z-logo
Premium
Cyclin‐D1 expression in node‐positive (N + ) and node‐negative (N − ) infiltrating human mammary carcinomas
Author(s) -
Collecchi, Paola,
Passoni Anna,
Rocchetta Marina,
Gnesi Elisa,
Baldini Editta,
Bevilacqua Generoso
Publication year - 1999
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19990420)84:2<139::aid-ijc8>3.0.co;2-y
Subject(s) - immunohistochemistry , cd1 , cyclin d1 , biology , mammary gland , pathology , flow cytometry , cancer research , breast cancer , cancer , microbiology and biotechnology , cell cycle , medicine , antigen , immunology , genetics , interleukin 21 , cd8
Cyclin‐D1 (CD1) expression was analyzed in human mammary carcinomas by immunohistochemical (IHC) and flow‐cytometry (FCM) methods: 52.5% and 50% of cases were strong expressors of CD1 by IHC and FCM analysis respectively. The percentage of CD1‐positive cells was especially high in node‐negative (N − ) estrogen‐receptor‐positive (ER + ) tumors, probably as a consequence of CD1 induction by estrogens in steroid‐responsive tissues. However, CD1 expression was not related to ER positivity in node‐positive tumors (N + ). An interesting relationship between CD1 expression and H 3 ‐thymidine labelling index (H 3 Td‐LI) was also found: CD1 and H 3 Td‐LI were unrelated in N − tumors, while high CD1 expression was observed in N + tumors with high DNA synthesis, as assessed by H 3 Td‐LI. The combined measurement of DNA and CD1 showed that 27 specimens were aneuploid, 19 of them (19/27; 70%) strongly expressing CD1. Further studies are needed to clarify the role of CD1 in DNA abnormality of breast tumors. However, we cannot exclude that the CD1 may be differently de‐regulated in the last phase of tumor progression, and that CD1 over‐expression may contribute to the aneuploidy of mammary carcinomas. Int. J. Cancer (Pred. Oncol.) 84:139–144, 1999. © 1999 Wiley‐Liss, Inc.

This content is not available in your region!

Continue researching here.

Having issues? You can contact us here