Pre-treatment inflammatory parameters predict survival from endometrial cancer: A prospective database analysis

There is evidence suggesting that pre-treatment clinical parameters can predict the probability of sphincter-preserving surgery in rectal cancer; however, to date, data on the predictive role of inflammatory parameters on the sphincter-preservation rate are not available. The aim of the present cohort study was to investigate the association between inflammation-based parameters and the sphincter-preserving surgery rate in patients with low-lying locally advanced rectal cancer (LARC). A total of 848 patients with LARC undergoing radiotherapy from 2004 to 2019 were retrospectively reviewed in order to identify patients with rectal cancer localized ≤ 6 cm from the anal verge, treated with neo-adjuvant radiochemotherapy (nRCT) and subsequent surgery. Univariable and multivariable analyses were used to investigate the role of pre-treatment inflammatory parameters, including the C-reactive protein (CRP), neutrophil-to-lymphocyte ratio (NLR), and platelet-to-lymphocyte ratio (PLR) for the prediction of sphincter preservation. A total of 363 patients met the inclusion criteria; among them, 210 patients (57.9%) underwent sphincter-preserving surgery, and in 153 patients (42.1%), an abdominoperineal rectum resection was performed. Univariable analysis showed a significant association of the pre-treatment CRP value (OR = 2.548, 95% CI: 1.584–4.097, p < 0.001) with sphincter preservation, whereas the pre-treatment NLR (OR = 1.098, 95% CI: 0.976–1.235, p = 0.120) and PLR (OR = 1.002, 95% CI: 1.000–1.005, p = 0.062) were not significantly associated with the type of surgery. In multivariable analysis, the pre-treatment CRP value (OR = 2.544; 95% CI: 1.314–4.926; p = 0.006) was identified as an independent predictive factor for sphincter-preserving surgery. The findings of the present study suggest that the pre-treatment CRP value represents an independent parameter predicting the probability of sphincter-preserving surgery in patients with low-lying LARC.

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Management of Elderly Patients with Early Stage Medically Inoperable Endometrial Cancer: Systematic Review and National Cancer Database Analysis

Brachytherapy ◽

10.1016/j.brachy.2017.04.011 ◽

2017 ◽

Vol 16 (3) ◽

pp. S16 ◽

Cited By ~ 1

Author(s):

Sunil W. Dutta ◽

Daniel M. Trifiletti ◽

Surbhi Grover ◽

Pamela Boimel ◽

Timothy N. Showalter

Keyword(s):

Systematic Review ◽

Endometrial Cancer ◽

Elderly Patients ◽

Early Stage ◽

National Cancer Database ◽

Database Analysis

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ENDOMETRIAL CANCER RISK IN BRCA MUTATION CARRIERS: A PROSPECTIVE DATABASE STUDY

10.26226/morressier.599bdc7ad462b80296ca12d1 ◽

2017 ◽

Author(s):

Neil Ryan

Keyword(s):

Endometrial Cancer ◽

Cancer Risk ◽

Brca Mutation ◽

Endometrial Cancer Risk ◽

Database Study ◽

Mutation Carriers ◽

Brca Mutation Carriers ◽

Prospective Database

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New pre-treatment eosinophil-related ratios as prognostic biomarkers for survival outcomes in endometrial cancer

BMC Cancer ◽

10.1186/s12885-018-5131-x ◽

2018 ◽

Vol 18 (1) ◽

Cited By ~ 6

Author(s):

Katarzyna Holub ◽

Albert Biete

Keyword(s):

Endometrial Cancer ◽

Prognostic Biomarkers ◽

Survival Outcomes ◽

Pre Treatment

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Prognostic value of different metastatic sites for patients with FIGO stage IVB endometrial cancer after surgery: A SEER database analysis

Journal of Surgical Oncology ◽

10.1002/jso.26102 ◽

2020 ◽

Author(s):

Hui Li ◽

Rusi Zhang ◽

Cuiying Chen ◽

Chuling Wu ◽

Haoliang Lin ◽

...

Keyword(s):

Endometrial Cancer ◽

Prognostic Value ◽

Figo Stage ◽

Seer Database ◽

Database Analysis ◽

Stage Ivb ◽

Metastatic Sites

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Brusatol Sensitizes Endometrial Hyperplasia and Cancer to Progestin by Suppressing Nrf2-Tet1-AKR1C1-Mediated Progestin Metabolism

10.21203/rs.3.rs-427970/v1 ◽

2021 ◽

Author(s):

Meiyan Hu ◽

Di Sun ◽

Jing Yu ◽

Yue Fu ◽

Zuoshu Qin ◽

...

