Home Blog of Signal Transduction Autophagy MEK Medical Therapy for Craniopharyngiomas

Category

Archives

Popular Post

ESKM, a novel therapeutic agent for sensitive and resistant PH+ leukemias

The mechanism of resistance to JAK2 inhibitor in myeloproliferative neoplasms patients

Effects of PARP inhibitors in BRCA gene-mutated ovarian cancer

DASATINIB; An inhibitor of Receptor Tyrosine Kinase

GP130/JAK/STAT3 signaling pathway induces multiple myeloma

Medical Therapy for Craniopharyngiomas

Craniopharyngiomas are rare benign neoplasms presenting in two different types, adamantinomatous (ACP) or papillary (PCP), which are molecularly and clinically distinct. Traditional treatment includes surgical resection and radiotherapy, which are accompanied by a number of debilitating complications because of the tumours' proximity to important brain structures. Recent advances in the understanding of molecular pathogenesis of craniopharyngiomas have opened horizons to medical therapeutic options. ACPs are mainly characterized by mutations of β-catenin, which activate Wingless/Int (Wnt), and alter the mitogen extracellular kinase (MEK)/extracellular signal-regulated kinase (ERK) pathway, as well as inflammatory, cellular senescence, programmed cell death and sonic hedgehog (SHH) pathways. PCPs are mainly characterized by Ras/Raf/MEK/ERK pathway activation secondary to BRAF-V600E mutations. MEK inhibitors, such as binimetinib, or anti-inflammatory mediators, such as tocilizumab or interferon, have been administered to patients with ACP and the efficacy is mostly favourable. On the other hand, BRAF inhibitors, such as dabrafenib or vemurafenib, either alone or in combination with the MEK inhibitors trametinib and cobimetinib, have been administered to patients with PCP resulting in favourable responses. A number of ongoing trials will shed light on schemes, doses, combined treatments and safety issues of the new molecular-targeted treatments, changing the management of patients with craniopharyngiomas by launching the era of personalized medicine in these rare neoplasms. We conducted a systematic review to identify case series or case reports with patients currently treated with systemic medical therapy.

Related Products

Cat.No. Product Name Information
S7007 Binimetinib (MEK162) Binimetinib (MEK162, ARRY-162, ARRY-438162) is a potent inhibitor of MEK1/2 with IC50 of 12 nM in a cell-free assay. Binimetinib induces G1 cell cycle arrest and apoptosis in human NSCLC cell lines and induces autophagy. Phase 3.

Related Targets

MEK Autophagy Apoptosis related