Rectal cancer and melanoma are linked by gene MIFT

Melanoma and rectal cancer may be associated to a same gene. A multicenter study published in Nature found that the oncogene MIFT could be related to susceptibility to both tumors. Inhibition of the effects of mutation of this gene may have therapeutic implications. The research involved Dr. And Dr. Susana Puig. Celia Badenas, Melanoma research team at the Institute of Biomedical Research August Pi i Sunyer (IDIBAPS) and the Department of Dermatology Hospital Clinic of Barcelona.

The MIFT is important in regulating the transcription of genes related to melanoma, and also responsible for the transcription of hypoxia inducible factor (HIF1A), related to genetic alterations that can lead to kidney cancer. The fact that several of the patients were diagnosed with both diseases when risk factors are so different from each tumor (ultraviolet radiation, number of nevi and melanoma skin to clear, and tobacco, obesity and hypertension for kidney cancer), was researchers to suspect that this match could be a genetic nexus between them, as they recently published in Nature.

Both the epidermis, which develops melanoma, and kidney, tissues are not receiving an adequate supply of oxygen, called hypoxic, which can cause oxidative stress that damages cells and leads to tumor. According to Dr. Puig, "smoking or hypertension may increase the oxidative stress and via HIF1A in the case of kidney cancer, while ultraviolet radiation would do the same to the skin," so that different risk factors trigger the same way to be carcinogenic.

The mutation identified in MITF is an activating mutation that selectively promotes the transcription of some genes. Develop a molecule that specifically block this mutation may have therapeutic implications, especially in patients with melanoma. This is because all melanomas studied expressed the gene MITF, regardless of whether or not mutated. However, in the case of kidney cancer only carriers of the mutation express MITF, so probably only the mutated, they are very rare, could benefit from a potential therapeutic anti-MITF. Carriers of the gene mutated MITF Mi-E318K have a 5 times greater risk of developing these cancers, or both.