Auto-antibodies to p53 and the Subsequent Development of Colorectal Cancer in a U.S. Prospective Cohort Consortium.


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:
12 2020
Historique:
received: 20 05 2020
revised: 01 08 2020
accepted: 21 09 2020
pubmed: 26 9 2020
medline: 22 12 2021
entrez: 25 9 2020
Statut: ppublish

Résumé

Auto-antibodies to tumor suppressor p53 are found in a subset of patients with colorectal cancer. A recent prospective study in the United States has reported a significant 1.8-fold increased odds for colorectal cancer development with prediagnostic seropositivity to p53. In this study, we sought to examine this association in a U.S. colorectal cancer cohort consortium to evaluate the potential utility of p53 auto-antibodies as an early biomarker for colorectal cancer. Auto-antibodies to p53 were measured in prediagnostic blood samples of 3,702 incident colorectal cancer cases and 3,702 controls, matched by age, race, and sex, from 9 U.S. prospective cohorts. The association of seropositivity to p53 with colorectal cancer risk, overall and by time between blood draw and diagnosis, was determined by conditional logistic regression. Overall, 5% of controls and 7% of cases were seropositive to p53, resulting in a statistically significant 33% increased colorectal cancer risk [odds ratio (OR), 1.33; 95% confidence interval (CI), 1.09-1.61]. By follow-up time, the association was only significant with colorectal cancer diagnoses within 4 years after blood draw (OR, 2.27; 95% CI, 1.62-3.19), but not thereafter (OR, 0.97; 95% CI, 0.76-1.24). In this large consortium of prospective cohorts, we found that prediagnostic seropositivity to tumor suppressor p53 was significantly associated with an over 2-fold increased odds of developing colorectal cancer within 4 years after blood draw. Our finding suggests that p53 seropositivity may not be a useful predictor of long-term colorectal cancer risk; however, it might be considered as a marker to aid in the early diagnosis of colorectal cancer.

Sections du résumé

BACKGROUND
Auto-antibodies to tumor suppressor p53 are found in a subset of patients with colorectal cancer. A recent prospective study in the United States has reported a significant 1.8-fold increased odds for colorectal cancer development with prediagnostic seropositivity to p53. In this study, we sought to examine this association in a U.S. colorectal cancer cohort consortium to evaluate the potential utility of p53 auto-antibodies as an early biomarker for colorectal cancer.
METHODS
Auto-antibodies to p53 were measured in prediagnostic blood samples of 3,702 incident colorectal cancer cases and 3,702 controls, matched by age, race, and sex, from 9 U.S. prospective cohorts. The association of seropositivity to p53 with colorectal cancer risk, overall and by time between blood draw and diagnosis, was determined by conditional logistic regression.
RESULTS
Overall, 5% of controls and 7% of cases were seropositive to p53, resulting in a statistically significant 33% increased colorectal cancer risk [odds ratio (OR), 1.33; 95% confidence interval (CI), 1.09-1.61]. By follow-up time, the association was only significant with colorectal cancer diagnoses within 4 years after blood draw (OR, 2.27; 95% CI, 1.62-3.19), but not thereafter (OR, 0.97; 95% CI, 0.76-1.24).
CONCLUSIONS
In this large consortium of prospective cohorts, we found that prediagnostic seropositivity to tumor suppressor p53 was significantly associated with an over 2-fold increased odds of developing colorectal cancer within 4 years after blood draw.
IMPACT
Our finding suggests that p53 seropositivity may not be a useful predictor of long-term colorectal cancer risk; however, it might be considered as a marker to aid in the early diagnosis of colorectal cancer.

