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A zebrafish whose melanocytes are labeled with green fluorescent protein (GFP) (top left), an enlarged view of GFP-labeled melanocytes (bottom left), and human stem cell-derived melanocytes grow in a culture dish (right)
Source: Dr.
Now, in your body, there are lurking thousands of cells with DNA errors that can cause cancer
The standard explanation is that it takes a certain number of genetic "hits" on the cell's DNA to push the cell to the edge
A good example is the mole
In order to solve this problem, Dr.
In a paper published in the journal Science on September 3, the researchers reported that the formation of melanoma depends on the so-called "oncogenic competence", which is the DNA mutation in the cell and the activation of the cell.
These findings explain why some cells can form cancer, while others do not.
From fish to human,
"When we look at these melanomas in zebrafish, we can see that there are many active genes that are more characteristic of embryonic cells than mature melanocytes," Dr.
To answer this question, Dr.
A few months later, they discovered that only fish that activate BRAF at the NC and MB stages can form tumors (what the researchers call "carcinogenicity")
The results are amazing
Therefore, to extend these results, Dr.
What is carcinogenic "ability"?
ATAD2 is a so-called chromatin modifier: it binds to chromosomal regions near genes and allows these genes to be turned on (technically, it is transcribed into messenger RNA and translated into protein)
In order to prove that ATAD2 played a decisive role, the scientists conducted additional experiments.
They took ATAD2 away or added it again
.
When scientists removed ATAD2 in a zebrafish model prone to melanoma, the cells lost the ability to form tumors
.
When they added it to MC cells, the cells acquired this ability
.
This tells researchers that ATAD2 is indeed a key lever of carcinogenicity
.
Using the large amount of clinical data provided by MSK and the Cancer Genome Atlas, they can prove that ATAD2 is important in cancer: patients with high ATAD2 content have a significantly lower survival rate, which indicates that it plays an important role in determining the cancer genome
.
It is not just mutation
scientists who say that their findings provide an important new perspective on the formation of cancer, in sharp contrast with traditional views
.
"The standard idea that has existed for decades is that you basically need two types of DNA mutations to get cancer: activated oncogenes and forbidden tumor suppressor genes.
Once you clear these two barriers, cancer will develop.
.
Now we have something completely different-carcinogenicity-which adds a third layer to the mix
.
"
The lead author of the study, Dr.
Baggiolini, a postdoctoral fellow in Studer's lab, compared the situation to a fire
.
"DNA mutation is like a lighted match: if you use the wrong wood or if the wood is wet, you may get a little flicker but no fire
.
But if you have the right wood, maybe some kind of fire, the whole thing will burn Get up
.
"
In this example, ATAD2 is the igniting material
.
In addition to targeting DNA mutations, developing a drug to eliminate this kind of ignition will be another way to treat cancer
.
Technologies with future potential The
hPSC technology developed by the team to study melanoma may prove to have a wide range of applications in personalized cancer treatment
.
White and Studer are using this technology to create disease models of cancer in individual patients
.
From the blood of patients, they can obtain cells to make hPSC
.
They can then introduce specific mutations that characterize the patient's tumor into these cells
.
Then, these genetically matched cells can be used to test a large number of drugs to see which drugs may benefit patients
.
This will bring these drugs back to the zebrafish, ensuring that they really work in live animals
.
Researchers believe that this intersection between cells in petri dishes and animal studies gives them the best chance of finding drugs that are effective for patients
.
"With hPSC, we can create patient-specific cancer disease models for any different tissue in the body, whether it comes from the brain, liver or other organs," Dr.
Studer said.
"I really hope this will become a routine part of care
.
"
These far-reaching results are the product of a decade of stable cooperation between two laboratories with different expertise, which may not be a coincidence
.
“It’s almost a cliché to say that science is better in collaboration, but in this case, it’s really important,” said Dr.
White
.
He added: "Everyone wants science to develop fast
.
We also want science to develop fast
.
But sometimes science must be slow to find the core truth
.
"
(Biology: Wanwen)
Original search:
Developmental chromatin programs determine oncogenic competence in melanoma
DOI 10.
1126/science.
abc1048
