Expression of Her2/neu, steroid receptors (ER and PR), Ki67 and p53 in invasive mammary ductal carcinoma associated with ductal carcinoma In Situ (DCIS) Versus invasive breast cancer alone.
OBJECTIVE
(a) To assess the expression patterns of HER2/neu, steroid receptors (ER and PR), Ki67 and p53 in invasive ductal cancer (IDC) and IDC associated with carcinoma in situ (IDC/DCIS) and (b) to determine if there is a differential expression of these molecular markers between IDC and IDC/DCIS.


METHODS
Paraffin-fixed breast cancer samples, diagnosed with only one histological invasive tumor (IDC (n=130), and IDC/DCIS (n=36) were analyzed by immunohistochemical means. The non-parametric Mann-Whitney and chi2 tests were used to evaluate any statistical differences between different groups. Significance was assumed at p<0.05.


RESULTS
A significant increase of the tumor grading was observed between IDC and IDC/DCIS (p<0.05). Her2/neu amplification was demonstrated in 49.6% of IDC compared to 31% of IDC/DCIS (p<0.05). ER expression showed no statistical differences between IDC and IDC/DCIS. The PR expression was demonstrated in 71% of IDC with significantly lower intensity than IDC/DCIS (p<0.05). The Ki67 expression was significantly higher (p<0.05) in IDC cases (64%) versus IDC/DCIS (49.7%). No differences were observed between IDC and IDC/DCIS for p53 expression.


CONCLUSIONS
We demonstrated significantly different expression patterns of Her2/neu, PR and Ki67 in IDC versus IDC/DCIS. Since these molecular markers play important roles in carcinogenesis and tumor progression, IDC/DCIS could be an important subtype of mammary invasive ductal cancer. Differences in expression of the evaluated markers might suggest a higher malignant potential of invasive carcinomas alone. The lower expression of Her2/neu and Ki67 in IDC/DCIS could implicate a less malignant behavior compared to a differentiated IDC. Additionally, these results might suggest that DCIS might be a malignant preform and the interaction with neoplastic tissue could result in an aggressive type of invasive tumor.
Mylonas
Ioannis
I
Ludwig-Maximilians University Munich, 1st Department of Obstetrics and Gynecology, 80337 Munich, Germany. Ioannis.mylonas@med.uni-muenchen.de
Makovitzky
Josef
J
Jeschke
Udo
U
Briese
Volker
V
Friese
Klaus
K
Gerber
Bernd
B
D001943:Breast Neoplasms / Q000378:metabolism* / Q000473:pathology; D002278:Carcinoma in Situ / Q000378:metabolism* / Q000473:pathology; D044584:Carcinoma, Ductal / Q000378:metabolism* / Q000473:pathology; D005260:Female; D018734:Genes, erbB-2; D006801:Humans; D007150:Immunohistochemistry; D019394:Ki-67 Antigen / Q000378:metabolism*; D009361:Neoplasm Invasiveness; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000378:metabolism*; D011960:Receptors, Estrogen / Q000378:metabolism*; D011980:Receptors, Progesterone / Q000378:metabolism*; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism*
D019394:Ki-67 Antigen; D018719:Erb-b2 Receptor Tyrosine Kinases; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D016159:Tumor Suppressor Protein p53