title: Tumor marker phenotype concordance in second primary breast cancer, California, 1999-2004.
abstract: Breast cancer is the most common cancer among women. It is estimated that 7% of women who have breast cancer will develop a subsequent second independent breast tumor within 10 years of the first. The status of estrogen (ER), progesterone (PR) and human growth hormone (HER2) receptors, individually and as phenotypic combinations, impacts the clinical course of breast cancer and may impact the course of subsequent primary tumors and patient survival. Our aims were to determine tumor marker phenotype concordance between first and second primary breast cancers (FPBC and SPBC), describe demographic and clinical characteristics, and examine first tumor treatments associated with phenotype concordance. A total of 76,209 cases of female invasive breast cancer were identified in the California Cancer Registry from 1999 to 2004. Of those, 1,407 women who had not undergone a prophylactic mastectomy, had information on the status of three tumor markers, and were diagnosed with an SPBC during the study period were selected. SPBCs were significantly smaller, diagnosed at a higher stage and were node positive. Patients whose FPBC was ER(+)/-/PR(+)/-/HER2- and triple negative (TN) (ER-/PR-/HER2-), often had concordant phenotypes for their SPBC. ER(+)/-/PR(+)/-/HER2+ and HER2-positive (ER-/PR-/HER2+) FPBCs, often had discordant phenotypes for their SPBC. ER(+)/-/PR(+)/-/HER2- SPBCs often lacked HER2 expression and were ER and/or PR positive. Tumor laterality and synchronicity significantly predicted concordance as did having a FPBC whose phenotypes were ER(+)/-/PR(+)/-/HER2+, HER2-positive and TN, while first primary tumor treatment with chemotherapy predicted discordance. The relationship between multiple primary breast cancer phenotype concordance and patient prognosis has yet to be determined. Our results indicate that SPBC surveillance strategies include consideration of FPBC phenotype. Although our results are provocative, they may have been influenced by current criteria used to determine tumor independence.
authors.affiliation: Chronic Disease Surveillance and Research Branch, Public Health Institute/California Department of Public Health, 1825 Bell Street, Suite 102, Sacramento, CA, 95825, USA. MBrown@ccr.ca.gov
authors.forename: Monica
authors.initials: M
authors.lastname: Brown
authors.forename: Katrina
authors.initials: K
authors.lastname: Bauer
authors.forename: Mary
authors.initials: M
authors.lastname: Pare
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D014408:Biomarkers, Tumor / Q000032:analysis*; D001943:Breast Neoplasms / Q000378:metabolism* / Q000473:pathology; D002140:California; D005260:Female; D006801:Humans; D008875:Middle Aged; D009367:Neoplasm Staging; D016609:Neoplasms, Second Primary / Q000378:metabolism* / Q000473:pathology; D010641:Phenotype; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000378:metabolism; D011960:Receptors, Estrogen / Q000378:metabolism; D011980:Receptors, Progesterone / Q000378:metabolism; D012042:Registries; D012189:Retrospective Studies
chemical_list: D014408:Biomarkers, Tumor; D018719:Erb-b2 Receptor Tyrosine Kinases; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone