectively). Male glioma and gastric cancer patients with TP53 mutations resulting in >5% transcriptional activity had 3.1-fold (95% CI, 2.4–3.8 P = 0.002 multivariate analysis hazard ratio ) and 4.6-fold (95% CI, 3.7–5.6 P = 0.001 multivariate analysis HR) lower risk of death as compared with patients harboring inactive (0% activity) p53 mutants. Pan-cancer survival analyses revealed a strong association between increased mutant p53 residual activity and improved survival in males with glioma and gastric adenocarcinoma (P = 0.002 and P = 0.02) that was not present in the female cohorts (P = 0.16 and P = 0.50). Survival was projected by stratifying patients according to their p53 mutant–specific residual transcriptional activity scores. ![]() This retrospective cohort analysis included 2,074 patients with sporadic TP53 mutations (403 unique mutations) and 1,049 germline TP53 mutation carriers (188 unique mutations). The objective of this study was to determine whether these biological differences have clinical significance. There is currently no clinical distinction between different TP53 mutations, despite increasing evidence that not all mutations have equally deleterious effects on the activity of the encoded tumor suppressor protein p53.
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