Molecular classification system identifies invasive breast carcinoma patients who are most likely and those who are least likely to achieve a complete pathologic response after neoadjuvant chemotherapy.
BACKGROUND
The molecular classification system categorizes invasive breast carcinomas according to their key driving biomarkers. In the current study, the authors evaluated whether response to neoadjuvant chemotherapy was correlated with the molecular classification groups.


METHODS
Using immunohistochemistry, the molecular classification group (luminal-A, luminal-B, HER-2-variant, HER-2-classic, and basal phenotype) was retrospectively determined in 68 breast cancer patients who received neoadjuvant treatment.


RESULTS
A total of 28 carcinoma patients (41.2%) achieved a compete pathologic response (CPR), including 2 of 15 patients classified as having luminal-A (13.3%), 4 of 16 patients classified as having luminal-B (25.0%), 10 of 12 patients classified as having HER-2-classic (83.3%), none of the 4 patients classified as having HER-2-variant, and 12 of 21 patients classified as having basal phenotype (57.1%) neoplasms. The CPR rate among patients with the HER-2-classic and basal neoplasms was 67% (22 of 33 neoplasms), compared with 17.1% (6 of 35 neoplasms) in the non-HER-2-classic/basal combined group (P < .001). Eleven carcinomas were initially diagnosed as invasive lobular carcinomas (pleomorphic and classic), 4 of which were luminal-A, 4 of which were luminal-B, 2 of which were HER-2-classic, and 1 of which was basal. On review, only 3 of these 11 cases remained classified as classic lobular carcinoma, all of which were classified as luminal-A, and none of these patients achieved a CPR. Four of the other 8 patients achieved a CPR.


CONCLUSIONS
The molecular classification system is useful for identifying carcinoma patients who are most likely and those who are least likely to achieve a CPR. In the current study, all the morphologically classic lobular carcinomas were classified as luminal-A neoplasms, which may explain the low rate of CPR reported.
Goldstein
Neal S
NS
Department of Anatomic Pathology, William Beaumont Hospital, Royal Oak, Michigan 48073, USA. NGoldstein@Beaumont.edu
Decker
David
D
Severson
Dawn
D
Schell
Scott
S
Vicini
Frank
F
Margolis
Jeffrey
J
Dekhne
Nayana S
NS
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000970:Antineoplastic Agents / Q000627:therapeutic use*; D014408:Biomarkers, Tumor / Q000378:metabolism; D001943:Breast Neoplasms / Q000145:classification* / Q000188:drug therapy / Q000378:metabolism; D018270:Carcinoma, Ductal, Breast / Q000145:classification / Q000188:drug therapy / Q000378:metabolism; D018275:Carcinoma, Lobular / Q000145:classification / Q000188:drug therapy / Q000378:metabolism; D017024:Chemotherapy, Adjuvant; D005260:Female; D006801:Humans; D008875:Middle Aged; D020360:Neoadjuvant Therapy; D009367:Neoplasm Staging; D010634:Phenobarbital / Q000378:metabolism; D011379:Prognosis; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000378:metabolism; D015996:Survival Rate; D016896:Treatment Outcome
D000970:Antineoplastic Agents; D014408:Biomarkers, Tumor; D010634:Phenobarbital; D018719:Erb-b2 Receptor Tyrosine Kinases