Cure Alveolar Soft Part Sarcoma International (iCureASPS)

From above link-

“Using a dual-drug combination to treat lung cancer could be an effective strategy for combating most lung cancer, shows new research from the University of Texas (UT) Southwestern’s Simmons Cancer Center. A press release from the school overviews the exciting new findings.
Lung cancer is the most common cause of cancer deaths in the United States among men and women and is responsible for 26 percent of all cancer mortalities nationwide, according to the National Cancer Institute. Researchers say their new two-pronged strategy is likely an effective treatment for non-small-cell lung cancer, which represents 85 percent of total cases in this country.
The drug combination, which utilizes one medication that targets epidermal growth factor receptors (a.k.a. EGFR), and another that targets tumor necrosis factor (TNF), appears to block lung cancer from using the latter as a route to escape treatment. Using a mouse model, researchers showed that when TNF is also blocked, the cancer becomes more sensitive to EGFR treatment. This finding, which was reported as part of a study published in the Journal of Clinical Oncology, has the potential to dramatically alter how doctors treat lung cancer.”


Tumor necrosis factor and cancer, buddies or foes?*



Abstract
Tumor necrosis factor (TNF) is a multifunctional cytokine that plays important roles in diverse cellular events such as cell survival, proliferation, differentiation, and death. As a pro-inflammatory cytokine, TNF is secreted by inflammatory cells, which may be involved in inflammation-associated carcinogenesis.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2631033/

Abstract from above link, continued-


TNF exerts its biological functions through activating distinct signaling pathways such as nuclear factor κB (NF-κB) and c-Jun N-terminal kinase (JNK). NF-κB is a major cell survival signal that is anti-apoptotic while sustained JNK activation contributes to cell death. The crosstalk between the NF-κB and JNK is involved in determining cellular outcomes in response to TNF. In regard to cancer, TNF is a double-dealer. On one hand, TNF could be an endogenous tumor promoter, because TNF stimulates cancer cells’ growth, proliferation, invasion and metastasis, and tumor angiogenesis. On the other hand, TNF could be a cancer killer. The property of TNF in inducing cancer cell death renders it a potential cancer therapeutic, although much work is needed to reduce its toxicity for systematic TNF administration. Recent studies have focused on sensitizing cancer cells to TNF-induced apoptosis through inhibiting survival signals such as NF-κB, by combined therapy. In this article we provide an overview of the roles of TNF-induced signaling pathways in cancer biology with specific emphasis on carcinogenesis and cancer therapy.

Too much TNF
“How Does TNF Cause Inflammation?”


If you have an immune system disease like rheumatoid arthritis (RA), you may have heard your doctor use the term TNF. It’s shorthand for tumor necrosis factor, a substance in your body that causes inflammation, or swelling.

It may surprise you to learn that inflammation can be a good thing. It happens when your immune system -- your body’s natural defense force -- is fighting a possible threat. For example, when you have a cold, your sinuses swell. When you get a cut, your finger turns warm and red. These things don’t feel good, but they show your immune system is doing its job


https://www.webmd.com/rheumatoid-arthri ... flammation

Too little TNF-


“Low levels of tumor necrosis factor alpha increase tumor growth by inducing an endothelial phenotype of monocytes recruited to the tumor site.”

https://www.ncbi.nlm.nih.gov/m/pubmed/19118019/