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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 [13826 Associated PubMed Articles listed on BioPortfolio]

MiR-19a negatively regulated the expression of PTEN and promoted the growth of ovarian cancer cells.

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The antitumor effects of entinostat in ovarian cancer require adaptive immunity.

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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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