Genetic assessment is crucial to address the correct treatment for advanced medullary thyroid cancer (MTC). Multi tyrosine kinase inhibitors (mTKIs) cabozantinib and vandetanib are good first line options, even vandetanib prescription is currently limited to RET mutated patients. Selective RET inhibitors such as pralsetinib could be a preferred upfront treatment in case of RET mutated MTC presenting common or gatekeeper RET mutations (e.g. M918T; V804L/M). Selpercatinib, otherwise, can be prescribed as the second line after disease progression to mTKIs. The best option for subsequent lines is to consider inclusion in clinical trials or alternatively other mTKIs such as sunitinib, sorafenib, lenvatinib, or pazopanib could be evaluated. New perspectives include next-generation RET inhibitors able to overcome resistance mechanisms responsible for disease progression to standard mTKIs and RET inhibitors, and immunotherapy for MTC presenting with high tumor mutational burden.
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http://dx.doi.org/10.1007/s11864-023-01145-5 | DOI Listing |
Clin Cancer Res
January 2025
University of Lyon System, Lyon, France.
The success of targeted therapies in oncogene-driven cancer is limited by adaptive or acquired treatment resistance, leading to disease progression. A recent study reports that YAP-dependent HER3 activation constitutes a therapeutic vulnerability of adaptive resistance to RET-targeted therapies in RET-altered cancers, highlighting a promising strategy to improve RET-inhibitor tumor responses.
View Article and Find Full Text PDFDrug Des Devel Ther
January 2025
The Key Laboratory of Molecular Pharmacology, Liaocheng People's Hospital, Liaocheng, Shandong, People's Republic of China.
Background: Melanoma is a highly lethal form of skin cancer, and effective treatment remains a significant challenge. SPP86 is a novel potential therapeutic drug. Nonetheless, the specific influence of SPP86 on autophagy, particularly its mechanisms in the context of DNA damage and apoptosis in human melanoma cells, remains inadequately understood.
View Article and Find Full Text PDFCancer Lett
January 2025
Peggy and Charles Stephenson Cancer Center, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA; Department of Pathology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA. Electronic address:
Anorexia is a major cause of cancer cachexia and is induced by growth differentiation factor-15 (GDF15), which activates the rearranged during transfection (RET) protein tyrosine kinase in the hindbrain through GDF family receptor α-like (GFRAL), raising the possibility of targeting RET for cancer cachexia treatment. RET-altered cancer patients treated with RET-selective kinase inhibitors gain weight, however, it is unclear whether this results from tumor regression that improves the overall health of patients. Thus, the potential of using a RET inhibitor to address cancer cachexia remains unknown.
View Article and Find Full Text PDFFront Oncol
December 2024
Dermatological Department, Tianjin Academy of Traditional Chinese Medicine Affiliated Hospital, Tianjin, China.
This study reports a 50-year-old patient presented with eczematous drug-eruption induced by selpercatinib after the treatment of non-small cell lung cancer (NSCLC). The patient has symmetric erythematous papules and plaques all over the body with dry, scaly skin accompanied by severe pruritus and visible scarring. After systemic treatment with glucocorticoids, the patient' skin lesions were reduced well.
View Article and Find Full Text PDFJ Med Chem
January 2025
School of Pharmacy and Food Engineering, Wuyi University, Jiangmen 529020, China.
The rearranged during transfection (RET) mutation such as the G810C mutation has significantly restricted the clinical application of selective RET inhibitors in the treatment of RET-driven cancers. This study designed and evaluated RET proteolysis targeting chimeras (PROTACs) based on selpercatinib (LOXO-292), identifying as a potent and selective RET PROTAC. effectively inhibited the proliferation of BaF3 cells with various RET mutations, showing IC values of 2.
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