Glejak wielopostaciowy, GBM - diagnoza, leczenie, nowości

[Crono5]

Rebooting Cancer Cells

written by Marc Levenson, Tech Live on Thursday, July 18, 2002

przedruk z:

http://www.g4tv.com/techtvvault/features/38961/Rebooting_Cancer_Cells.html


Researchers have found a way to turn cancerous cells back to normal.
It's almost like the computer restart function known as "Ctrl + Alt + Del." Stanford researchers, trying a novel genetic approach, have "rebooted" some cancer cells' genetic programming so they revert to normal, noncancerous cells. Tonight's "Tech Live" reports.

It's similar to computer functions. Dr. Dean Felsher found that when a cancer-causing gene is briefly turned off and then turned back on, "You're giving the cell a chance to restore its normal programs," he said.

No one's sure what happens, or why, but the technique coaxed laboratory cancer cells to revert to their normal function. And for a normal cell, that means if it senses cancer, it triggers what's called apoptosis -- programmed cell death. In simple terms, the cell commits suicide.

"That can result in a permanent change in a cancer cell," Felsher said.

Just the beginning

The technique still needs years of research, but it means hope for patients like Debbie Nako, who's at Stanford Medical Center for chemotherapy to treat colon cancer.

Chemotherapy drugs attack cancer, but they're not able to aim well, so they kill healthy cells too. That's why some cancer patients lose hair or feel nauseous. In Debbie Nako's case, "You get buzzing feeling in your veins," she said.

Her oncologist, Dr. Cheryl Cho, acknowledges the need for more targeted cancer drugs. "The goal would be to develop agents that you could actually use to target the genes that Dr. Felsher's found."

The new field of proteomics takes the Human Genome Project -- the government-sponsored project to map human DNA -- to its next level. Researchers worldwide are finding proteins that genes make to identify the targets for disease. The researchers then develop drugs to aim right at those diseases.

In the case of cancer cell "reboot" drugs, Felsher admits there's a long road ahead.

"This is only a small part of the puzzle for the treatment for cancer," he said.

But for Nako, just knowing that science is working toward a better way to treat cancer is therapy in itself. "It would be worth my life, yes," she said.

To read more about Felsher's research, read Cancer Coaxed to Self-Destruct.


Cancer coaxed to self-destruct

Stanford Report, July 10 , 2002
By AMY ADAMS

przedruk z:
http://news-service.stanford.edu/news/2002/july10/cancer.html


Researchers at the medical center have tricked cancer cells into self-destructing by briefly disabling a cancer-causing gene. Although the gene revs back up after deactivation, the brief hiatus gives the affected cells a chance to alter their cancerous destiny. This work in mice could open new avenues for treating some human cancers, researchers believe.

Cancer usually results after a cell accumulates a handful of mutations in cancer-related genes called oncogenes or tumor-suppressor genes. Researchers had thought that cancer cells would side-step attempts to fix any single genetic change, especially after treatment ends. But in a study published in the July 5 issue of Science, researchers found that by briefly tinkering with only one mutant gene they could forever alter the course of the cancer.

"Nobody had ever seen that turning off a cancer gene for a few days caused irreversible change," said Dean Felsher, MD, PhD, assistant professor of oncology and lead researcher on the study. "Most people thought that cancer would come back once treatment that turned off an oncogene stopped."

Felsher and his colleagues worked with a gene called MYC, which normally tells a cell when to grow or divide. In many types of cancers, such as lymphoma, breast, colon, and prostate, this gene produces excess protein that allows the rapid growth characteristic of cancer cells. "Anything you learn about MYC should be applicable to a lot of tumors," Felsher said. He added that because the gene is so important, any results may carry significant weight.

Felsher created bone cancer cells containing an altered version of MYC that could be shut down by adding a molecular off switch. He then injected those cells into mice, which went on to develop bone cancer. When he fed mice the off switch, MYC production stopped and the cancer cells quickly reverted to normal bone cells. After 10 days, he stopped treatment, allowing the gene to resume churning out protein. Instead of restarting cancerous growth, the cells died.

Mice that had their MYC gene switched off for 10 days survived four times longer than untreated mice with bone cancer. The cancer resurfaced in some of the treated mice, but went back into remission with another round of temporary MYC-disabling treatment. "You don't always need to shut the oncogene off permanently," Felsher said. "That could change the way you think about treating cancer."

Felsher cautioned that his current results may not apply to all cancers. His previous work shows that MYC - like all oncogenes - is a complicated gene that can contribute to cancer by many different mechanisms. Depending on which role the gene is playing in the cell, the effects of shutting it off may vary. "We are trying to understand the genetics of when shutting off MYC will work," Felsher said.