Abstract
We have previously shown that a higher percentage of circulating CD3+ T lymphocytes undergo spontaneous apoptosis in cancer patients as compared with normal controls. Prolactin (PRL) has been reported to inhibit apoptosis in various cell types, including a Nb2 rat lymphoma cell line. In addition, there is evidence that the human PRL-antagonist hPRL-G129R induces apoptosis in breast cancer cell lines. We investigated a possible relationship between prolactin receptor (PRL-R) expression and apoptosis of CD3+ T lymphocytes, as well as PRL plasma levels, in patients with breast cancer. Peripheral blood mononuclear cells of patients (n = 11) and sex-matched normal controls (n = 12) were stained with AnnexinV, anti-Fas mAb (CD95), mouse antihuman PRL-R mAb B6.2, anti-CD3 mAb and respective isotype control mAbs. Multicolor flow cytometry was used to compare expression of these markers on T cell. In patients, 37 ± 19% (median ± SD) of CD3+ cells bound AnnexinV, marking early apoptosis of T lymphocytes compared with 17 ± 10% in controls (P <0.004). Furthermore, 82 ± 15% of the CD3+ T cells were Fas+ in patients, compared with 51 ± 9% in controls (P <0.0001). All CD3+ T lymphocytes were positive for PRL-R expression in breast cancer patients, as well as in normal control individuals. The mean fluorescence intensity of PRL-R on T lymphocytes of breast cancer patients was 106-172 (median 119) compared with 87-176 (median 123), suggesting no difference in PRL-R expression on T lymphocytes in patients versus controls. PRL plasma levels were comparable in patients and normal controls (4.8 ± 3.4 ng/ml versus 9.8 ± 4.6 ng/ml). In concordance with these findings, PRL was not able to inhibit the onset of apoptosis of Jurkat cells, a thymic lymphoma cell line, incubated with Fas cross-linking CH-11 mAb. These results indicate that PRL/PRL-R might not be involved in modulating Fas/Fas ligand interactions, which are, in part, responsible for apoptosis of T lymphocytes, leading to excessive turnover of T cells in the circulation of patients with breast cancer.
Highlights
Lymph node biopsy is important as a prognostic factor, and influences therapy
In this study we determined the in vivo cell kinetics along the spectrum of apparently normal epithelium, hyperplasia, preinvasive lesions and invasive carcinoma, in breast tissues affected by fibrocystic changes in which preinvasive and/or invasive lesions developed, as a model of breast carcinogenesis
This study was undertaken to determine the effect of wound healing drainages and postsurgical sera obtained from breast carcinoma (BC) patients on proliferation of dormant BC cells and to assess the role of HER2 oncoprotein in this proliferation
Summary
Lymph node biopsy is important as a prognostic factor, and influences therapy. In the transition from normal epithelium to hyperplasia and from preinvasive lesions to invasive carcinoma, the net growth of epithelial cells results from a growth imbalance in favour of proliferation. The objective of this study was to assess the efficacy of hyperbaric oxygen therapy in symptomatic patients after breast cancer treatment. Conclusion: Hyperbaric oxygen therapy should be considered as a treatment option for patients with persisting symptomatology following breast-conserving therapy. We hypothesized that COX-2 expression was associated with that of vascular endothelial growth factor (VEGF) and proliferating cell nuclear antigen (PCNA) in human breast cancer. Conclusion: COX-2 expression is significantly associated with increased cellular proliferation and angiogenesis in invasive breast cancer. Recent studies have demonstrated that the sentinel node biopsy (SNB) is a reliable and minimally invasive method for determining the axillary node status in patients with breast cancer. Conclusion: Overexpression of episialin strongly inhibits fat secretion, and critically affects timing of involution of the lactating mammary gland
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
