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Featured Articles

Cancer Cells Transform Normal Stem Cells Into Cancer Stem Cells.

Date: Tuesday, April 17, 2012

The influence of cancer cells on their neighbors is something that is being actively studied.  In this research, human prostate cells were exposed to arsenic, a chemical known to cause cancer.  Arsenic is a relevant chemical to study because it is a common contaminant in drinking water around the world. The prostate cells exposed to arsenic turned into malignant cancer cells.

The arsenic-transformed cells were then placed in culture near (but not touching) normal prostate stem cells. 
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Cancer: Running A Critical Cellular Pathway BACKWARDS!

Date: Wednesday, November 30, 2011

Cancer cells grow in an unregulated manner.  To be able to grow and divide, the cells need large amounts of energy and resources. 

The Krebs cycle, also called the tricarboxcylic acid cycle (TCA), or citric acid cycle (CAC), is a central part of cell metabolism and normally provides cells with several useful products.  This pathway takes in a breakdown product of glucose, called acetyl-CoA, and produces usable forms of energy (GTP) and
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Creating Cancer Killers.

Date: Monday, August 15, 2011

Cells of the immune system are able to fight off infection and to kill cancer cells. Unfortunately, cancer cells frequently develop ways to hide from the immune system and are able to avoid being killed.  New results show that immune cells from patients with cancer can be modified and turned into potent killers of cancer cells.

The treatment was used in patients with chronic lymphcytic leukemia (CLL).  In CLL, the cancer cells are white blood cells.  B cells, a type of white blood cell have a protein on their surface called CD19.  This protein helps normal B cells perform their job, the production of antibodies.  CD19 is also found on cancerous B cells.
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Cancer cells are addicted to oncogenes.

Date: Thursday, March 24, 2011

This is the first in a series of featured articles that have been chosen to highlight key aspects of cancer biology and treatment.  These articles may be older but they clearly present the defining 'Hallmarks of cancer'.

In this research, mice were genetically engineered to produce too much of two different oncogenes.  The first is MYC, a transcription factor that drives cell division forward.  To control the types of cancer arising in the mice, the researchers created a version of the MYC genet that would only be active in B lymphocytes (B cells).
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Reactivation of tumor suppressor may not be enough to stop cancer.

Date: Friday, February 25, 2011

Tumor suppressor genes ususally function to limit cell growth.  Loss of tumor suppressors is a critical step in the development of cancer.  One of the most important tumor suppressors is p53 (or TP53).  The p53 protein integrates signals affecting a cell (growth factors, DNA damage, oncogene signaling, etc.). The result of p53 activation can be either the suspension of cell division or the death of the cell via apoptosis.

Because p53 activity is lost in over half of all cancers, of any origin, there has been lots of research into what would happen to cancer cells if p53 could be re-activated.
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