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Current or recent smoking is associated with more variable telomere length in prostate stromal cells and prostate cancer cells
Author(s) -
Joshu Corinne E.,
Peskoe Sarah B,
Heaphy Christopher M.,
Kenfield Stacey A.,
Mucci Lorelei A.,
Giovannucci Edward L.,
Stampfer Meir J.,
Yoon Ghilsuk,
Lee Thomas K.,
Hicks Jessica L.,
De Marzo Angelo M.,
Meeker Alan K.,
Platz Elizabeth A.
Publication year - 2018
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/pros.23462
Subject(s) - telomere , prostate cancer , stromal cell , medicine , cancer , prostate , telomerase , oncology , cancer cell , pathology , biology , genetics , gene
Background Current and recent smoking have been associated with a greater risk of prostate cancer recurrence and mortality, though the underlying mechanism is unknown. Methods To determine if telomere shortening, which has been associated with poor outcomes, may be a potential underlying mechanism, we prospectively evaluated the association between smoking status and telomere length in 567 participants in the Health Professionals Follow‐up Study, who were surgically treated for prostate cancer. Using tissue microarrays (TMA), we measured telomere length in cancer and benign tissue, specifically stromal cells in the same TMA spot using a telomere‐specific fluorescence in situ hybridization assay. Smoking status was collected via questionnaire 2‐years before diagnosis. Adjusting for age, pathologic stage and grade, the median and standard deviation of the per‐cell telomere signals were determined for each man for stromal cells and cancer cells by smoking categories. In sub‐analyses, we restricted to men without major co‐morbidities diagnosed before prostate cancer. Results Overall, there were no associations between smoking status and telomere length or variability in stromal cells or cancer cells. However, among men without comorbidities, current smokers and former smokers who quit <10 years ago had the most variable telomere length in stromal cells (29.3% more variable than never smokers; P ‐trend = 0.0005) and in cancer cells (27.7% more variable than never smokers; P ‐trend = 0.05). Among men without comorbidities, mean telomere length did not differ by smoking status in stromal cells or cancer cells. Conclusion Telomere variability in prostate cells may be one mechanism through which smoking influences poor prostate cancer outcomes.