Quantitative phosphoproteomics revealed interplay between Syk and Lyn in the resistance to nilotinib in chronic myeloid leukemia cells

Gioia, Romain; Leroy, Cédric; Drullion, Claire; Lagarde, Valérie; Étienne, Gabriel; Dulucq, Stéphanie; Lippert, Éric; Roche, Serge; Mahon, François‐Xavier; Pasquet, Jean‐Max

doi:10.1182/blood-2010-10-313692

Cited by 88 publications

(71 citation statements)

References 39 publications

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“…In addition, IPA suggests that enhanced signaling from phospholipase Cg1 (PLCg1) and upregulation of cytoplasmic tyrosine kinases such as Lyn, Fyn, and Syk may contribute to accelerated proliferation rate of BCR-ABL1 Abl1 2/2 cells overexpressing receptor tyrosine kinase Kit (supplemental Figure 2). [22][23][24][25] Moreover, upregulation of Pdgfa, Vegfb, Vegfc, and Csf1 expression in BCR-ABL1 Abl1 2/2 cells implicates autocrine stimulation of cell growth.…”

Section: Abl1 Inhibits Proliferation Of Bcr-abl1-expressing Leukemia mentioning

confidence: 99%

Normal ABL1 is a tumor suppressor and therapeutic target in human and mouse leukemias expressing oncogenic ABL1 kinases

Dasgupta

Koptyra

Hoser

et al. 2016

Blood

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Section: Abl1 Inhibits Proliferation Of Bcr-abl1-expressing Leukemia mentioning

confidence: 99%

Normal ABL1 is a tumor suppressor and therapeutic target in human and mouse leukemias expressing oncogenic ABL1 kinases

Dasgupta

Koptyra

Hoser

et al. 2016

Blood

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“…Thus these data need to be corroborated in larger, welldefined patient cohorts. In addition to its potential role in AML, Axl was upregulated upon development of imatinib resistance in a CML cell line [220], and has very recently been linked to resistance to nilotinib [221]. Axl also plays a role in B-cell chronic lymphocytic leukemia, because it is constitutively activated in these leukemia cells and acts as a docking site for nonreceptor kinases [222].…”

Section: Tamr Gas6 and Protein S In Leukemiamentioning

confidence: 99%

Macrophage–tumor crosstalk: role of TAMR tyrosine kinase receptors and of their ligands

Schmidt

Ben-Batalla

Schultze

et al. 2011

Cell. Mol. Life Sci.

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Ample clinical and preclinical evidence indicates that macrophages interact with tumor cells as well as with virtually all populations of host cells present in the tumor microenvironment. This crosstalk can strongly promote malignancy, but also has in principle the potential to inhibit tumor growth. Thus, it is of the utmost importance to improve our understanding of the mechanisms driving the pro- and antimalignant behavior of tumor-associated macrophages (TAMs) in order to develop better anticancer therapies. In this review, we discuss the biological consequences of reciprocal interactions between TAMs, cancer cells, endothelial cells, fibroblasts and other leukocyte subfractions within tumors. It was recently elucidated that tumors specifically educate macrophages to secrete growth arrest-specific gene 6 (Gas6), the common ligand of the Tyro3, Axl, Mer receptor (TAMR) family. In turn, Gas6 fosters tumor growth by promoting cancer cell proliferation. Therefore, the Gas6-TAMR axis might represent a novel target for disrupting tumor-macrophage crosstalk. We summarize here what is known about TAMR and their ligands in (human) cancer biology. In order to shed more light on the role of macrophages in human cancer, we additionally provide an overview of what is currently known about the prognostic impact of TAMs in human cancer.

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“…39 The same applies to Nilotinib. 40 Axl overexpression and/or activation has been related to resistance to chemotherapy in some other cancer types ; gastrointestinal stromal tumor cell lines 41 , rhabdomyosarcoma 42 , HER-2 positive breast tumor cells 43 , cutaneous squamous cell carcinoma (SCC) 44 , Kaposi sarcoma 45 and ovarian cancer. 46 Drugs targeting Axl are currently under investigation.…”

Section: Gas6/axl In Different Cancer Typesmentioning

confidence: 99%

Tiroid Kanserinde Tirozin Kinaz İnhibitörleri: Axl/Gas6 Yolağı Gizli Bir Hedef Olabilir mi?

Işildak¹

2013

UHOD

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Tyrosine kinase inhibitors are molecules that block various intracellular signaling pathways. Trials with some tyrosine kinase inhibitors showed promising results in thyroid cancer. They are thought to owe their antitumor property mainly to their effect on vascular endothelial growth factor receptor which is important in angiogenesis. Axl is a receptor tyrosine kinase shown to be involved in proliferation migration and survival of cells. Recent studies implied axl in thyroid cancer development. In this review, we aimed to discuss the mechanism of action of tyrosine kinase inhibitors in general and specifically focus on the axl/gas6 signaling pathway. Tirozin kinaz inhibitörleri çeflitli intraselüler sinyal yolaklar›n› bloke eden molekülleridir. Baz› tirozin kinaz inhibitörleriyle yap›lan çal›flma-lar, tiroid kanserinde ümit verici olduklar›n› göstermifltir. Antitümör özelliklerini bafll›ca, anjiogenezde önemli olan vasküler endotelyal büyüme fakötrü reseptörü üzerindeki etkilerine borçlu olduklar› düflünülmektedir. Axl, hücrelerin ço¤almas›, göçü ve sa¤kal›m›nda rolü oldu¤u gösterilmifl bir reseptör tirozin kinazd›r. Yak›n zamanda yap›lan çal›flmalar tiroid kanseri gelifliminde axl'yi iflaret etmektedir. Bu derlemede, genel olarak tirozin kinaz inhibitörlerinin etkisini tart›flmak ve özellikle axl/gas6 sinyal yola¤› üzerinde durmak istedik.Anahtar Kelimeler: Tirozin kinaz inhibitörü, axl/gas6 sinyali, Tiroid kanseri ULUSLARARASı HEMATOLOJI-ONKOLOJI DERGISI

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Quantitative phosphoproteomics revealed interplay between Syk and Lyn in the resistance to nilotinib in chronic myeloid leukemia cells

Cited by 88 publications

References 39 publications

Normal ABL1 is a tumor suppressor and therapeutic target in human and mouse leukemias expressing oncogenic ABL1 kinases

Normal ABL1 is a tumor suppressor and therapeutic target in human and mouse leukemias expressing oncogenic ABL1 kinases

Macrophage–tumor crosstalk: role of TAMR tyrosine kinase receptors and of their ligands

Tiroid Kanserinde Tirozin Kinaz İnhibitörleri: Axl/Gas6 Yolağı Gizli Bir Hedef Olabilir mi?

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