New-Onset Diabetes after an Obesity-Related Cancer Diagnosis and Survival Outcomes in the Women's Health Initiative.


Journal

Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
ISSN: 1538-7755
Titre abrégé: Cancer Epidemiol Biomarkers Prev
Pays: United States
ID NLM: 9200608

Informations de publication

Date de publication:
02 10 2023
Historique:
received: 23 03 2023
revised: 20 06 2023
accepted: 07 08 2023
medline: 3 10 2023
pubmed: 17 8 2023
entrez: 17 8 2023
Statut: ppublish

Résumé

Individuals diagnosed with an obesity-related cancer (ORC survivors) are at an elevated risk of incident diabetes compared with cancer-free individuals, but whether this confers survival disadvantage is unknown. We assessed the rate of incident diabetes in ORC survivors and evaluated the association of incident diabetes with all-cause and cancer-specific mortality among females with ORC in the Women's Health Initiative cohort (N = 14,651). Cox proportional hazards regression models stratified by exposure-risk periods (0-1, >1-3, >3-5, >5-7, and >7-10 years) from ORC diagnosis and time-varying exposure (diabetes) analyses were performed. Among the ORC survivors, a total of 1.3% developed diabetes within ≤1 year of follow-up and 2.5%, 2.3%, 2.3%, and 3.6% at 1-3, 3-5, 5-7, and 7-10 years of follow-up, respectively, after an ORC diagnosis. The median survival for those diagnosed with diabetes within 1-year of cancer diagnosis and those with no diabetes diagnosis in that time frame was 8.8 [95% confidence interval (CI), 7.0-14.5) years and 16.6 (95% CI, 16.1-17.0) years, respectively. New-onset compared with no diabetes as a time-varying exposure was associated with higher risk of all-cause (HR, 1.27; 95% CI, 1.16-1.40) and cancer-specific (HR, 1.17; 95% CI, 0.99-1.38) mortality. When stratified by exposure-risk periods, incident diabetes in ≤1 year of follow-up was associated with higher all-cause (HR, 1.76; 95% CI, 1.40-2.20) and cancer-specific (HR0-1, 1.82; 95% CI, 1.28-2.57) mortality, compared with no diabetes diagnosis. Incident diabetes was associated with worse cancer-specific and all-cause survival, particularly in the year after cancer diagnosis. These findings draw attention to the importance of diabetes prevention efforts among cancer survivors to improve survival outcomes.

Sections du résumé

BACKGROUND
Individuals diagnosed with an obesity-related cancer (ORC survivors) are at an elevated risk of incident diabetes compared with cancer-free individuals, but whether this confers survival disadvantage is unknown.
METHODS
We assessed the rate of incident diabetes in ORC survivors and evaluated the association of incident diabetes with all-cause and cancer-specific mortality among females with ORC in the Women's Health Initiative cohort (N = 14,651). Cox proportional hazards regression models stratified by exposure-risk periods (0-1, >1-3, >3-5, >5-7, and >7-10 years) from ORC diagnosis and time-varying exposure (diabetes) analyses were performed.
RESULTS
Among the ORC survivors, a total of 1.3% developed diabetes within ≤1 year of follow-up and 2.5%, 2.3%, 2.3%, and 3.6% at 1-3, 3-5, 5-7, and 7-10 years of follow-up, respectively, after an ORC diagnosis. The median survival for those diagnosed with diabetes within 1-year of cancer diagnosis and those with no diabetes diagnosis in that time frame was 8.8 [95% confidence interval (CI), 7.0-14.5) years and 16.6 (95% CI, 16.1-17.0) years, respectively. New-onset compared with no diabetes as a time-varying exposure was associated with higher risk of all-cause (HR, 1.27; 95% CI, 1.16-1.40) and cancer-specific (HR, 1.17; 95% CI, 0.99-1.38) mortality. When stratified by exposure-risk periods, incident diabetes in ≤1 year of follow-up was associated with higher all-cause (HR, 1.76; 95% CI, 1.40-2.20) and cancer-specific (HR0-1, 1.82; 95% CI, 1.28-2.57) mortality, compared with no diabetes diagnosis.
CONCLUSIONS
Incident diabetes was associated with worse cancer-specific and all-cause survival, particularly in the year after cancer diagnosis.
IMPACT
These findings draw attention to the importance of diabetes prevention efforts among cancer survivors to improve survival outcomes.

Identifiants

pubmed: 37590895
pii: 728488
doi: 10.1158/1055-9965.EPI-23-0278
doi:

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1356-1364

Subventions

Organisme : NCI NIH HHS
ID : F99 CA264400
Pays : United States
Organisme : NCI NIH HHS
ID : U01 CA272529
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA042014
Pays : United States
Organisme : NCI NIH HHS
ID : K07 CA222060
Pays : United States
Organisme : NCI NIH HHS
ID : K00 CA264400
Pays : United States

Informations de copyright

©2023 American Association for Cancer Research.

Auteurs

Prasoona Karra (P)

Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, Utah.
Cancer Control and Population Sciences, Huntsman Cancer Institute, Salt Lake City, Utah.
Department of Epidemiology, Geisel School of Medicine at Dartmouth College, Lebanon, New Hampshire.

Sheetal Hardikar (S)

Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, Utah.
Cancer Control and Population Sciences, Huntsman Cancer Institute, Salt Lake City, Utah.
Department of Population Health Sciences, University of Utah, Salt Lake City, Utah.

Maci Winn (M)

Cancer Control and Population Sciences, Huntsman Cancer Institute, Salt Lake City, Utah.
Department of Population Health Sciences, University of Utah, Salt Lake City, Utah.

Garnet L Anderson (GL)

Fred Hutchinson Cancer Research Center, Seattle, Washington.

Benjamin Haaland (B)

Cancer Control and Population Sciences, Huntsman Cancer Institute, Salt Lake City, Utah.
Department of Population Health Sciences, University of Utah, Salt Lake City, Utah.

Benjamin Krick (B)

Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, Utah.
Cancer Control and Population Sciences, Huntsman Cancer Institute, Salt Lake City, Utah.

Cynthia A Thomson (CA)

The University of Arizona Cancer Center, Tucson, Arizona.

Aladdin Shadyab (A)

Herbert Wertheim School of Public Health and Human Longevity Science, University of California, San Diego, La Jolla, California.

Juhua Luo (J)

Indiana University, Bloomington, Indiana.

Nazmus Saquib (N)

Sulaiman AlRajhi University, Kingdom of Saudi Arabia, Al Bukayriyah, Saudi Arabia.

Howard D Strickler (HD)

Albert Einstein College of Medicine, Bronx, New York.

Rowan Chlebowski (R)

The Lundquist Institute, Torrance, California.

Rhonda S Arthur (RS)

Albert Einstein College of Medicine, Bronx, New York.

Scott A Summers (SA)

Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, Utah.

William L Holland (WL)

Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, Utah.

Thunder Jalili (T)

Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, Utah.

Mary C Playdon (MC)

Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, Utah.
Cancer Control and Population Sciences, Huntsman Cancer Institute, Salt Lake City, Utah.
Department of Population Health Sciences, University of Utah, Salt Lake City, Utah.

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