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Cell Biology
& Cytogenetics

Frost Trees

Index of Articles

Updated: August 9, 2007

Epigenetics

Genes Sleeping on the Job

New Therapies Based on a Better Understanding of Cell Biology

Chromatin 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.

 

Target Mitochondrion

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

mitochondrion 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

cellular adhesion 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

gene chart 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.

 

Clonal Evolution

Acquired Resistance to Therapy by Selection

The Nature of CLL: How the Disease Grows and Evolves

evolution diagram 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

p53 protein 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

 

Genetics

Genetic Mutations and Their Effect on Overall Survival

Important Paper Identifies Common Genetic Abnormalities

The difference between good prognosis and poor prognosis for a CLL patient resides at least in part on the particular genetic abnormality that characterizes the patient's disease. Stilgenbauer, Dohner, et al., lay out some basic correlative data on common mutations and survival expectations associated with them. Therapy choices should be made based on the risk associated with each type of abnormality. To learn more, read our review of their paper, Genetic Abnormalities in Blood Cancers.

 

 

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