While some cancers are known to be caused by mutations in key genes, genetic mutation does not always tell the full story. Epigenetic changes—which do not affect the DNA sequence itself, but rather the degree to which a gene is expressed—can play an important role in cancer as well. Such is the case with acute lymphoblastic leukemia (ALL), the most common form of cancer in children, which has a low incidence of genetic mutation but often coincides with abnormal epigenetic behavior.
Damon Runyon News
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 second class of Damon Runyon Quantitative Biology Fellows, announced this month, will apply the tools of computational biology to generate and interpret cancer research data at extraordinary scale and resolution. From RNA sequencing data that pinpoints tumor cells to their exact location to three-dimensional models of cell-cell interaction, their projects extend the boundaries of what is possible in cancer research, allowing them to tackle fundamental biological and clinical questions.
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 American Association for Cancer Research (AACR) is the oldest and largest cancer research organization in the world. Its Fellows, selected through a rigorous peer review process, are scientists from a range of disciplines whose work has “propelled significant innovation and progress against cancer.”
Damon Runyon is delighted to announce the unanimous election of Carlos Arteaga, MD, and Levi Garraway, MD, PhD, to its Board of Directors.
In early April, Damon Runyon Quantitative Biology Fellows and distinguished leaders from our selection committee discussed pioneering a new field at the nexus of laboratory-based cancer research and data science.
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.