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1.  Upregulated Expression of Indoleamine 2, 3-Dioxygenase in Primary Breast Cancer Correlates with Increase of Infiltrated Regulatory T Cells In Situ and Lymph Node Metastasis 
IDO has been reported to induce immunotolerance and promote metastasis in solid malignancy, but the mechanisms involved were not fully understood. In this study, the expression of IDO in primary breast cancer was examined and the correlation between the expression levels of IDO and the densities of Foxp3+ Tregs in situ was studied. The IDO stably-expressing CHO cells(IDO/CHO) were generated to evaluate the induction of Foxp3+ Tregs after coculturing with CD3+ T cells in vitro. The IDO expression in cancer was higher than that in benign diseases both at RNA and protein levels. The IDO expression was significantly upregulated in tumors of more advanced stages and with more extensive lymph node metastasis, and displayed positive linear correlation with the density of Foxp3+ Tregs. We further demonstrated that CD4+CD25+CD127− Tregs could be amplified by coculturing CD3+ T cells with IDO/CHO cells in vitro which displayed increasing Foxp3 expression both at mRNA and protein levels. Our results implied that up-regulation of IDO in primary breast cancer may inhibit local immune surveillance and promote metastasis by favoring development and infiltration of Foxp3+ Tregs in the tumor microenvironment.
PMCID: PMC3202140  PMID: 22110525
2.  Quality of Life after Autologous Peripheral Blood Stem Cell Transplantation and High-Dose Chemotherapy in High-Risk Breast Cancer Patients 
Breast Care  2009;4(6):379-386.
As long-term survivors of breast cancer after autologous peripheral blood stem cell transplantation (ASCT) are becoming more numerous, studies addressing the issue of long-term follow-up are necessary. In this study, we report on the quality of life (QOL) after ASCT and high-dose chemotherapy (HDCT).
Patients and Methods
The QOL questionnaire version 3.0 by the European Organization for Research and Treatment of Cancer (EORTC QLQ-C30 version 3.0) was filled in by patients and healthy controls at 5 time points. After obtaining the results, we analyzed the correlation between QOL and the effect factors.
Some functions got significantly worse, and some symptoms got more serious after ASCT and HDCT. However, most of them improved with time and were comparable to the healthy controls after 5 years. QOL was in part related to age, tumor characteristics, educational level, marriage status, and income.
Evaluating QOL allows medical workers to fully understand a patient's state of health, and aid the estimation and selection of clinical treatment methods as well as improve recovery.
PMCID: PMC2942001  PMID: 20877673
Quality of life; Autologous peripheral blood stem cell transplantation; High-risk breast cancer
3.  CD4+T Cells in CIKs (CD4+ CIKs) Reversed Resistance to Fas-Mediated Apoptosis Through CD40/CD40L Ligation Rather Than IFN-γ Stimulation 
Background: Cytokine-induced killer cells (CIKs) are nonspecific antitumor effectors with superior advantages. CD4+ CIKs can induce Fas-dependent apoptosis in sensitive Raji cells. Here, a Fas-dependent apoptosis was detected in resistant breast cancer MDA-MB-231 cells, and underlying mechanisms were discriminated. Methods: Amplification of CIKs and purification of CD4+ CIKs were performed in 15 patients with malignant solid tumors. The expression of CD40L and soluble cytokines in CD4+ CIKs were analyzed. The apoptotic rates of tumor cells and the expression of Fas on membranes were detected using flow cytometry assay. The specific blocking antibodies against FasL, CD40L, and interferon-γ (IFN-γ) were added to abolish their effects. The changes of 4 apoptosis-related genes (Bcl-2, Bax, Fas-associating protein with death domain [FADD], and FLICE inhibitory protein [c-FLIP]) in MDA-MB-231 cells cocultured with CD4+ CIKs were measured by real-time quantitative reverse-transcriptase polymerase chain reaction after 6 hours and 24 hours with or without blocking antibodies. Results: Upregulated expression of membrane-attached CD40L and dramatically increased secretion of soluble CD40L and IFN-γ were identified in CD4+ CIK. The susceptibility to Fas-mediated apoptosis of insensitive MDA-MB-231 cells was elevated after being pretreated with supernatants from CD4+ CIK. After coculture with CD4+ CIK, apoptosis in MDA-MB-231 cells paralleled with enhanced expression of Fas was blocked fully by either anti-FasL or anti-CD40L, but only partly by anti-IFN-γ antibodies. The anti-CD40L monoclonal antibody (McAb) rather than anti-IFN-γ McAb induced significant increase of c-FLIP, which negatively correlated with the apoptosis observed in MDA-MB-231 cells. Conclusions: Apoptosis in MDA-MB-231 cells induced by CD4+ CIK is Fas-dependent. The reversion of Fas resistance is mediated through CD40/CD40L ligation rather than IFN-γ stimulation by inhibiting synthesis of c-FLIP.
PMCID: PMC2936940  PMID: 18593367
CD40/CD40L ligation; IFN-γ; apoptosis; Fas-dependent; breast cancer
4.  Synchronous infiltrating ductal carcinoma and primary extramedullary plasmacytoma of the breast 
Extramedullary plasmacytomas are seldom solitary and usually progress to diffuse myelomatosis. Plasmacytomas of the breast are rare, especially when not associated multiple myeloma. Synchronous infiltrating ductal carcinoma and primary extramedullary plasmacytoma of the breast have not previously reported.
Case presentation
A 27-years-old woman with an untreated upper outer quadrant breast mass for 1-year was referred to our cancer hospital for surgical evaluation of increasing breast pain. Postoperatively, microscopic examination revealed an infiltrating ductal carcinoma complicated by an extramedullary plasmacytoma divided by fibrous tissue in one section. Following surgery, the patient received chemotherapy for the carcinoma and radiotherapy for the plasmacytoma.
In this case, careful histopathology examination was essential to make the correct diagnosis and therapy for these synchronous lesions. The patient finished chemotherapy and radiotherapy without significant adverse effects.
PMCID: PMC2680856  PMID: 19393076

Results 1-4 (4)