Send to:

Choose Destination
See comment in PubMed Commons below
Am J Obstet Gynecol. 2009 Apr;200(4):457.e1-5. doi: 10.1016/j.ajog.2008.12.012. Epub 2009 Feb 6.

Tissue microarray analysis of hormonal signaling pathways in uterine carcinosarcoma.

Author information

  • 1Division of Gynecologic Oncology, Department of Obstetrics and Gynecology and Women's Health, Albert Einstein Cancer Center, Albert Einstein College of Medicine, Bronx, NY, USA.



To evaluate the relationship of hormone (estrogen receptor alpha, estrogen receptor beta, progesterone receptor) and growth factor receptor (insulin-like growth factor receptor, human epidermal growth factor receptor 2) expression with disease progression in uterine carcinosarcoma.


Immunohistochemistry was performed on tissue arrays using standard methodology. Differences between groups were evaluated by the Wilcoxon rank-sum test. Interactions between tumor stage and receptor expression were determined by linear trend analysis.


Compared with normal endometrium, carcinosarcomas exhibited low estrogen receptor alpha and progesterone receptor expression (all P < .01), but overexpressed estrogen receptor beta (P = .02). Estrogen receptor beta expression increased in advanced stage disease (P = .02). Insulin-like growth factor receptor expression was lower in carcinosarcoma compared with normal endometrium (P = .01). Human epidermal growth factor receptor 2 expression was elevated and increased with disease progression (P < .01).


In uterine carcinosarcoma, estrogen receptor beta expression is elevated and increases with disease progression, whereas estrogen receptor alpha and progesterone receptor are suppressed. Human epidermal growth factor receptor 2 expression is increased, whereas insulin-like growth factor receptor is lower than in normal endometrium. These data support a potential role for estrogen receptor beta in disease progression via crosstalk with human epidermal growth factor receptor 2.

[PubMed - indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science Icon for PubMed Central
    Loading ...
    Write to the Help Desk