Identifiants

pubmed: 32972968
pii: 1055-9965.EPI-20-0780
doi: 10.1158/1055-9965.EPI-20-0780
pmc: PMC7710535
mid: NIHMS1632879
doi:

Substances chimiques

Autoantibodies 0
TP53 protein, human 0
Tumor Suppressor Protein p53 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

2729-2734

Subventions

Organisme : NHLBI NIH HHS
ID : HHSN268201600002C
Pays : United States
Organisme : NHLBI NIH HHS
ID : HHSN268201600018C
Pays : United States
Organisme : NCI NIH HHS
ID : U01 CA182934
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA190428
Pays : United States
Organisme : NHLBI NIH HHS
ID : HHSN268201600003C
Pays : United States
Organisme : NCI NIH HHS
ID : UM1 CA186107
Pays : United States
Organisme : NHLBI NIH HHS
ID : HHSN268201600004C
Pays : United States
Organisme : NHLBI NIH HHS
ID : HHSN268201600001C
Pays : United States
Organisme : NCI NIH HHS
ID : UM1 CA167552
Pays : United States
Organisme : NCI NIH HHS
ID : R00 CA215314
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA040360
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA077955
Pays : United States
Organisme : NCI NIH HHS
ID : P01 CA087969
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL034595
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK058404
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA092447
Pays : United States
Organisme : NCI NIH HHS
ID : U01 CA167552
Pays : United States
Organisme : NCI NIH HHS
ID : UM1 CA182934
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK058587
Pays : United States
Organisme : NCI NIH HHS
ID : U01 CA202979
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA097193
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA071789
Pays : United States
Organisme : NCI NIH HHS
ID : U01 CA164973
Pays : United States

Informations de copyright

©2020 American Association for Cancer Research.

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Auteurs

Julia Butt (J)

Infections and Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany. j.butt@dkfz-heidelberg.de.
Cancer Control and Population Sciences Program, Duke Cancer Institute, and Department of Population Health Sciences, Duke University, Durham, North Carolina.

William J Blot (WJ)

Division of Epidemiology, Vanderbilt University Medical Center, Nashville, Tennessee.

Kala Visvanathan (K)

Department of Epidemiology, Johns Hopkins School of Public Health, Baltimore, Maryland.

Loïc Le Marchand (L)

Epidemiology Program, University of Hawai'i Cancer Center, Honolulu, Hawaii.

Lynne R Wilkens (LR)

Epidemiology Program, University of Hawai'i Cancer Center, Honolulu, Hawaii.

Yu Chen (Y)

Department of Population Health, New York University School of Medicine, New York, New York.

Howard D Sesso (HD)

Brigham and Women's Hospital, Boston, Massachusetts.
Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts.

Lauren Teras (L)

Behavioral and Epidemiology Research Group, American Cancer Society, Atlanta, Georgia.

Marc D Ryser (MD)

Department of Population Health Sciences, and Department of Mathematics, Duke University, Durham, North Carolina.

Terry Hyslop (T)

Cancer Control and Population Sciences Program, Duke Cancer Institute, and Department of Population Health Sciences, Duke University, Durham, North Carolina.
Department of Biostatistics and Bioinformatics, Duke University, Durham, North Carolina.

Sylvia Wassertheil-Smoller (S)

Department of Epidemiology & Population Health, Albert Einstein College of Medicine, Bronx, New York.

Lesley F Tinker (LF)

Cancer Prevention Program, Division of Public Health Sciences at Fred Hutchinson Cancer Research Center, Seattle, Washington.

John D Potter (JD)

Centre for Public Health Research, Massey University, Wellington, New Zealand.
Fred Hutchinson Cancer Research Center, Seattle, Washington.

Mingyang Song (M)

Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts.
Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, Massachusetts.
Clinical and Translational Epidemiology Unit and Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts.

Sonja I Berndt (SI)

Infections and Immunoepidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, Maryland.

Tim Waterboer (T)

Infections and Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany.

Michael Pawlita (M)

Infections and Cancer Epidemiology, German Cancer Research Center (DKFZ), Heidelberg, Germany.

Meira Epplein (M)

Cancer Control and Population Sciences Program, Duke Cancer Institute, and Department of Population Health Sciences, Duke University, Durham, North Carolina.

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