It’s important to note that standard cancer treatments (surgery, chemotherapy, and radiation) can always be optimized and improved. In fact, there are currently many life-enhancing advancements for almost every type of cancer.
This article shows how the standard treatment for Acute Myeloid Leukemia can be optimized.
Since the genetic subtypes of each cancer usually have varying prognoses and responses to treatment, it is important to determine the specific subtype for each patient. The subtypes of most cancers are determined by the types of cell surface proteins (immunophenotyping) and the chromosomal changes (translocations).
Therefore, it is fundamental that the treatment you engage in is optimized for your particular molecular signature – and not just the most common form of treatment available through your local cancer agency.
The following section shows how the standard treatment for Acute Myeloid Leukemia can be optimized.
The five year survival for standard AML treatment with 7+3 (cytarabine and daunorubicin) varies from 15-70% and relapse rates vary from 78-33%, depending on the genetic subtype (Grimwade et al. 1998). The effectiveness of standard treatment (referred to as 7+3) on patients with specific genetic signatures is indicated below.
The prognostic chromosomal rearrangements for standard treatment of AML (7+3) are as follows:
Good Prognosis: AML cases with chromosomal rearrangements such as t(8;21), t(15;17), inv(16) have a five year survival rate of 70% and a relapse rate of 33%.
Intermediate Prognosis: AML cases with chromosomal rearrangements such as normal, +8, +21, +22, del(7q), del(9q) or abnormal 11q23, have a five year survival rate of 48% and a relapse rate of 50%.
Poor Prognosis: AML cases with chromosomal rearrangements such as -5, -7, del(5q), abnormal 3q or complex cytogenetics, have a five year survival rate of 15% and a relapse rate of 78%.
As you can see, the outlook for patients with poor prognosis rearrangements is not good. The next section outlines a significant improvement in treating these patients.
For AML patients harboring abnormal chromosome 3q, there are some concerns with standard treatment. Genetically, AML is a heterogeneous disease with 40% of cases based on primary chromosome translocations or inversions that encode fusion proteins (Shing et al., 2007).
Based on cytogenetic and immune based data, patients with an abnormal 3q chromosome most likely have the MEL1S fusion protein driving their disease. The loss of the p53 tumour suppressor gene usually accompanies this genetic rearrangement. Since the standard treatment was not designed to target cells expressing this fusion protein, it is unlikely to achieve remission in this case.
Furthermore, the 7+3 regime is only effective when the chemotherapeutic agents are combined in a specific ratio. Since the genes that metabolize these agents as well as individual patient’s health varies greatly, maintaining this narrow therapeutic window is challenging.
In CPX-351, cytarabine and daunorubicin are encapsulated within liposomes in a 5:1 ratio, allowing for the synergistic drug ratio to be maintained in the blood plasma for 24 hours post-injection, which is a significant improvement.
Results from pre-clinical studies have shown that despite using sub-MTD daunorubicin doses, CPX-351 exhibited superior therapeutic activity, maintenance of synergistic drug ratios in bone marrow, and high proportions of long-term survivors compared to standard free-drug cocktails (Lim et al., 2010).
While this variation may not appear significant in long-term management of AML, it is important to note that with every therapeutic approach and type of cancer examined, we have identified many similar examples of life-enhancing updates and improvements.
If you have AML and are interested in receiving CPX-351, please contact Celator.
This article was first published on June 16, 2011, written by Alex Rolland .
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