ArticleHaematologica2018
Maternal embryonic leucine zipper kinase inhibitor OTSSP167 has preclinical activity in multiple myeloma bone disease.
Article in Haematologica, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Maternal Embryonic Leucine Zipper Kinase (Biology · 2026Review
- Computational identification of Moracin G and Isolonchocarpin as potent MELK inhibitors for anticancer drug discovery.Scientific reports · 2025Article
- Re-programming by a six-factor-secretome in the patient tumor ecosystem during nutrient stress and drug response.iScience · 2024Article
- siRNA-Mediated MELK Knockdown Induces Accelerated Wound Healing with Increased Collagen Deposition.International journal of molecular sciences · 2023Article
- Targeting Ferroptosis in Colorectal Cancer.Metabolites · 2022Review
- Microtubule affinity regulating kinase 4 promoted activation of the NLRP3 inflammasome-mediated pyroptosis in periodontitis.Journal of oral microbiology · 2022Article
- Analysis of crucial genes, pathways and construction of the molecular regulatory networks in vascular smooth muscle cell calcification.Experimental and therapeutic medicine · 2021Article
- Inhibition of MELK produces potential anti-tumour effects in bladder cancer by inducing G1/S cell cycle arrest via the ATM/CHK2/p53 pathway.Journal of cellular and molecular medicine · 2020Article
- Inhibition of MELK Protooncogene as an Innovative Treatment for Intrahepatic Cholangiocarcinoma.Medicina (Kaunas, Lithuania) · 2019Article
- Targeting PKCι-PAK1 signaling pathways in EGFR and KRAS mutant adenocarcinoma and lung squamous cell carcinoma.Cell communication and signaling : CCS · 2019Article
- Exosomes play a role in multiple myeloma bone disease and tumor development by targeting osteoclasts and osteoblasts.Blood cancer journal · 2018Article
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple myeloma bone disease is characterized by an uncoupling of bone remodeling in the multiple myeloma microenvironment, resulting in the development of lytic bone lesions. Most myeloma patients suffer from these bone lesions, which not only cause morbidity but also negatively impact survival. The development of novel therapies, ideally with a combined anti-resorptive and bone-anabolic effect, is of great interest because lesions persist with the current standard of care, even in patients in complete remission. We have previously shown that MELK plays a central role in proliferation-associated high-risk multiple myeloma and its inhibition with OTSSP167 resulted in decreased tumor load. MELK inhibition in bone cells has not yet been explored, although some reports suggest that factors downstream of MELK stimulate osteoclast activity and inhibit osteoblast activity, which makes MELK inhibition a promising therapeutic approach. Therefore, we assessed the effect of OTSSP167 on bone cell activity and the development of myeloma-induced bone disease. OTSSP167 inhibited osteoclast activity
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