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Hope for a cure is provided by research on the molecular drilling of skin cancer cells

According to research that opens the door to potential new treatments for the condition, skin cancer cells create "molecular drills" in order to infiltrate healthy tissues and spread throughout the body.

The London Institute of Cancer Research has identified the gene that promotes tumour growth.

Melanoma cells growing in 3D skin-like material in the lab created drills, which researchers were able to photograph using robotic microscopy.
The drills aid tumour cells in adhering to and poking holes through nearby cells and structures, enabling the cancer to spread outside of the place where it first starts and into further tissues and organs.

“This is the first time this type of cell shape change has been associated with any type of metastatic cancer,” said Chris Bakal, professor of cancer morphodynamics at the Institute of Cancer Research in London.

Since the 1990s, the number of new cases of melanoma has more than doubled in the UK, where the disease now affects more than 16,000 people annually. Tumors may frequently be removed by surgeons in the early stages, but as the cancer spreads to other body areas, it becomes more challenging to cure.

A 3D matrix rich in collagen, one of the key proteins in skin, was used by Bakal and his colleagues to grow melanoma cells. They uncovered a particular gene, ARHGEF9, which was essential to the development of the molecular drills by selectively removing genes from the cancer cells.

All human cells contain the gene, however in adults it mostly only becomes active in brain cells to aid in the formation of new connections. The gene enables neurons to create their own drill-like structures far earlier in human development, which aids in the spread of the cells throughout the body and the wiring of the nervous system.

The researchers explain how turning off the ARHGEF9 gene in melanoma cells destabilised the molecular drills, preventing the cancer from attaching to and boring into neighbouring tissues. Their findings are published in the journal iScience.

The discovery gives rise to expectations for novel treatments for melanoma and perhaps other malignancies, such neuroblastoma, which may spread similarly. Despite being connected to a variety of neurological illnesses, the ARHGEF9 gene is thought to be more crucial during early development than in adulthood. If so, creating medications that block the gene could prevent the spread of melanoma without having any negative side effects.

Drugs that target the gene may be more selective to cancer cells and therefore less hazardous as the gene is highly active in metastatic cells and less so in many other normal cells.

“We feel that disarming the drill is likely to have widespread application,” said Bakal, though he suspects the process will not be relevant for all melanomas. Beyond paving the way for future treatments, the work may have much broader implications for understanding cancer. “This work could ultimately change how we think about cancer cells and tumours. Specifically, neurons interact in large networks to form brains, talk via neurotransmitters, and propagate information through electricity,” said Bakal. Our work is showing that many cancer cells may act similarly to form these networks and that tumours might almost be ‘brain-like’. The drills or sensors we identified here could be one way that cancer cells plug into this network and relay information to each other.”

The outcomes, according to Dr. Sam Godfrey of Cancer Research UK, were positive. According to him, these results will enable future study to concentrate on the function of this target in melanoma and whether it could also benefit in the treatment of some malignancies that affect adolescents and young adults.

New diagnostic procedures and melanoma patient treatments will become available as we learn more about the biology of this illness.

Hope for a cure is provided by research on the molecular drilling of skin cancer cells

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