They find the key gene in the development of lymphatic cancer

One multidisciplinary team research led by the Charité University Hospital from Berlin and the Goethe University from Frankfurt am Main hidentified a gene up to now unknown that conditions development from tumors at lymphatic apparatus, which opens up new possibilities in the cancer treatment from lymphatic glands.

The team has examined the genes that are modified en the lymphatic cancer for identify a key process at developing from illness and in the repair of genetic damage that, according to the scientists in the study published today in the journal Nature Communications, could open a new therapeutic approach.

At lymphatic cancer I know alter several signaling routes of the cells, including what is known as SUMOylation, a targeted modification from protein that changes its properties and determines, for example, its useful life or location in the cell.

“In our study, we were able to identify a previously unknown cancer gene that regulates this central signaling pathway in tumor diseases and could represent a point of attack for new therapies.” says Professor Ulrich Keller, director of the Medical Clinic with a focus on hematology, oncology and tumor immunology at the Charité Campus Benjamin Franklin.

With the purpose of identify Y characterize these points of central change, The team of scientists searched systematically genes That modify in the lymphomas, that is, the tumors of the lymphatic glands.

To do this, they used a so-called transposon system, with which the genes in the model can be turned on and off randomly by “skipping” sections of the genome to examine their effect on tumor development.

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“In recent years, numerous large sequencing studies have accurately characterized the genome of tumor diseases and illustrated the complexity and heterogeneity of the underlying changes using molecular maps.” explains the doctor Markus Schick, team leader and principal investigator of the Medical Clinic specializing in hematology, oncology and tumor immunology in Charité and first author of the study.

But Schick regrets that “the fact that such deviations often just happen in small groups from patients makes it difficult interpretation from his meaning”.

“Thanks to our approach, we have now been able to discover numerous previously unknown cancer genes, including the SENP6 gene, which is lost in about a third of all lymphoma patients. Based on this, we clarify its functional mechanism and develop a strategy. therapy “, adds the researcher.

The gene role at Cancer up to now it was not known. The pencoded SENP6 protein thus remove the SUMO modifications other proteins in the cell and therefore, controls their interactions with each other.

The research team has now been able show that directed deactivation from SENP6 leads al development of cancer, that is, it is a tumor suppressor gene.

In the healthy cellss, SENP6 plays a central role on the repair of DNA damage. After the gene is lost, this function is impaired and damage to genetic material accumulates, ultimately contributing to the development of cancer.

However, the tumor formation after the loss of SENP6 might be effectively suppressed by means of the inhibition of therepair enzyme of ADN PARP with the help of drugs that have already been approved for the treatment of breast cancer.

Professor Keller explains that “With our findings, we were able to establish SENP6 as a biomarker for the success of treatment with these PARP inhibitors. We are currently investigating in which other tumor diseases, in addition to lymphomas, the mechanism just described contributes to the development of cancer.”

“The goal of personalized medicine is treatments that are precisely tailored to individual patients. Therefore, the next step is clinical trials to test these inhibitors as a new specific treatment option for cancers characterized by loss of blood. SENP6 “, Keller points out.

“In addition, there are combination therapies that are still used infrequently, but have enormous potential, especially if used based on the patient’s own tumor biology,” Add. EFE

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