Keyword(s):

Endometrial Cancer ◽

Endometrial Hyperplasia ◽

Synergistic Effects ◽

Cell Counting ◽

Luciferase Reporter ◽

Dot Blot ◽

Promoter Regions ◽

Nrf2 Target Gene ◽

Pre Treatment ◽

Progestin Therapy

Abstract BackgroundProgestin resistance is the main obstacle for the conservative therapy to maintain fertility in women with endometrial hyperplasia and cancer. Up to 30% of endometrial cancers fail to respond to progestin, a rate that has not significantly changed due to the lack of a detailed understanding of progestin resistance.MethodsCell Counting Kit-8 (CCK-8) assays were used to detect the synergistic effects of brusatol in combination with progestin. Using commercial kits, the conversion of progestin to 20α-dihydroxyprogesterone following btusatol treatment or AKR1C1 silence was investigated. The correlation betwwen AKR1C1 expression profile and prgestin response was further analyzed in paired endometrial hyperplasia and cancer samples from the same individuals before and after progestin therapy. The effects of brusatol-mediated reversal of progestin resistance was explored in both mouse xenograft and human organoid models. DNA dot blot, HMeDIP, and dural-luciferase reporter assays were performed to uncover the mechanism through which brusatol inhibits AKR1C1 and sensitizes endometrial hyperplasia and cancer to progestin.ResultsBrusatol sensitizes endometrial cancer cell to progestin by downregulating the expression of Nrf2 and its target AKR1C1. Increased AKR1C1 facilitated production of 20-α-dihydroxyprogeserone and was associated with declined progesterone. Suppression of AKR1C1 by brusatol resulted in decreased progesterone catabolism and maintained potent progesterone to inhibit endometrial cancer growth. Aberrant overexpression of AKR1C1 was found in paired endometrial hyperplasia and cancer samples from the same individuals with progestin resistance, whereas attenuated or loss of AKR1C1 was observed in post-treatment samples with well progestin response as compared with paired pre-treatment tissues. Tet1 was identified as a novel Nrf2 target gene. It in turn upregulated AKR1C1 expression by increasing hydroxymethylation levels in its promoter regions. ConclusionsWe found that Nrf2-Tet1-AKR1C1 axis plays an essential role in progestin resistance, and brusatol sensitizes endometrial hyperplasia and cancer to progestin by suppressing Nrf2-Tet1-AKR1C1-mediated progestin metabolism. Our findings suggest that AKR1C1 expression pattern may serve as an important biomarker of progestin resistance in endometrial hyperplasia and cancer .

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Body mass index and attitudes towards health behaviors among women with endometrial cancer before and after treatment

International Journal of Gynecological Cancer ◽

10.1136/ijgc-2019-000999 ◽

2019 ◽

Vol 30 (2) ◽

pp. 187-192

Author(s):

Ross Harrison ◽

Hui Zhao ◽

Charlotte C Sun ◽

Shuangshuang Fu ◽

Shannon D Armbruster ◽

...

Keyword(s):

Body Mass Index ◽

Endometrial Cancer ◽

Health Behavior ◽

Health Behaviors ◽

Cancer Survivors ◽

Body Mass ◽

Post Treatment ◽

Treatment Changes ◽

The Mean ◽

Pre Treatment

IntroductionSome experts have argued that obesity-related malignancies such as endometrial cancer are a “teachable moment” that lead to meaningful changes in health behaviors. It is unclear if endometrial cancer survivors lose weight following treatment. Our goal with this investigation was to evaluate post-treatment changes in body mass index (BMI) and attitudes towards health behaviors in endometrial cancer survivors.MethodsIncident endometrial cancer cases undergoing surgery between 2009–2015 were identified in the Marketscan Commercial database and linked with BMI data and health behavior questionnaires from the Marketscan Health Risk Assessment database. Patients were excluded for insufficient BMI data. Standard statistical methods, including the two-sample Wilcoxon rank sum test, χ2 test, and McNemar’s test, were used.Results655 patients with a median age of 54 (IQR 49-58) were identified and analyzed. Median duration of follow-up was 595 days (IQR 360–1091). Mean pre- and post-treatment BMI was 35.5 kg/m2 (median 35.0; IQR 27.0–42.3) and 35.6 kg/m2 (median 34.3; IQR 28.0–42.0), respectively. Median BMI change in the entire cohort was 0 kg/m2 (IQR −1.0 to 2.0). Weight gain (n=302; 46.1%) or no change in weight (n=106; 16.2%) was seen in most patients. Among the 302 patients who gained weight, the mean pre-treatment BMI was 34.0 kg/m2 and mean increase was 2.8 kg/m2 (median 2.0; IQR 1.0–3.4). Among the 247 cases who lost weight, the mean pre-treatment BMI was 38.6 kg/m2 and mean decrease was 3.2 kg/m2 (median 2.0; IQR 1.0–4.0). No pre- to post-treatment differences were observed in health behavior questionnaires regarding intention to better manage their diet, exercise more, or lose weight.DiscussionMost endometrial cancer survivors gain weight or maintain the same weight following treatment. No post-treatment changes in attitudes regarding weight-related behaviors were observed. The systematic delivery of evidence-based weight loss interventions should be a priority for survivors of endometrial cancer.

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