Objective To estimate the incidence of caesarean scar pregnancy (CSP) and to describe the management outcomes associated with this condition. Design A national cohort study using the UK Early Pregnancy Surveillance Service (UKEPSS). Setting 86 participating Early Pregnancy Units. Population All women diagnosed in the participating units with CSP between November 2013 and January 2015. Methods Cohort study of women identified through the UKEPSS monthly mailing system. Main outcome measures Incidence, clinical outcomes and complications. Results 102 cases of CSP were reported, with an estimated incidence of 1.5 per 10 000 (95% CI 1.1–1.9) maternities. Full outcome data were available for 92 women. Management was expectant in 21/92 (23%), medical in 15/92 (16%) and surgical in 56/92 (61%). The success rates of expectant, medical and surgical management were 43% (9/21), 46% (7/15) and 96% (54/56), respectively. The complication rates were 15/21 (71%) with expectant, 9/15 (60%) with medical and 20/56 (36%) with surgical management. Discharge from care (median number of days) was 82 (range 37–174) with expectant, 21 (range 10–31) with medical and 11 (range 4–49) with surgical management. Conclusions Surgical management appears to be associated with a high success rate, low complication rate and short post‐treatment follow up. Tweetable abstract Surgery for CSP appears to be successful, with low complication rates and short post‐treatment follow up.
To investigate possible causes of the variable response to treatment in pediatric B-precursor acute lymphoblastic leukemia (ALL) and to establish potential novel therapeutic targets, we used ionizing radiation (IR) exposure as a model of DNA damage formation to identify tumors with resistance to p53-dependent apoptosis. Twenty-one of 40 ALL tumors responded normally to IR, exhibiting accumulation of p53 and p21 proteins and cleavage of caspases 3, 7, and 9 and of PARP1. Nineteen tumors exhibited apoptotic resistance and lacked PARP1 and caspase cleavage; although 15 of these tumors had normal accumulation of p53 and p21 proteins, examples exhibited abnormal expression of TRAF5, TRAF6, and cIAP1 after IR, suggesting increased NF-B prosurvival signaling as the mechanism of apoptotic resistance. The presence of a hyperactive PARP1 mutation in one tumor was consistent with such increased NF-B activity. PARP1 inhibition restored p53-dependent apoptosis after IR in these leukemias by reducing NF-B DNA binding and transcriptional activity. In the remaining 4 ALL tumors, apoptotic resistance was associated with a TP53 mutation or with defective activation of p53. We conclude that increased NF-B prosurvival signaling is a frequent mechanism by which B-precursor ALL tumors develop apoptotic resistance to IR and that PARP1 inhibition may improve the DNA damage response of these leuke-
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.