As researchers study the genetics of DLBCL, they are constantly identifying new genes and proteins that are associated with either promoting or inhibiting the growth of the lymphoma. These genetic differences are significant because they can become the targets of new therapies that are designed to destroy cancer-causing genes in cells affected by DLBCL.
A team of researchers determined that a protein called KMT2D plays a role in suppressing B-cell lymphomas. According to their research, the KMT2D gene (which makes the KMT2D protein) is one of the most frequently mutated genes found in DLBCL. When KMT2D is healthy, it helps promote normal B-cell activity, but when the KMT2D gene mutates early in DLBCL, it encourages the growth of cancerous cells. This study, in combination with other research, suggests that identifying treatments that can kill cells that do not have the KMT2D protein is a logical approach for fighting cancer by targeting the lymphoma cells when they are first developing.
Another example involves interactions between a specific chromosome and a specific gene known as TP53 that helps suppress DLBCL. Deletion of the p arm of chromosome 17 (17p) occurs in up to 20 percent of DLBCL cases. Scientists think this deletion might be an important factor in DLBCL initially forming cells and tumors and developing into full-blown disease.(15) If this proves to be correct, then finding medications that specifically target and kill cells with a 17p deletion might be another approach to DLBCL treatment.
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