A new research reveals the reason it’s so difficult to treat certain types of cancers is that they have an ability to “camouflage” to protect their existence.
This is common with aggressive cancers such as breast cancer which the study discovered it has a “master switch” that appears to control the dynamic behavior.
The switch in question is called Sox10. And it’s said to control growth and invasion into the surrounding tissues, on most triple-negative breast cancers that have proven hard to treat.
It’s a Major Leap in Cancer Research
The understanding is, cancer cells have an ability to reprogram to form new cell types, evolve to become drug resistant and spread first to other parts of the body through metastasizing and the gene Sox10 is behind this.
The fact that this one switch appears to dictate tumor cell behaviors, it means researchers can find ways to manipulate what happens inside cancer cells. Hopes are that this will help us finally put an end to the tricky survival behavior observed in stubborn tumors.
The researchers believe this work represents a significant milestone in understanding cancer and might present new avenues for treating and diagnosing breast tumors.
Why Triple-Negative Breast Cancer is so Stubborn
Geoffrey M.Wahl, senior author of the report (Salk Institute) which also appears in the journal Cancer Cell explains that two things make these cancer types so hard to treat. First, is their ability to invade new areas in the body — a process called metastasis and second is their heterogeneity or the fact that the cells exist in different forms.
“In precision medicine, we call this impression, reason being if we decide to target one type of cell, along the way others cells in the same tumor “camouflage” or change to become drug-resistant,” Wahl explains. The same is also thought with certain types of intractable cancers.
During fetal and embryonic growth, cells multiply by division and move to various parts of the organism then change to be able to perform the native functions in that area, what we call “plasticity.”
After a certain age, adult cells switch this plasticity property off, however for unknown reasons they get reawakened and transform to become cancerous.
In the study, the researchers began by investigating the DNA cells found in areas of the mouse mammary, which is coiled in a bundle called chromatin. But it was noted that the package was uncoiling to make certain genes easily accessible, something the team said gave them the first clue as to what exact genes could have been active during development.
The conclusion on chromatin analysis implies that both subpopulation and fetal cells of breast cancer cells, around the same region of the genome, become accessible, which ideally is the same areas where a master gene switch Sox10 is known to bind to DNA to trigger a range of developmental processes.
The Master Sox10 Switch
Chi-Yen Chung, a fellow Salk associate in the research and author likewise points out that in fetal cells, being the most “plastic”, they discovered that binding sites for Sox10 appeared so open and accessible than the healthy adult cells, which often have more closed chromatin and appear more inflexible.
After that, the team was able to demonstrate that Sox10 indeed bind to genes in the open areas to activate them, which basically regulates genes responsible for mobility, cell type, and different other key features that gave breast cancer the ability to metastasize and evolve.
The breast tumor cells with a higher concentration of Sox10 turned to become more primitive and developed the ability to move. All this happened in a dramatic way that the researchers wanted to see what happens if they could prohibit Sox10 from binding to the particular genes. So they proceeded with the experiment this time without access to Sox10 and the result was, none of the breast tumor cells that were programmed to become cancerous could form tumors.
This is great news to cancer patients; however, scientists say they still need to analyze Sox10 to confirm if it might have an impact on normal cell functions for safety.