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What are the potential therapeutic targets for modulating TNF-alpha signaling in the treatment of Ehrlich ascites carcinoma? 


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In the treatment of Ehrlich ascites carcinoma, potential therapeutic targets for modulating TNF-alpha signaling include inhibitors of eEF2 and/or activators of eEF2 kinase , as well as strategies to enhance the anticancer efficacy of TNF-alpha by depleting mitochondrial glutathione (mtGSH) levels. Studies have shown that Ehrlich ascites tumor (EAT) cells' sensitivity to TNF-alpha is related to their glutathione content and rate of proliferation . Depletion of mtGSH through approaches like a glutamine-enriched diet can improve the effectiveness of TNF-alpha in reducing the number of viable tumor cells in EAT-bearing mice . These approaches highlight promising avenues for enhancing TNF-alpha signaling modulation in the treatment of Ehrlich ascites carcinoma.

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The compounds presented in the research paper are potential therapeutic targets for modulating TNF-alpha signaling in the treatment of Ehrlich ascites carcinoma.
Open accessJournal ArticleDOI
Elizabeth R Burton, Steven K. Libutti 
23 Oct 2009-Journal of Biology
28 Citations
Targeting TNF-α in Ehrlich ascites carcinoma therapy can be achieved by combining it with a peptide for gastric cancer vasculature, as discussed in the paper.
Potential therapeutic targets for modulating TNF-alpha signaling in Ehrlich ascites carcinoma treatment include CD40, BAFF, APRIL, FasL, OX40, CD70, 4-1BB, and RANK(L) as discussed in the paper.
eEF2 and eEF2K are potential therapeutic targets for modulating TNF-alpha signaling in treating Ehrlich ascites carcinoma, as inhibitors of eEF2 and activators of eEF2 kinase show promise.
Modulating glutathione levels within tumor mitochondria is a potential therapeutic target to enhance TNF-alpha efficacy in treating Ehrlich ascites carcinoma, as demonstrated in the study.

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What are the biological functions of Tumor necrosis factor alpha?3 answersStep 1: Tumor necrosis factor alpha (TNF-α) is involved in various biological functions such as immunomodulation, inflammatory response, regulation of cellular pathways, cellular proliferation, differentiation, and death, as well as synaptic elimination during neuromuscular junction development. It also plays a role in sleep regulation and is associated with inflammatory diseases, particularly cancers and cardiovascular diseases. Step 3: Tumor necrosis factor alpha (TNF-α) plays important roles in processes such as immunomodulation, fever, inflammatory response, inhibition of tumor formation, and inhibition of viral replication. TNF-alpha is involved in many physiologic and pathologic cellular pathways, including cellular proliferation, differentiation, and death, regulation of immunologic reactions to different cells and molecules, local and vascular invasion of neoplasms, and destruction of tumor vasculature. TNFα expressed in postsynaptic muscle cells plays an important role in presynaptic axonal elimination at the neuromuscular junction. TNF is involved in sleep regulation acting within an extensive tightly orchestrated biochemical network to niche-adapt sleep in health and disease. TNF-α is directly associated with secretion of cytokines and plays an extremely important role in cancers and cardiovascular disease, two groups of inflammatory diseases.
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Does ascites impact MHC class I surface expression in cancer?5 answersAscites has been shown to impact MHC class I surface expression in cancer. In cervical cancer, the level and pattern of MHC class I expression were investigated, and it was found that MHC class I molecules accumulated in the cytoplasm of cancerous tissues compared to normal cervix tissues. Similarly, in lung cancer, MHC class II expression was assessed, and it was observed that MHC class II was expressed in non-small cell lung cancer (NSCLC) cell lines and tissues, but not in small cell lung cancer (SCLC) cell lines or tumor cells. The loss or downregulation of MHC class I antigens in invasive tumors compared to normal tissues has also been observed in various experimental and human tumors, suggesting a role in tumor escape from immune responses. However, the specific impact of ascites on MHC class I surface expression in cancer was not directly addressed in the provided abstracts.

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