Article citationsMore>>
Siekmann, I.-K., Dierck, K., Prall, S., Klokow, M., Strauss, J., Buhs, S., Wrzeszcz, A., Bockmayr, M., Beck, F., Trochimiuk, M., Gottschling, K., Martens, V., Khosh-Naucke, M., Gerull, H., Müller, J., Behrmann, L., Blohm, M., Zahedi, R.P., Jeremias, I., Sickmann, A., Nollau, P. and Horstmann, M.A. (2018) Combined Inhibition of Receptor Tyrosine and p21-Activated Kinases as a Therapeutic Strategy in Childhood ALL. Blood Advances, 2, 2554-2567.
https://doi.org/10.1182/bloodadvances.2018020693
has been cited by the following article:
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TITLE:
Angiogenic and FLT3 Receptors Expression in Acute Lymphoblastic Leukemia in Pediatric Age Group
AUTHORS:
Mona Hilmy Alrayes, Reham Hammad, Mohamed Abd Alazim Hussein EL Baddiny, Maha Saleh Madbouly Ibrahim, Mahmoud Hammad
KEYWORDS:
Childhood Leukemia, Angiogenesis, Vascular Endothelial Growth Factor Receptors, FLT3, Acute Lymphoblastic Leukemia
JOURNAL NAME:
Journal of Cancer Therapy,
Vol.10 No.6,
June
24,
2019
ABSTRACT: Angiogenesis
has an important role in pathophysiology of cancer. FMS-like tyrosine kinase 3
(FLT3) is implicated in hematopoietic malignancies. Their role in childhood
acute lymphoblastic leukemia (ALL) pathogenesis needs more enlightenment.
Expression of vascular endothelial growth factor receptor-1 and -2 (VEGFR-1 and
-2), as well as FLT3 were assessed by flow cytometry in bone marrow (BM) blasts
of 55 newly diagnosed children with ALL. Patients included B cell ALL (B-ALL)
group (n = 41) and T cell ALL (T-ALL) group (n = 14). Comparison between groups
revealed a significant increase in blasts percent (%) expressing FLT3 and FLT3
intensity detected in B-ALL group (p = 0.004
and p = 0.02, respectively). In B-ALL patients, a significant positive
correlation was seen between blasts % expressing FLT3 and blasts percentage
infiltrating BM (r = 0.405; p = 0.009), also positive correlation was seen
between % of blasts expressing VEGFR-1 and VEGFR-2 (r = 0.704; p 0.001). In T-ALL group, blast % expressing FLT3
revealed significant positive correlations with blast %
expressing VEGFR-1, and those expressing VEGFR-2 (r = 0.627; p = 0.016, and r =
0.654; p = 0.011, respectively). In
addition, significant correlation was seen in blasts % expressing all; FLT3,
VEGFR-1 and -2, with blasts % expressing stem cell marker CD34 (r = 0.826; p = 0.001,
r = 0.596; p = 0.041, and r = 0.798; p = 0.002, respectively). Conclusion:
Expression of VEGFR-1, VEGFR-2 and FLT3 were demonstrated and linked on
leukemic blasts of ALL which highlights their role in pathogenesis. FLT3
expression plays a role in facilitating blasts proliferation in BM in B-ALL.
FLT3, VEGFR-1 and -2 could be used in future profiling of CD34+ leukemic stem cell pool in T-ALL.
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