Associations between cigarette smoking, hormone therapy, and folate intake with incident colorectal cancer by TP53 protein expression level in a population-based cohort of older women

Lori S. Tillmans, Robert A. Vierkant, Alice H. Wang, Niloy Jewel Samadder, Charles F. Lynch, Kristin E. Anderson, Amy J. French, Robert W. Haile, Lisa J. Harnack, John D. Potter, Susan L Slager, Thomas Christopher Smyrk, Stephen N Thibodeau, James R Cerhan, Paul John Limburg

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Cigarette smoking (CS), hormone therapy (HT), and folate intake (FI) are each thought to influence colorectal cancer risk, but the underlying molecular mechanisms remain incompletely defined. The TP53 (p53) protein, encoded by the TP53 tumor-suppressor gene that is commonly mutated in colorectal cancer, can be readily assessed to differentiate biologically distinct colorectal cancer subtypes. In this prospective cohort study, we examined CS-, HT-, and FI-Associated colorectal cancer risks by TP53 protein expression level among Iowa Women's Health Study (IWHS) participants. The IWHS recruited 41,836 randomly selected Iowa women, ages 55 to 69 years, with a valid driver's license at study entry in 1986. Self-reported exposure variables were assessed at baseline. Incident colorectal cancer cases were ascertained by annual linkage with the Iowa Cancer Registry. Archived, paraffin-embedded tissue specimens were collected and evaluated for TP53 protein expression by immunohistochemistry. Multivariate Cox regression models were fit to estimate relative risks (RR) and 95% confidence intervals (CI) for associations between CS, HT, or FI and TP53-defined colorectal cancer subtypes. Informative environmental exposure and protein expression data were available for 492 incident colorectal cancer cases: 222 (45.1%) TP53 negative, 72 (14.6%) TP53 low, and 198 (40.2%) TP53 high. Longer duration (>5 years) of HT was inversely associated with TP53 high colorectal cancers (RR, 0.50; 95% CI, 0.27-0.94). No other statistically significant associations were observed. These data support possible heterogeneous effects from HT on TP53-related pathways of colorectal carcinogenesis in older women.

Original languageEnglish (US)
Pages (from-to)350-355
Number of pages6
JournalCancer Epidemiology Biomarkers and Prevention
Volume23
Issue number2
DOIs
StatePublished - Feb 2014

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Tumor Suppressor Protein p53
Folic Acid
Colorectal Neoplasms
Smoking
Hormones
Population
Women's Health
Therapeutics
Confidence Intervals
Environmental Exposure
Licensure
Tumor Suppressor Genes
Proportional Hazards Models
Paraffin
Registries
Carcinogenesis
Cohort Studies
Immunohistochemistry
Prospective Studies

ASJC Scopus subject areas

  • Epidemiology
  • Oncology
  • Medicine(all)

Cite this

Associations between cigarette smoking, hormone therapy, and folate intake with incident colorectal cancer by TP53 protein expression level in a population-based cohort of older women. / Tillmans, Lori S.; Vierkant, Robert A.; Wang, Alice H.; Samadder, Niloy Jewel; Lynch, Charles F.; Anderson, Kristin E.; French, Amy J.; Haile, Robert W.; Harnack, Lisa J.; Potter, John D.; Slager, Susan L; Smyrk, Thomas Christopher; Thibodeau, Stephen N; Cerhan, James R; Limburg, Paul John.

In: Cancer Epidemiology Biomarkers and Prevention, Vol. 23, No. 2, 02.2014, p. 350-355.

Research output: Contribution to journalArticle

Tillmans, Lori S. ; Vierkant, Robert A. ; Wang, Alice H. ; Samadder, Niloy Jewel ; Lynch, Charles F. ; Anderson, Kristin E. ; French, Amy J. ; Haile, Robert W. ; Harnack, Lisa J. ; Potter, John D. ; Slager, Susan L ; Smyrk, Thomas Christopher ; Thibodeau, Stephen N ; Cerhan, James R ; Limburg, Paul John. / Associations between cigarette smoking, hormone therapy, and folate intake with incident colorectal cancer by TP53 protein expression level in a population-based cohort of older women. In: Cancer Epidemiology Biomarkers and Prevention. 2014 ; Vol. 23, No. 2. pp. 350-355.
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abstract = "Cigarette smoking (CS), hormone therapy (HT), and folate intake (FI) are each thought to influence colorectal cancer risk, but the underlying molecular mechanisms remain incompletely defined. The TP53 (p53) protein, encoded by the TP53 tumor-suppressor gene that is commonly mutated in colorectal cancer, can be readily assessed to differentiate biologically distinct colorectal cancer subtypes. In this prospective cohort study, we examined CS-, HT-, and FI-Associated colorectal cancer risks by TP53 protein expression level among Iowa Women's Health Study (IWHS) participants. The IWHS recruited 41,836 randomly selected Iowa women, ages 55 to 69 years, with a valid driver's license at study entry in 1986. Self-reported exposure variables were assessed at baseline. Incident colorectal cancer cases were ascertained by annual linkage with the Iowa Cancer Registry. Archived, paraffin-embedded tissue specimens were collected and evaluated for TP53 protein expression by immunohistochemistry. Multivariate Cox regression models were fit to estimate relative risks (RR) and 95{\%} confidence intervals (CI) for associations between CS, HT, or FI and TP53-defined colorectal cancer subtypes. Informative environmental exposure and protein expression data were available for 492 incident colorectal cancer cases: 222 (45.1{\%}) TP53 negative, 72 (14.6{\%}) TP53 low, and 198 (40.2{\%}) TP53 high. Longer duration (>5 years) of HT was inversely associated with TP53 high colorectal cancers (RR, 0.50; 95{\%} CI, 0.27-0.94). No other statistically significant associations were observed. These data support possible heterogeneous effects from HT on TP53-related pathways of colorectal carcinogenesis in older women.",
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AU - Samadder, Niloy Jewel

AU - Lynch, Charles F.

AU - Anderson, Kristin E.

AU - French, Amy J.

AU - Haile, Robert W.

AU - Harnack, Lisa J.

AU - Potter, John D.

AU - Slager, Susan L

AU - Smyrk, Thomas Christopher

AU - Thibodeau, Stephen N

AU - Cerhan, James R

AU - Limburg, Paul John

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