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Gen tunggal ternyata sel-sel kanker kolorektal  yang kembali ke jaringan normal pada tikus

Date:

June 18, 2015

Source:

Cell Press

Summary:

Strategi anti - kanker umumnya melibatkan proses membunuh sel-sel tumor . Namun , sel-sel kanker bukannya dapat  dibujuk untuk kembali ke jaringan normal hanya dengan mengaktifkan gen tunggal . Para peneliti menemukan bahwa untuk memulihkan ke tingkat normal dari gen kanker kolorektal manusia pada tikus berhenti pertumbuhan tumornya  dan re-established fungsi usus yang normal  hanya dalam waktu empat hari ....more

Single gene
turns colorectal cancer cells back into normal tissue in mice

Date:

June 18, 2015

Source:

Cell Press

Summary:

Anti-cancer strategies generally involve killing off tumor cells. However,
cancer cells may instead be coaxed to turn back into normal tissue simply by
reactivating a single gene. Researchers found that restoring normal levels of a
human colorectal cancer gene in mice stopped tumor growth and re-established
normal intestinal function within only four days.

..............................

Anti-cancer strategies generally involve killing off tumor cells. However,
cancer cells may instead be coaxed to turn back into normal tissue simply by
reactivating a single gene, according to a study published June 18th in the
journal Cell. Researchers found
that restoring normal levels of a human colorectal cancer gene in mice stopped
tumor growth and re-established normal intestinal function within only 4 days.
Remarkably, tumors were eliminated within 2 weeks, and signs of cancer were prevented
months later. The findings provide proof of principle that restoring the
function of a single tumor suppressor gene can cause tumor regression and
suggest future avenues for developing effective cancer treatments.

Colorectal cancer is the second leading cause of cancer-related death in
developed countries, accounting for nearly 700,000 deaths worldwide each year.
"Treatment regimes for advanced colorectal cancer involve combination
chemotherapies that are toxic and largely ineffective, yet have remained the
backbone of therapy over the last decade," says senior study author Scott
Lowe of the Memorial Sloan Kettering Cancer Center.

Up to 90% of colorectal tumors contain inactivating mutations in a tumor
suppressor gene called adenomatous polyposis coli (Apc). Although these
mutations are thought to initiate colorectal cancer, it has not been clear
whether Apc inactivation also plays a role in tumor growth and survival once
cancer has already developed.

"We wanted to know whether correcting the disruption of Apc in
established cancers would be enough to stop tumor growth and induce
regression," says first author Lukas Dow of Weill Cornell Medical College.
This question has been challenging to address experimentally because attempts
to restore function to lost or mutated genes in cancer cells often trigger
excess gene activity, causing other problems in normal cells.

To overcome this challenge, Lowe and his team used a genetic technique to
precisely and reversibly disrupt Apc activity in a novel mouse model of
colorectal cancer. While the vast majority of existing animal models of
colorectal cancer develop tumors primarily in the small intestine, the new
animal model also developed tumors in the colon, similar to patients.
Consistent with previous findings, Apc suppression in the animals activated the
Wnt signaling pathway, which is known to control cell proliferation, migration,
and survival.

When Apc was reactivated, Wnt signaling returned to normal levels, tumor
cells stopped proliferating, and intestinal cells recovered normal function.
Tumors regressed and disappeared or reintegrated into normal tissue within 2
weeks, and there were no signs of cancer relapse over a 6-month follow-up
period. Moreover, this approach was effective in treating mice with malignant
colorectal cancer tumors containing Kras and p53 mutations, which are found in
about half of colorectal tumors in humans.

Although Apc reactivation is unlikely to be relevant to other types of
cancer, the general experimental approach could have broad implications.
"The concept of identifying tumor-specific driving mutations is a major
focus of many laboratories around the world," Dow says. "If we can
define which types of mutations and changes are the critical events driving
tumor growth, we will be better equipped to identify the most appropriate
treatments for individual cancers."

For their own part, Lowe and his team will next examine the consequences of
Apc reactivation in tumors that progress beyond local invasion to produce
distant metastases. They will also continue to investigate why Apc is so
effective at suppressing colon tumor growth, with the goal of one day mimicking
this effect with drug treatments.

"It is currently impractical to directly restore Apc function in
patients with colorectal cancer, and past evidence suggests that completely
blocking Wnt signaling would likely be severely toxic to normal intestinal
cells," Lowe says. "However, our findings suggest that small
molecules aimed at modulating, but not blocking, the Wnt pathway might achieve
similar effects to Apc reactivation. Further work will be critical to determine
whether WNT inhibition or similar approaches would provide long-term
therapeutic value in the clinic."







Story Source:

The above post is reprinted from materials provided by Cell Press. Note:
Materials may be edited for content and length.







Journal Reference:

1.   
Lukas E. Dow, Kevin P. O’Rourke, Janelle Simon, Darjus F.
Tschaharganeh, Johan H. van Es, Hans Clevers, Scott W.
Lowe. Apc Restoration Promotes Cellular Differentiation and
Reestablishes Crypt Homeostasis in Colorectal Cancer. Cell,
2015; 161 (7): 1539 DOI:10.1016/j.cell.2015.05.033

http://www.sciencedaily.com/releases/2015/06/150618134241.htm

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