INF-γ Cancer Research Results

INF-γ, interferon gamma: Click to Expand ⟱
Source:
Type:
IFN-γ is a cytokine produced primarily by activated T lymphocytes (CD4⁺ Th1, CD8⁺ cytotoxic T cells) and natural killer (NK) cells.
– It plays a central role in orchestrating immune responses against pathogens and tumor cells by enhancing antigen presentation and activating immune effector mechanisms.

– IFN-γ can promote antitumor immunity by activating macrophages, NK cells, and cytotoxic T lymphocytes.
– It enhances the presentation of tumor antigens, thereby facilitating the immune system’s ability to target and eliminate cancer cells.
• Its expression and signaling within the tumor microenvironment are generally associated with a robust immune response and, in many cases, a favorable prognosis—particularly in tumors deemed "immunologically hot."

• Dual Role:
– While IFN-γ typically supports immune-mediated tumor suppression, chronic exposure to IFN-γ within the tumor microenvironment may contribute to immune editing and the selection of tumor cell variants that are resistant to immune attack.
Scientific Papers found: Click to Expand⟱
1688- SSE,    Potential Role of Selenium in the Treatment of Cancer and Viral Infections
- Review, Var, NA
IL2↑, in mice promoted T cell receptor signaling that pushed T cell differentiation toward a Th1 phenotype by increasing interleukin -2 (IL-2) and interferon gamma (INF-γ) production
INF-γ↑,
Th1 response↑, 18 human subjects treated with 200 μg selenium-enriched broccoli daily for three days showed that selenium supplementation resulted in substantially higher levels of both Th1 and Th2 cytokines secreted by peripheral blood mononuclear cells
Th2↑,
Dose↑, Wang et al. on hens supplemented selenium (5 mg/kg, 10 mg/kg, and 15 mg/kg) orally for three time periods (15, 30, and 45 days) found that excessive selenium intake leads to a substantial reduction in the amount of IFN-γ and IL-2 cytokines
AntiCan∅, after 5.5 years, the results of this study revealed no relationship between selenium supplementation and prostate cancer risk reduction in men with low selenium levels
Risk↑, instead, they discovered that taking selenium supplements raised the high-grade prostate cancer risk in men who had high selenium levels
chemoP↑, selenium provided protection of normal tissues from drug-induced toxicity
Hif1a↓, Selenium down-regulates HIFs,
VEGF↓, leading to the subsequent down-regulation in expression of several genes including those involved in angiogenesis such as vascular endothelial growth factor (VEGF)
selectivity↑, Selenium also helps with DNA repair in response to DNA-damaging agents, which improves the effectiveness of chemotherapeutic agents by protecting normal cells from their toxicity.
*GADD45A↑, selenium protected WT-MEF from DNA damage in a p53-dependent manner by increasing the expression of p53-dependent DNA repair proteins such as XPC, XPE, and Gadd45a. Thus, cells lacking p53, such as tumor cells, did not receive the same protection
NRF2↓, a defined dose and schedule of selenium down-regulates and up-regulates Nrf2 in tumor tissue and normal tissue, respectively
*NRF2↑, a defined dose and schedule of selenium up-regulates Nrf2 in normal tissue
ChemoSen↑, These differential effects were associated with selective sensitization of tumor tissues to subsequent treatment with chemotherapy. Overactivation of Nrf2 increases the expression of MRPs, consequently decreasing the effectiveness of chemotherapy .
angioG↓, The inhibition of hypoxia-induced activation of HIF-1α and VEGF by knocking down Nrf2 suppresses angiogenesis, demonstrating a crosstalk mechanism between Nrf2 and HIF-1α in angiogenesis
PrxI↓, Selenium was shown to reduce drug detoxification and increase cytotoxic effects of anti-cancer drugs in tumor cells through suppression of the Nrf2/Prx1 pathway,
ChemoSideEff↓, showed that selenium supplementation attenuated the cardiotoxic effects of doxorubicin by decreasing oxidative stress and inflammation through Nrf2 pathway activation
eff↑, combination of niacin and selenium reduced the reactive oxygen species generated by sepsis and diminished the resultant lung injury by upregulating Nrf2 signaling


Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

NRF2↓, 1,   PrxI↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   Hif1a↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

IL2↑, 1,   INF-γ↑, 1,   Th1 response↑, 1,   Th2↑, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   Dose↑, 1,   eff↑, 1,   selectivity↑, 1,  

Functional Outcomes ⓘ

AntiCan∅, 1,   chemoP↑, 1,   ChemoSideEff↓, 1,   Risk↑, 1,  
Total Targets: 17

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

NRF2↑, 1,  

DNA Damage & Repair ⓘ

GADD45A↑, 1,  
Total Targets: 2

Scientific Paper Hit Count for: INF-γ, interferon gamma
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:1170  State#:%  Dir#:2
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