As diseases go, cancer is the ultimate shape shifter. Thought to start with just a single mutation in the DNA of a single cell, it spawns generation after generation of quirky, out-of-control progeny whose genetic instability results in many additional mutations and wild proliferation leading to solid tumors and blood cancers.
Moreover, even when scientists discover drugs capable of reining in its destructive behavior, it tends to outsmart them by morphing, freeing itself to head once more down its renegade path.
Cancer is on course to overtake heart disease as the leading killer of Americans, but despite the urgent need to find new therapies and prevention strategies, scientists conducting cancer research are still working their way through a maze of unparalleled complexity. For one thing, cancer actually refers to more than 100 different diseases. All are fundamentally disorders of tissue growth regulation, and nearly all are caused by abnormalities in the affected cells’ genetic material. Yet that inherent heterogeneity means that researchers continually are racing to keep up with a collection of especially dynamic and perplexing adversaries.
In 1971, President Richard M. Nixon signed the National Cancer Act, dramatically increasing funding for cancer research and launching “our great crusade against cancer [which] should be a cause for new hope among people everywhere.” Throughout the intervening decades, Salk Institute researchers have been at the front lines of that fight. Their studies of the diverse genetic mutations that drive the development of individual cancers have resulted in important contributions that have increased understanding and helped change the landscape for cancer treatment.
Research in the Cancer Center is divided into three programs: Metabolism and Cancer, Mouse Models and Stem Cells, and Growth Control and Genomics Stability. Faculty members in each area are listed below.
Metabolism and Cancer
|Janelle Ayres||Ron Evans||Tony Hunter|
|Marc Montminy||Joseph Noel||Satchidananda Panda|
|Reuben Shaw||Ye Zheng|
Mouse Models and Stem Cells
|Senyon Choe||Fred Gage||Joseph Ecker|
|Juan Carlos Izpisua Belmonte||Chris Kintner||Julie Law|
|Kuo-Fen Lee||Greg Lemke||Axel Nimmerjahn|
|Samuel Pfaff||John Thomas||Inder Verma|
Growth Control and Genomic Stability
|Beverly Emerson||Martin Hetzer||Katherine Jones|
|Jan Karlseder||Björn Lillemeier||Vicki Lundblad|
|Clodagh O'Shea||Geoffrey Wahl||Lei Wang|
Diabetes drug could hold promise for lung cancer patients
January 29, 2013
Cold viruses point the way to new cancer therapies
October 16, 2012
Salk findings may give clinicians a way to detect cancer earlier
September 7, 2011
The battle of the morphogens: How to get ahead in the nervous system
September 1, 2011
A new ending to an old "tail"
April 21, 2011
The stemness of cancer cells
December 13, 2010
Mobilizing the repair squad: Critical protein helps mend damaged DNA
December 24, 2009
Good fences make good neighbors:
May 15, 2009
July 17, 2014
Scientists at the Salk Institute have identified a gene responsible for stopping the movement of cancer from the lungs to other parts of the body, indicating a new way to fight one of the world's deadliest cancers.
By identifying the cause of this metastasis—which often happens quickly in lung cancer and results in a bleak survival rate—Salk scientists are able to explain why some tumors are more prone to spreading than others. The newly discovered pathway, detailed today in Molecular Cell, may also help researchers understand and treat the spread of melanoma and cervical cancers. Read more>>
January 29, 2013
Ever since discovering a decade ago that a gene altered in lung cancer regulated an enzyme used in therapies against diabetes, Reuben Shaw has wondered if drugs originally designed to treat metabolic diseases could also work against cancer.
The growing evidence that cancer and metabolism are connected, emerging from a number of laboratories around the world over the past 10 years, has further fueled these hopes, though scientists are still working to identify what tumors might be most responsive and which drugs most useful. Read more>>
October 16, 2012
Adenovirus, a type of cold virus, has developed molecular tools—proteins—that allow it to hijack a cell\'s molecular machinery, including large cellular machines involved in growth, replication and cancer suppression. The Salk scientists identified the construction of these molecular weapons and found that they bind together into long chains (polymers) to form a three-dimensional web inside cells that traps and overpowers cellular sentries involved in growth and cancer suppression. The findings, published October 11 in Cell, suggest a new avenue for developing cancer therapies by mimicking the strategies employed by the viruses. Read more>>
March 11, 2012
The well-being of living cells requires specialized squads of proteins that maintain order. Degraders chew up worn-out proteins, recyclers wrap up damaged organelles, and-most importantly-DNA repair crews restitch anything that resembles a broken chromosome. If repair is impossible, the crew foreman calls in executioners to annihilate a cell. As unsavory as this last bunch sounds, failure to summon them is one aspect of what makes a cancer cell a cancer cell. Read more>>
February 07, 2012
Reviving a theory first proposed in the late 1800s that the development of organs in the normal embryo and the development of cancers are related, scientists at the Salk Institute for Biological Studies have studied organ development in mice to unravel how breast cancers, and perhaps other cancers, develop in people. Their findings provide new ways to predict and personalize the diagnosis and treatment of cancer. Read more>>