engleski

Differences in immunohistochemical features between invasive breast cancers and DCIS lesions from a single population, based on a consecutive case series of 1, 248 patients

Background: If all breast cancer types evolve from DCIS lesions, speed of tissue invasion can be calculated from breast tumor type distributions among DCIS lesions and among invasive cancers (Tumour Biol 2013 ; 34:1-7.). Methods: Histologic data of 68 DCIS and 1, 180 invasive ductal cancer (IDC) patients were collected and analyzed. Results: ER+PgR- phenotype was more common in Luminal B2 than among the pooled Luminal A&B1 (p=0.0002), more in Luminal B1 than in Luminal A (p=0.0167). The same phenotype was associated with age older than 54 in Luminal B1 and in B2 patients. HER2 type cancers were more often in older patients (p=0.0038). Tumor progression from DCIS to IDC was found 39% faster than the average in Luminal B1 tumors, supporting the clinical importance of this tumor type. The rare combination of low Ki-67 in HER2 type cancers (only 14% of HER2 type cancers) showed very slow transition to IDC (only 53.55% of the average speed), while the triple negative cancers were faster than the average, almost despite the Ki-67 value (104.63% for the low and 114.27% for the high Ki-67 tumors). In three tumor types with positive steroid receptors the ER+PgR- phenotype showed slower IDC transition than the ER+PgR+ phenotype of the same tumor type (speed difference of 38% for Luminal A, 46% for Luminal B1 and 67% for Luminal B2 with Ki67>14%). Triple-negative tumors in younger patients were 24% faster than the expected average, while in HER2 type tumors, in younger patients the tissue invasion speed was 20% below the expected values. Conclusions: The relative tissue invasion speed differed substantialy among our patients. Differences depended on tumor types, steroid expression phenotypes and age. It seemed that in ER+PgR- tumors, if ligand binding to ERs does not promote PgR expression, it also does not stimulate the tissue invasion. In triple negative tumors, an age dependent premenopausal mechanism seems possible as an accelerator of tissue invasion, while the invasion of HER2 overexpressed tumors in older patients possibly depended on an unidentified mechanism that takes more time to be acquired, so it was less present in premenopausal patients.

breast cancer types; invasive ductal breast cancer; DCIS; phenotype

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