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There are two types of genes that, if mutated, can lead to cancer. One set of genes directs cell growth – a mutation in one of these genes can cause cells to grow uncontrollably, like a gas pedal stuck to the car floor. The other set of genes function as the “brakes,” telling cells when to slow down, correct replication mistakes, or undergo apoptosis (programmed cell death). These are called tumor suppressor genes, and as the name implies, a disruption in their function can allow the growth of tumors.
Established by an Act of Congress in 1863, the National Academy of Sciences (NAS) is the body of distinguished researchers “charged with providing independent, objective advice to the nation on matters related to science and technology.” Election to membership is among the highest honors a scientist can receive. This year, three Damon Runyon alumni join the NAS ranks, bringing the total number of Damon Runyon alumni in NAS to 89.
By the time patients experience symptoms, their tumors contain a genetically diverse collection of cancer cells, each with an accumulation of mutations. If we could better understand the sequence of events that leads from a single mutation to a heterogeneous population of tumor cells, earlier detection and intervention might be possible. However, attempts to trace this evolution where it has already occurred (in model organisms, immortalized cell lines, or patient samples) face significant challenges.
The KRAS gene, responsible for encoding a protein that serves as an “on/off” switch for cell growth, is one of the most commonly mutated genes in cancer. The frequency and nature of its mutation differ across cancer types, however, with the highest occurrence of mutation found in cancers of the colorectum, pancreas, lung, and blood plasma.
The tumor, once an indistinct mass of heterogeneous cells, is gaining single-cell resolution. Until recently, even distinguishing between healthy cells and malignant cells within a tumor sample presented a challenge.
Nearly all human cancers, and particularly blood cancers, involve dysregulated gene expression – the wrong genes are switched on or the right ones are switched off. The molecule responsible for switching genes on and off is called a transcription factor. Identifying which transcription factor is misbehaving and how is often the key to developing effective cancer treatments.
A new study demonstrates the staying power of the immune response generated by a personalized cancer vaccine called NeoVax, which works by targeting specific proteins on each patient’s tumor cells to activate the body's immune system against the cancer.
Pancreatic cancer is one of the most difficult forms of cancer to treat effectively. Standard courses of chemotherapy drugs often come up short for patients, leading to a dismal 5-year relative survival rate of just 10%. And while the past few years’ transformative breakthroughs in immunotherapy have drastically improved the prognosis for many patients diagnosed with other forms of cancer, most pancreatic cancers have proved frustratingly resistant to immunotherapy alone.
This year, thirteen Damon Runyon alumni were chosen as American Association for the Advancement of Science (AAAS) Fellows in honor of their invaluable contributions to science and technology.
To understand all the genetic alterations driving melanoma, Damon Runyon Clinical Investigator Eliezer Van Allen, MD, and his colleagues at Dana-Farber Cancer Institute have assembled the largest molecular dataset on this disease and used it to uncover new details that may help in diagnosis and treatment.