Out of the 50 patients, only six were female (12.0%), and all these female patients presented with an immature T-ALL phenotype (pro T-ALL and pre T-ALL).
The highest percentage of patients (56.0%) presented with an immature T-ALL phenotype (pro- and pre-T-ALL) (CD4-, CD8-), whereas 24.0% of cases expressed features of maturing T-ALL phenotype (cortical) (CD4+, CD8+).
The average age of patients with immature T-ALL, maturing (cortical) T-ALL, and mature (medullary) T-ALL were 19.9, 20.5, and 17.3 years, respectively (p = 0.060).
The average bone marrow blast cell percentages were 77.7%, 88.6%, and 72.3% in the immature T-ALL, maturing T-ALL, and mature T-ALL groups, respectively, and was not statistically significant (p = 0.060).
T-ALL comprises approximately 20% of all ALL cases [1, 2, 14].
With cytoplasmic CD3 as the most specific T-cell marker expressed in all maturation stages, there are pro-T (CD7+), pre-T (CD2+ and/or CD5+ and/or CD8+), cortical T (CD1a+), and medullary T (surface CD3+, CD1a-) subtypes of T-ALL based on progressive stages of differentiation .
Ma et al., "The TCR [gamma][delta] repertoire and relative gene expression characteristics of T-ALL cases with biclonal malignant vS1 and VS2 T cells," DNA and Cell Biology, vol.
They screened 26,400 molecules and identified the novel molecular compound Lenaldekar (LDK) as effective in eliminating immature zebrafish T-cells and targeting human T-ALL cell lines without causing major toxicity to other cell types.
After confirming LDK's effectiveness in vitro, the investigators then tested its efficacy in zebrafish and mouse models of human T-ALL.
After testing a number of patient samples, researchers found that LDK was active against the vast majority of primary leukaemia samples, demonstrating its effectiveness beyond T-ALL.
Using a technique called serial transplantation, the research team studied T-ALL in zebrafish and selected cancer cells from those in which the disease advanced more rapidly for further testing.
This method allowed the research team to zero in on genes associated with T-ALL's most aggressive forms.