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How Our Immune System Can Help Fight Cancer

2014-08-27 03:16:53 | BioPortfolio

Summary

There is growing evidence that our immune system can help fight cancer. This has stimulated interest in the development and application of tumor vaccines for several human solid tumors, including epithelial ovarian cancer (EOC). A major obstacle to the development of these vaccines is that there are specialty cells called regulatory T cells that prevent the immune system from attacking all of our organs. These regulatory T cells also prevent our immune system for attacking cancer cells.

Indoleamine 2,3-dioxygenase (IDO), an enzyme that degrades an essential amino acid tryptophan that is necessary for T cells to multiply, however regulatory T cells are less susceptible to low levels of tryptophan, and can still multiply. This allows cancer growth and progression. This may be explained by genetic polymorphisms (changes) in the IDO gene, which may alter its function. Five of these changes in the IDO gene have been described. In this research project, we are asking if you would donate a small piece of your tumor and ascites to see if we can examine your IDO gene in the tumor cells and see if any of these gene changes are present. We hope that this will help us understand how the immune system works in EOC.

We hypothesize that genetic polymorphisms within the IDO gene alter its enzymatic activity and affect the outcome of ovarian cancer patients. These findings have the potential to translate into a method for predicting successful immunotherapy.

Study Design

Observational Model: Case-Only, Time Perspective: Prospective

Conditions

Ovarian Cancer

Location

Winthrop-University Hospital
Mineola
New York
United States
11501

Status

Not yet recruiting

Source

Winthrop University Hospital

Results (where available)

View Results

Links

Published on BioPortfolio: 2014-08-27T03:16:53-0400

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Assessment of the Minimal Residual Disease in Ovarian Cancer From Circulating Tumor DNA and Immune Repertoire

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Toremifene in Treating Patients With Ovarian Cancer

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PubMed Articles [14171 Associated PubMed Articles listed on BioPortfolio]

Risk of epithelial ovarian cancer among women with benign ovarian tumors: a follow-up study.

The importance of benign ovarian tumors as precursors or risk markers for ovarian cancer is not fully understood. Studies on the association between benign ovarian tumors and ovarian cancer have provi...

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Ovarian cancer is the one of the most deadly gynecologic malignancy among cancer related death in women. However, the treatment for ovarian cancer is still limited. In this study, we aimed to explore ...

Low BCL7A expression predicts poor prognosis in ovarian cancer.

Ovarian cancer is a common gynaecological cancer with a poor prognosis that poses a serious threat to human life and health. It is essential to explore the possible prognostic biomarkers of ovarian ca...

Dysregulation of pseudogene/lncRNA-hsa-miR-363-3p-SPOCK2 pathway fuels stage progression of ovarian cancer.

Ovarian cancer is one of the most common and lethal cancer types in women. The molecular mechanism of ovarian cancer progression is still unclear.

LINC00339 promotes cell proliferation, migration, and invasion of ovarian cancer cells via miR-148a-3p/ROCK1 axes.

Ovarian cancer is one of the most common malignant tumors of female genital organs. Long non-coding RNAs play an important role in the progression of ovarian cancer. In the present study, we aimed at ...

Medical and Biotech [MESH] Definitions

Autosomal dominant HEREDITARY CANCER SYNDROME in which a mutation most often in either BRCA1 or BRCA2 is associated with a significantly increased risk for breast and ovarian cancers.

An antineoplastic agent used to treat ovarian cancer. It works by inhibiting DNA TOPOISOMERASES, TYPE I.

Cessation of ovarian function after MENARCHE but before the age of 40, without or with OVARIAN FOLLICLE depletion. It is characterized by the presence of OLIGOMENORRHEA or AMENORRHEA, elevated GONADOTROPINS, and low ESTRADIOL levels. It is a state of female HYPERGONADOTROPIC HYPOGONADISM. Etiologies include genetic defects, autoimmune processes, chemotherapy, radiation, and infections.

Cessation of ovarian function after MENARCHE but before the age of 40, without or with OVARIAN FOLLICLE depletion. It is characterized by the presence of OLIGOMENORRHEA or AMENORRHEA, elevated GONADOTROPINS, and low ESTRADIOL levels. It is a state of female HYPERGONADOTROPIC HYPOGONADISM. Etiologies include genetic defects, autoimmune processes, chemotherapy, radiation, and infections.

A homolog of p53 TUMOR SUPPRESSOR PROTEIN that encodes full-length trans-activating and N-terminally-truncated (DeltaN) isoforms. Detection of splice variants and isoforms in the nervous system (human TELENCEPHALON, CHOROID PLEXUS; CEREBROSPINAL FLUID), embryonic tissue, human BREAST CANCER; OVARIAN CANCER, suggest roles in cellular differentiation.

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