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Biology subjects

Gandhi, D.

Publications and source records attributed to Gandhi, D..

2 recordsLinked to original sources

AXL mediates mast cell survival and resistance to tyrosine kinase inhibitors in mastocytosis

Mastocytosis is a clonal disorder driven by KIT mutations, but resistance to tyrosine kinase inhibitors (TKIs) remains a major challenge. Following the discovery of an AXL L197M mutation in a patient with congenital aggressive mastocytosis, we demonstrated unexpected wild-type AXL expression in neoplastic mast cells (MCs) across mastocytosis subtypes, challenging current views concerning mastocytosis pathophysiology. AXL was undetectable in steady-state MCs but several factors, including IFN- and IFN-{beta}, induced its expression, consistent with the inflammatory nature of mastocytosis and the high interferon levels in patient plasma. Ectopic expression of WT or L197M AXL in the ROSA KIT D816V cell line enhanced proliferation and survival by upregulating pSTAT5, pSTAT3, pFAK, p-p38, survivin and BCL2. Both AXL forms conferred resistance to the KIT inhibitor PKC412/midostaurin by sustaining BCL2, MCL1, and BCL-XL expression while reducing caspase-3 activation. L197M AXL induced slightly stronger resistance to apoptosis than WT, but this difference was not significant. Combined KIT and AXL targeting (PKC412+R428) restored TKI sensitivity by downregulating BCL-XL, Livin and cIAP1, and activating caspase-3, highlighting the therapeutic potential of dual KIT/AXL pathway inhibition. Importantly, neoplastic MCs from a mast cell leukemia patient harboring the KIT F522C mutation and unresponsive to PKC412 strongly expressed AXL and displayed marked in vitro sensitivity to R428 alone, highlighting AXL as a potential therapeutic target in aggressive mastocytosis not driven by KIT D816V. These findings identify AXL as a previously unrecognized driver of malignant MC survival and TKI resistance, and support AXL inhibition as a promising therapeutic strategy in aggressive mastocytosis. Key Points- AXL is aberrantly expressed in neoplastic mast cells, driving survival and resistance to KIT inhibition in mastocytosis. - Dual KIT and AXL inhibition restores TKI sensitivity in KIT-mutant mastocytosis. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=182 SRC="FIGDIR/small/686205v1_ufig1.gif" ALT="Figure 1"> View larger version (40K): org.highwire.dtl.DTLVardef@1569c9eorg.highwire.dtl.DTLVardef@1445b32org.highwire.dtl.DTLVardef@bf3565org.highwire.dtl.DTLVardef@14a94f0_HPS_FORMAT_FIGEXP M_FIG C_FIG

cancer biology↗

ribosomal DNA instability as a potential cause of karyotype evolution

Karyotype refers to the configuration of the genome into a set of chromosomes. The karyotype difference between species is expected to impede various biological processes, such as chromosome segregation or meiotic chromosome pairing, potentially contributing to incompatibility. Karyotypes can rapidly change between closely related species and even among populations of the same species. However, the forces driving karyotype evolution are poorly understood. Here we describe a unique karyotype of a D. melanogaster strain isolated from the Seychelles archipelago. This strain has lost the ribosomal DNA (rDNA) locus on the X chromosome. Because the Y chromosome is the only other rDNA-bearing chromosome, all females carry at least one Y chromosome as the source of rDNA. Interestingly, we found that the strain also carries a truncated Y chromosome (YS) that is stably maintained in the population despite its inability to support male fertility. Our modeling and cytological analysis suggest that the Y chromosome has a larger negative impact on female fitness than the YS chromosome. Moreover, we generated an independent strain that lacks X rDNA and has a karyotype of XXY females and XY males. This strain quickly evolved multiple karyotypes: two new truncated Y chromosomes (similar to YS), as well as two independent X chromosome fusions that contain the Y-derived rDNA fragment, eliminating females dependence on the Y chromosome. Considering that Robertsonian fusions frequently occur at rDNA loci in humans, we propose that rDNA loci instability is a driving force of karyotype evolution.

genetics↗