Tumorigenesis is the process involved in the production of a new tumor or tumors.
Cancer starts when key cellular signals run amok, driving uncontrolled cell growth. But scientists at the Stanford University School of Medicine report that lowering levels of one cancer signal under a specific threshold reverses this process in mice, returning tumor cells to their normal, healthy state. The finding could help target cancer chemotherapy to tumors while minimizing side effects for the body's healthy cells.
The molecular profile of cancer stem cells that initiate metastatic colon tumors is significantly different from those responsible for primary tumors, according to new research from a team at Weill Cornell Medical College.
In a collaborative effort, researchers from Boston University School of Medicine (BUSM) have discovered that deletions or mutations within the TFAP2A gene (Activating Enhancer-Binding Protein) result in the distinctive clefting disorder Branchio-Oculo-Facial syndrome (BOFS).
In a discovery that could lead to the development of new treatments for gastric cancer, scientists at the Melbourne Branch of the international Ludwig Institute for Cancer Research (LICR) have discovered what appears to be the primary driver of tumor development in the stomach.
Using a common virus as a tool for investigating abnormal cell proliferation, a team led by scientists at Cold Spring Harbor Laboratory (CSHL) has succeeded in clarifying an intricate series of biochemical steps that shed light on a way that cancer can begin.
Tapping into a growing body of knowledge about the origins and progression of cancer, researchers are now developing and testing new preventive therapies to stop it in its tracks.
Researchers at the National Sun Yat-Sen University and Kaohsiung Medical University, Kaohsiung, Taiwan have revealed a new mechanism by which nonsteroidal anti-inflammatory drugs (NSAIDs) attenuate tumor invasion and metastasis.
In a G&D paper published online ahead of its April 1 print publication date, Dr. William Kaelin (Dana Farber Cancer Institute) and colleagues identify a potential new neuronal tumor suppressor.
A new study provides valuable insight into a previously undescribed mechanism that regulates a prominent cancer-associated protein.
Preliminary research has found an association between certain microRNA expression patterns and poor survival and treatment outcomes for colon cancer, according to a study in the January 30 issue of JAMA: The Journal of the American Medical Association.
Like fine china and crystal, which tend to be used sparingly, stem cells divide infrequently.
Scientists report that an evolutionarily conserved transcription factor may have both positive and negative effects on the growth of tumors, depending on whether or not the tumor cells have enough oxygen.
Two independent papers in the December 1st issue of G&D detail how human RecQ helicases regulate homologous recombination and protect genome stability.
Researchers at the University of Texas M. D. Anderson Cancer Center have found a protein that enables cellular survival during periods of low oxygen, or hypoxia, which also is key for development of many kinds of cancer.
A stem cells' immediate neighborhood, a specialized environment also known as the stem cell niche, provides crucial support needed for stem cell maintenance.
Kaposi's sarcoma herpesvirus (KSHV) is a human tumor virus and an etiological agent for Kaposi's sarcoma (KS).
A new study provides evidence that noncoding RNAs and interactions between noncoding genes play a much greater role in human cancer than was previously understood.
In an upcoming Genes & Development paper, Dr. Christopher Counter and colleagues at the Duke University Medical Center have identified IL6 as a new target in the battle against Ras-induced cancers.
PLoS ONE has just published a study which defines a gene locus on chromosome 1 that predicts prognosis of brain tumor patients and may even set the basis for the development of more efficient drugs to combat brain cancer.
When the activity of individual genes it is longer required, there are two main mechanisms responsible for the “switching off”, mainly DNA methylation and the Polycomb protein complex. Sometimes, these mechanisms lose their efficiency and some of the genes that should be "switched off" remain active.