Updated: August 9, 2007
Genes Sleeping on the Job
New Therapies Based on a Better Understanding of Cell Biology
An interesting new clinical trial has opened up for CLL patients, one that may have potential for low toxicity as well as good efficacy. As a refreshing change from the usual heavy doses of chemotherapy, this trial is based on using very low doses of drugs, often as little as ten times lower than the amounts used under standard regimens. The rationale for this approach is equally interesting. The DNA in a cell's nucleus is a vast library of information which normally defines and regulates how the cell functions. In cancer cells, however, the information retrieval mechanism is often at fault. The idea here is to use just enough drugs to correct this fault, and thereby allow the cancer cell to kill itself. Click here to read Epigenetics.
Promising New Approaches Bypass the Usual Cellular Control Points and May Level the Playing Field for Bucket C Patients
New Research on Attacking Mitochondria in B-CLL Cells
Several recent research articles have opened up exciting new opportunities in the treatment of CLL. These feature new small molecule drugs that take an entirely different approach to targeting CLL cells. In this new approach to treating CLL, it seems to make no difference if you are IgVH mutated or unmutated, CD38 positive or not, chemo-naïve or have been through the wars with every chemotherapy drug known to man. In fact, there are some indications that heavily pretreated and late Rai stage patients may respond better to this approach. To learn more about these exciting new drugs on the horizon, read Target Mitochondrion.
Adhesion, Homing and Resistance
Why Peripheral Blood Numbers Do Not Tell the Whole Story – and Why CLL Cells Are Hard to Kill
It's a Tale of Adhesion Factors, Chemokine Trails, Receptors and Blockers
The behavior of CLL as a disease and the different characteristics exhibited by strains with different clonal genetic aberrations are all related to cellular chemistry. We examine a number of critical aspects such as resistance to therapies, bulkiness of lymph nodes, infiltration of bone marrow and the support structure for CLL cells in their preferred environments. We also look at some futuristic possibilities for therapies in this article, Adhesion, Homing and Resistance to Therapy.
Cytogenetics of ATM and TP53 Genes
Gatekeepers of our Health
These Genes Are Critical to the Natural History of CLL
The TP53 gene and the ATM gene play a critical role in the behavior of CLL cells. We explore the roles of these genes in the life of a normal cell and their malfunction in cancer. Modern FISH analysis focusing on these genes helps identify the risk characteristics and aggressiveness of a given patient's CLL and therefore is an important prognostic tool. Click here to read Cytogenetics of ATM and TP53.
Acquired Resistance to Therapy by Selection
The Nature of CLL: How the Disease Grows and Evolves
In this article we review important new research into the mechanisms by which clonal B-CLL cells become more aggressive and harder to kill. This is Darwinian selection at the cellular level. We look at the implications for treatment strategy and offer a new approach to managing the disease in Clonal Evolution.
p53: The Anti-Tumor Gene Located on Chromosome 17p
The Tumor Suppressor Gene and its Associated Protein
The Worst Cytogenetic Mutation in CLL
Deletion of the gene at chromosomal location 17p13.1 is really bad news in CLL — and most other cancers. This article discusses the function of the gene and describes how its associated protein works to repair DNA damage — or, if the damage is too great, to trigger cellular suicide. Read about it in The p53 Gene
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