Mutational analysis of candidate tumor-associated genes in acute megakaryoblastic leukemia

Bhat, Rukhmi; Malinge, Sébastien; Gamis, Alan S.; Sorrell, April; Hilden, Joanne M.; Ketterling, Rhett P.; Paietta, Elisabeth; Tallman, Martin S.; Crispino, John D.

doi:10.1038/leu.2009.159

Cited by 4 publications

(1 citation statement)

References 7 publications

(13 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Classical treatments are usually toxic and non-specific, and are associated with difficulties (Cervio et al, 2012), such as economic burden (O'Donnell et al, 2012) and poor tolerance to myelo-suppressive chemotherapy, especially in elderly patients (Wiernik,, Masato Takimoto 2,5 this protein in the rearrangement of the actin cytoskeleton (Verdijk et al, 2004). Also, in megakaryoblastic leukaemic cell lines, the expression of scinderin, another actinregulatory protein, induces differentiation, maturation and apoptosis (Bhat et al, 2009). The actin cytoskeleton is an essential scaffold for integrating membrane and intracellular function, whose dynamics are regulated by a number of accessory proteins (Sato, 2012).…”

Section: Introductionmentioning

confidence: 99%

Gelsolin Induces Promonocytic Leukemia Differentiation Accompanied by Upregulation of p21CIP1

Shirkoohi¹,

Fujita²,

Darmanin³

et al. 2012

Asian Pacific Journal of Cancer Prevention

View full text Add to dashboard Cite

Section: Introductionmentioning

confidence: 99%

Gelsolin Induces Promonocytic Leukemia Differentiation Accompanied by Upregulation of p21CIP1

Shirkoohi¹,

Fujita²,

Darmanin³

et al. 2012

Asian Pacific Journal of Cancer Prevention

View full text Add to dashboard Cite

Prolymphocytic Leukemia: New Insights in Diagnosis and in Treatment

et al. 2017

View full text Add to dashboard Cite

B cell prolymphocytic leukemia (B-PLL) diagnosis remains challenging in the absence of clear immunophenotypic or cytogenetic signature and overlap with mantle cell lymphoma. New molecular defects have been identified in T cell prolymphocytic leukemia (T-PLL), especially in the JAK STAT pathway. Like in chronic lymphocytic leukemia (CLL), B-PLL treatment depends on the presence of TP53 dysfunction. In T-PLL, alemtuzumab still remains the standard of care. Allogeneic transplantation is the only curable option. Thanks to reduced intensity conditioning regimens, it has become accessible to a larger number of patients. PLL prognosis remains poor with conventional therapies. However, great advances in the understanding of both T- and B-PLL pathogenesis lead to promising new therapeutic agents.

show abstract