Wednesday 23 March 2022

New therapy may stop metastasis in triple-negative breast cancer

 

  • Scientists have shown that the expression of the oncoprotein MYC is altered in the majority of cancers.
  • Scientists have also demonstrated that inhibiting MYC can reduce tumor progression.
  • However, some scientists have concerns that inhibiting MYC may inadvertently promote the spread of cancer.
  • In the present study, researchers found that the MYC inhibitor Omomyc stopped the spread of triple-negative breast cancer in mice.

The study, which appears in the journal Cancer Research Communications, offers hope that Omomyc may also be effective in humans.

The oncoprotein MYC plays a role in promoting most human forms of cancer. Oncoproteins are produced by genes that promote cancer. Scientists have found that MYC encourages the proliferation of cancer cells and increases their survival.

While MYC’s role in the development of tumors is clear, scientists are split on whether MYC promotes metastasis — the spread of tumors to other parts of a person’s body.

Some scientists suggest MYC encourages this spread, while others indicate it inhibits the spread of tumors.

Consequently, the scientists behind the present study wanted to get more information to help resolve this debate.

Medical News Today spoke to Dr. Laura Soucek of the Vall D’hebron Institute of Oncology, Barcelona, Spain, and the study’s corresponding author.

“My laboratory has been focusing on MYC, a ‘most wanted’ target in cancer therapy, since its inception,” said Dr. Soucek.

“With this latest work, we aimed at shedding light on a controversial subject in MYC biology. In fact, while MYC had a well-established role in primary tumor progression, its role in metastasis was still not clear, since there were contrasting reports in the literature suggesting both a pro-metastatic and antimetastatic function for it, so that caution was recommended when using an MYC inhibitor in a metastatic setting.”

“Essentially, they were telling us that inhibiting MYC could well help in treating primary tumors but at the same time could promote new metastases. Since novel MYC inhibitors are finally reaching the clinic and are being tested in advanced metastatic patients, it was a priority for us and for the entire MYC biology field to clarify this risk.”

Dr. Soucek and her colleagues have developed the MYC inhibitor Omomyc, and in previous research have shown its effects on inhibiting tumor growth.

In the present study, the researchers were particularly interested in the effects Omomyc might have on metastasis in triple-negative breast cancerTrusted Source, an aggressive form of cancer that is difficult for clinicians to treat.

“We focused on triple-negative breast cancer, the most aggressive subtype of breast cancer, which often presents metastasis already at diagnosis. Nowadays, metastases are the real challenge in cancer treatment because of their frequent resistance to therapy,” explained Dr. Soucek.

After examining the effects of Omomyc on in vitro cells and then in mice, Dr. Soucek and her colleagues found promising results.

“Our data in pre-clinical models — cells and animal models — show that MYC inhibition by Omomyc has a profound effect on different aspects of the metastatic process, both preventing establishment of the metastatic lesions and reducing them in number and volume once they are already formed,” said Dr. Soucek.

“In some cases, metastases were even eradicated,” says Dr. Daniel Massó-Vallés, a previous postdoctoral researcher at the cancer research company Peptomyc and the first author of the study.

Dr. Pavani Chalasani — of the College of Medicine Tucson, University of Arizona — spoke to MNT, praising the study. Dr. Chalasani was not involved in the research.

“The authors present very interesting, novel, and exciting results on MYC inhibition as a potential treatment option,” noted Dr. Chalasani.

Dr. Soucek said that plans were already afoot to test whether Omomyc also inhibited tumor development and metastasis in humans.

Source: Medical News Today

No comments:

Post a Comment