AXL as a Target in Breast Cancer Therapy

Colavito, Sierra A.

doi:10.1155/2020/5291952

Cited by 52 publications

(56 citation statements)

References 132 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The availability of targeted drugs against specific RTKs or their signaling molecules has also stimulated this axis of investigations. A growing interest in the EMT-associated RTK Axl, for which commercial inhibitors are being assessed in clinical trials [91][92][93], may be underlined. Although herein we will not debate the exact nature of the relationships linking EMT and Cancer-Stem Cells (CSCs) [94,95], it is important to note that EMT induces the expression of stem cell attributes [96,97] and that certain EMT and CSC markers are often coexpressed in tumor cells.…”

Section: Epithelial-mesenchymal Transitions: Impact On Ctc Phenotypicmentioning

confidence: 99%

EMT-Associated Heterogeneity in Circulating Tumor Cells: Sticky Friends on the Road to Metastasis

Genna

Vanwynsberghe

Villard

et al. 2020

Cancers

View full text Add to dashboard Cite

Epithelial–mesenchymal transitions (EMTs) generate hybrid phenotypes with an enhanced ability to adapt to diverse microenvironments encountered during the metastatic spread. Accordingly, EMTs play a crucial role in the biology of circulating tumor cells (CTCs) and contribute to their heterogeneity. Here, we review major EMT-driven properties that may help hybrid Epithelial/Mesenchymal CTCs to survive in the bloodstream and accomplish early phases of metastatic colonization. We then discuss how interrogating EMT in CTCs as a companion biomarker could help refine cancer patient management, further supporting the relevance of CTCs in personalized medicine.

show abstract

Section: Epithelial-mesenchymal Transitions: Impact On Ctc Phenotypicmentioning

confidence: 99%

EMT-Associated Heterogeneity in Circulating Tumor Cells: Sticky Friends on the Road to Metastasis

Genna

Vanwynsberghe

Villard

et al. 2020

Cancers

View full text Add to dashboard Cite

show abstract

“…The receptor tyrosine kinase Axl, which binds Gas6 and functions in the clearance of phagocytic cells during the innate immune response ( 70 ), is also enriched in this population. Interestingly, Axl is overexpressed in human breast cancers and a number of Axl inhibitors are currently in clinical trials ( 72 – 74 ). Although Axl marks classically activated macrophages in innate immunity, Axl inhibition in immune cells was shown to induce an anti-tumor response in mouse models, which was potentiated by PD-1/PD-L1 inhibitors.…”

Section: Discussionmentioning

confidence: 99%

Diverse Macrophage Populations Contribute to the Inflammatory Microenvironment in Premalignant Lesions During Localized Invasion

et al. 2020

View full text Add to dashboard Cite

Myeloid cell heterogeneity remains poorly studied in breast cancer, and particularly in premalignancy. Here, we used single cell RNA sequencing to characterize macrophage diversity in mouse pre-invasive lesions as compared to lesions undergoing localized invasion. Several subpopulations of macrophages with transcriptionally distinct profiles were identified, two of which resembled macrophages in the steady state. While all subpopulations expressed tumor-promoting genes, many of the populations expressed pro-inflammatory genes, differing from reports in tumor-associated macrophages. Gene profiles of the myeloid cells were similar between early and late stages of premalignancy, although expansion of some subpopulations occurred. These results unravel macrophage heterogeneity in early progression and may provide insight into early intervention strategies that target macrophages.

show abstract

“…Axl was initially discovered during a screen for genes involved in the progression of chronic myeloid leukaemia (CML) to blast crisis [7][8][9]. It is expressed in numerous embryonic tissues and is thought to be involved in mesenchymal and neural development.…”

Section: Axlmentioning

confidence: 99%

The Role of the Receptor Tyrosine Kinase Axl in Carcinogenesis and Development of Therapeutic Resistance: An Overview of Molecular Mechanisms and Future Applications

Wium

Ajayi-Smith

Paccez

et al. 2021

Cancers

View full text Add to dashboard Cite

Resistance to chemotherapeutic agents by cancer cells has remained a major obstacle in the successful treatment of various cancers. Numerous factors such as DNA damage repair, cell death inhibition, epithelial–mesenchymal transition, and evasion of apoptosis have all been implicated in the promotion of chemoresistance. The receptor tyrosine kinase Axl, a member of the TAM family (which includes TYRO3 and MER), plays an important role in the regulation of cellular processes such as proliferation, motility, survival, and immunologic response. The overexpression of Axl is reported in several solid and hematological malignancies, including non-small cell lung, prostate, breast, liver and gastric cancers, and acute myeloid leukaemia. The overexpression of Axl is associated with poor prognosis and the development of resistance to therapy. Reports show that Axl overexpression confers drug resistance in lung cancer and advances the emergence of tolerant cells. Axl is, therefore, an important candidate as a prognostic biomarker and target for anticancer therapies. In this review, we discuss the consequence of Axl upregulation in cancers, provide evidence for its role in cancer progression and the development of drug resistance. We will also discuss the therapeutic potential of Axl in the treatment of cancer.

show abstract

AXL as a Target in Breast Cancer Therapy

Cited by 52 publications

References 132 publications

EMT-Associated Heterogeneity in Circulating Tumor Cells: Sticky Friends on the Road to Metastasis

EMT-Associated Heterogeneity in Circulating Tumor Cells: Sticky Friends on the Road to Metastasis

Diverse Macrophage Populations Contribute to the Inflammatory Microenvironment in Premalignant Lesions During Localized Invasion

The Role of the Receptor Tyrosine Kinase Axl in Carcinogenesis and Development of Therapeutic Resistance: An Overview of Molecular Mechanisms and Future Applications

Contact Info

Product

Resources

About