Elliott Elliott Head Breast Cancer Research and Treatment Center

Baton Rouge, LA, United States

Elliott Elliott Head Breast Cancer Research and Treatment Center

Baton Rouge, LA, United States
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Elliott R.L.,Elliott Elliott Head Breast Cancer Research and Treatment Center | Elliott R.L.,Sallie Astor Burdine Breast Foundation | Head J.F.,Elliott Elliott Head Breast Cancer Research and Treatment Center | Head J.F.,Sallie Astor Burdine Breast Foundation
Surgical Oncology | Year: 2013

Purpose: Beginning in 1995 breast cancer patients were vaccinated in the adjuvant setting with an autologous, allogeneic whole cell vaccine to evaluate the effect on host lymphocyte immunity and disease specific survival. Methods: The breast cancer patients had host lymphocyte immunity against tumor associated antigens evaluated by a Lymphocyte Blastogenesis Assay (LBA) before vaccination. Thirty-seven patients with depressed immunity were vaccinated in the adjuvant setting. Patients were given six intradermal injections (three weekly followed by three monthly). Ten weeks after the last injection the LBA was repeated. Results: Some patients experienced slight pain and swelling at the injection site with slight chills and fever, but there were no severe toxicities. The vaccinated patients had a mean follow-up of 12.7 years with mean follow-up of 8.9 and 9.2 years for the patients with normal and depressed immunity, respectively, in the historic control. The 10 year survival was 95% (20 of 21 patients) in the normal immunity historic control, 59% (33 of 56 patients) in the depressed immunity historic control and 89% (33 of 37 patients) in the patients with depressed immunity that were vaccinated in the present clinical trial. The disease specific survival of the vaccinated patients with depressed immunity in this trial is significantly greater than that of the historic controls of unvaccinated patients with depressed immunity to their tumor associated antigens. Conclusion: This study confirms the importance of maintaining good host lymphocyte immunity after completion of standard therapy and validates the value of cancer immunotherapy in the adjuvant setting. © 2013 Elsevier Ltd. All rights reserved.


Elliott R.L.,Elliott Elliott Head Breast Cancer Research and Treatment Center | Jiang X.P.,Elliott Elliott Head Breast Cancer Research and Treatment Center | Phillips J.T.,Elliott Elliott Head Breast Cancer Research and Treatment Center | Barnett B.G.,Elliott Elliott Head Breast Cancer Research and Treatment Center | Head J.F.,Elliott Elliott Head Breast Cancer Research and Treatment Center
Cancer Biotherapy and Radiopharmaceuticals | Year: 2011

Human leukocyte antigen G (HLA-G) is an immunotolerant nonclassical major histocompatibility complex Class Ib molecule. It is expressed by trophoblastic placental cells during pregnancy to protect the fetus from maternal alloreactivity. HLA-G is overexpressed in tumors and involved in cancer immune evasion. Reverse transcription-polymerase chain reaction and immunohistochemistry (IHC) were used to examine HLA-G expression in normal mammary and breast cancer cell lines and normal and human breast cancer tissues. Reverse transcription-polymerase chain reaction confirmed that normal epithelial MCF-12A cells had no HLA-G mRNA expression, whereas cancer cell lines MCF-7, T47D, and MDA-MB-231 and NCI/Adr-Res had various levels of HLA-G mRNA expression. Twelve (12) normal and 38 breast cancer tissues were examined by IHC. Fifty-eight (58) percent (22/38) of cancers had medium to strong staining to HLA-G, whereas only 8% (1/12) of normal breast tissues had medium to strong staining, and the difference was significant (p < 0.05). HLA-G staining was found in the membranes and cytoplasm of cancer cells. In conclusion, breast cancer cells overexpress HLA-G mRNA and protein, and this probably contributes to immune evasion. © Copyright 2011, Mary Ann Liebert, Inc.


Jiang X.P.,Elliott Elliott Head Breast Cancer Research and Treatment Center | Elliott R.L.,Elliott Elliott Head Breast Cancer Research and Treatment Center | Head J.F.,Elliott Elliott Head Breast Cancer Research and Treatment Center
Anticancer Research | Year: 2010

Since malignant cells often have a high demand for iron, we hypothesize that breast cancer cells may alter the expression of iron transporter genes including iron importers [transferrin receptor (TFRC) and solute carrier family 11 (proton-coupled divalent metal ion transporters), member 2 (SLC11A2)] and the iron exporter SLC40A1 (ferroportin), and additionally that the growth of breast cancer can be inhibited by manipulating iron transporter gene expression. To test our hypothesis, reverse transcription polymerase chain reaction (RT-PCR) was used to determine mRNA expression of iron transporter genes in normal human mammary epithelial MCF-12A cells and human breast cancer MCF-7 cells. Antisense oligonucleotides were employed to suppress the expression of TFRC gene in the 4T1 mammary adenocarcinoma in both cell culture and a mouse tumor model. We found the following: i) the MCF-7 cells have higher expression of TFRC and SLC11A2 compared with MCF-12A epithelia; ii) SLC40A1 was only expressed in MCF-12A epithelia but not in MCF-7 cells; iii) iron increased mRNA levels of the SLC11A2 gene in both MCF-12A and MCF-7 cells; iv) TFRC antisense oligonucleotides reduced TFRC mRNA levels and intracellular total iron, and inhibited the proliferation of the 4T1 cells in cell culture; v) TFRC antisense oligonucleotide inhibited tumor growth and lung metastases in the 4T1 mammary adenocarcinoma mouse model. In conclusion, breast cancer cells up-regulate the expression of iron importer genes and down-regulate the expression of iron exporter SLC40A1 to satisfy their increased demand for iron. Suppression of transferrin receptor by antisense results in inhibition of tumor growth and lung metastasis in the 4T1 mammary adenocarcinoma mouse model.


PubMed | Elliott Elliott Head Breast Cancer Research and Treatment Center
Type: Journal Article | Journal: Anticancer research | Year: 2010

Since malignant cells often have a high demand for iron, we hypothesize that breast cancer cells may alter the expression of iron transporter genes including iron importers [transferrin receptor (TFRC) and solute carrier family 11 (proton-coupled divalent metal ion transporters), member 2 (SLC11A2)] and the iron exporter SLC40A1 (ferroportin), and additionally that the growth of breast cancer can be inhibited by manipulating iron transporter gene expression. To test our hypothesis, reverse transcription polymerase chain reaction (RT-PCR) was used to determine mRNA expression of iron transporter genes in normal human mammary epithelial MCF-12A cells and human breast cancer MCF-7 cells. Antisense oligonucleotides were employed to suppress the expression of TFRC gene in the 4T1 mammary adenocarcinoma in both cell culture and a mouse tumor model. We found the following: i) the MCF-7 cells have higher expression of TFRC and SLC11A2 compared with MCF-12A epithelia; ii) SLC40A1 was only expressed in MCF-12A epithelia but not in MCF-7 cells; iii) iron increased mRNA levels of the SLC11A2 gene in both MCF-12A and MCF-7 cells; iv) TFRC antisense oligonucleotides reduced TFRC mRNA levels and intracellular total iron, and inhibited the proliferation of the 4T1 cells in cell culture; v) TFRC antisense oligonucleotide inhibited tumor growth and lung metastases in the 4T1 mammary adenocarcinoma mouse model. In conclusion, breast cancer cells up-regulate the expression of iron importer genes and down-regulate the expression of iron exporter SLC40A1 to satisfy their increased demand for iron. Suppression of transferrin receptor by antisense results in inhibition of tumor growth and lung metastasis in the 4T1 mammary adenocarcinoma mouse model.

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