Publications by authors named "Hodaya Malka"

Cancer cells depend on specific oncogenic pathways or present a genetic alteration that leads to a particular disturbance. Still, personalized and targeted biological therapy remains challenging, with current efforts generally yielding disappointing results. Carefully assessing onco-target molecular pathways can, however, potently assist with such efforts for the selection of patient populations that would best respond to a given drug treatment.

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Article Synopsis
  • Post-translational modifications of G-protein coupled receptors (GPCRs) are crucial in regulating tissue health and cancer, specifically in protease-activated receptors (PARs), which are less understood.
  • The study identifies RNF43, an E3 ubiquitin ligase, as a negative regulator of PARs that promotes PAR degradation and impacts colon cancer growth by altering signaling pathways.
  • Additionally, RNF43's expression is significantly higher in certain colon cancer models where PAR is absent, suggesting its role in promoting cancer stem cell characteristics and β-catenin activity relevant to tumor development.
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While the role of G-protein-coupled receptors (GPCR) in cancer is acknowledged, their underlying signaling pathways are understudied. Protease-activated receptors (PAR), a subgroup of GPCRs, form a family of four members (PAR1-4) centrally involved in epithelial malignancies. PAR4 emerges as a potent oncogene, capable of inducing tumor generation.

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The essential role of G-protein coupled receptors (GPCRs) in tumor growth is recognized, yet a GPCR based drug in cancer is rare. Understanding the molecular path of a tumor driver gene may lead to the design and development of an effective drug. For example, in members of protease-activated receptor (PAR) family (e.

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