Dysphagia often occurs in cancer patients. The primary causes of dysphagia in cancer patients include new local dissemination of cancer cells or metastatic brain lesions, which needs to be accurately differentiated. Dermatomyositis is often associated with cancer and may manifest before or after the cancer diagnosis. Although early diagnosis and immunotherapy can improve dermatomyositis, its identification may be delayed in cancer patients due to complex comorbidities. We report a case of a 33-year-old woman with metastatic breast cancer who presented with dysphagia. The primary consideration was metastatic lesions. However, subsequent diagnosis revealed dermatomyositis.Symptoms, including facial swelling, dysarthria, and dysphagia, emerged 26 months after the cancer diagnosis. No new metastatic lesion was identified through imaging studies. A videofluoroscopic study (VFSS) revealed velopharyngeal insufficiency, reduced pharyngeal contraction, and excessive pharyngeal residue with silent aspiration. After a combination of further clinical, laboratory, and muscle biopsy findings, dermatomyositis was identified as the actual cause of dysphagia. The patient was treated with immunosuppressive and rehabilitative swallowing therapies, which improved her symptoms. This case underscores the critical importance of accurately identifying and promptly treating dysphagia in cancer patients. It particularly emphasizes the need to recognize dermatomyositis as a potential differential diagnosis in cancer patients presenting with dysphagia.

Dysphagia often occurs in cancer patients. The primary causes of dysphagia in cancer patients include new local dissemination of cancer cells or metastatic brain lesions, which needs to be accurately differentiated. Dermatomyositis is often associated with cancer and may manifest before or after the cancer diagnosis. Although early diagnosis and immunotherapy can improve dermatomyositis, its identification may be delayed in cancer patients due to complex comorbidities. We report a case of a 33-year-old woman with metastatic breast cancer who presented with dysphagia. The primary consideration was metastatic lesions. However, subsequent diagnosis revealed dermatomyositis.Symptoms, including facial swelling, dysarthria, and dysphagia, emerged 26 months after the cancer diagnosis. No new metastatic lesion was identified through imaging studies. A videofluoroscopic study (VFSS) revealed velopharyngeal insufficiency, reduced pharyngeal contraction, and excessive pharyngeal residue with silent aspiration. After a combination of further clinical, laboratory, and muscle biopsy findings, dermatomyositis was identified as the actual cause of dysphagia. The patient was treated with immunosuppressive and rehabilitative swallowing therapies, which improved her symptoms. This case underscores the critical importance of accurately identifying and promptly treating dysphagia in cancer patients. It particularly emphasizes the need to recognize dermatomyositis as a potential differential diagnosis in cancer patients presenting with dysphagia.

Dysphagia often occurs in cancer patients. The primary causes of dysphagia in cancer patients include new local dissemination of cancer cells or metastatic brain lesions, which needs to be accurately differentiated. Dermatomyositis is often associated with cancer and may manifest before or after the cancer diagnosis. Although early diagnosis and immunotherapy can improve dermatomyositis, its identification may be delayed in cancer patients due to complex comorbidities. We report a case of a 33-year-old woman with metastatic breast cancer who presented with dysphagia. The primary consideration was metastatic lesions. However, subsequent diagnosis revealed dermatomyositis.Symptoms, including facial swelling, dysarthria, and dysphagia, emerged 26 months after the cancer diagnosis. No new metastatic lesion was identified through imaging studies. A videofluoroscopic study (VFSS) revealed velopharyngeal insufficiency, reduced pharyngeal contraction, and excessive pharyngeal residue with silent aspiration. After a combination of further clinical, laboratory, and muscle biopsy findings, dermatomyositis was identified as the actual cause of dysphagia. The patient was treated with immunosuppressive and rehabilitative swallowing therapies, which improved her symptoms. This case underscores the critical importance of accurately identifying and promptly treating dysphagia in cancer patients. It particularly emphasizes the need to recognize dermatomyositis as a potential differential diagnosis in cancer patients presenting with dysphagia.

Dysphagia often occurs in cancer patients. The primary causes of dysphagia in cancer patients include new local dissemination of cancer cells or metastatic brain lesions, which needs to be accurately differentiated. Dermatomyositis is often associated with cancer and may manifest before or after the cancer diagnosis. Although early diagnosis and immunotherapy can improve dermatomyositis, its identification may be delayed in cancer patients due to complex comorbidities. We report a case of a 33-year-old woman with metastatic breast cancer who presented with dysphagia. The primary consideration was metastatic lesions. However, subsequent diagnosis revealed dermatomyositis.Symptoms, including facial swelling, dysarthria, and dysphagia, emerged 26 months after the cancer diagnosis. No new metastatic lesion was identified through imaging studies. A videofluoroscopic study (VFSS) revealed velopharyngeal insufficiency, reduced pharyngeal contraction, and excessive pharyngeal residue with silent aspiration. After a combination of further clinical, laboratory, and muscle biopsy findings, dermatomyositis was identified as the actual cause of dysphagia. The patient was treated with immunosuppressive and rehabilitative swallowing therapies, which improved her symptoms. This case underscores the critical importance of accurately identifying and promptly treating dysphagia in cancer patients. It particularly emphasizes the need to recognize dermatomyositis as a potential differential diagnosis in cancer patients presenting with dysphagia.

BACKGROUND: Glycogen synthase kinase 3beta (GSK3beta) is a ubiquitous serine/threonine kinase that is regulated by serine phosphorylation at 9. Recent studies have reported the beneficial effects of a number of the pharmacological GSK3beta inhibitors in rodent models of septic shock. Since most of the GSK3beta inhibitors are targeted at the ATP-binding site, which is highly conserved among diverse protein kinases, the development of novel non-ATP competitive GSK3beta inhibitors is needed. METHODS: Based on the unique phosphorylation motif of GSK3beta, we designed and generated a novel class of GSK3beta inhibitor (GSK3i) peptides. In addition, we investigated the effects of a GSK3i peptide on lipopolysaccharide (LPS)-stimulated cytokine production and septic shock. Mice were intraperitoneally injected with GSK3i peptide and monitored over a 7-day period for survival. RESULTS: We first demonstrate its effects on LPS-stimulated pro-inflammatory cytokine production including interleukin (IL)-6 and IL-12p40. LPS-induced IL-6 and IL-12p40 production in macrophages was suppressed when macrophages were treated with the GSKi peptide. Administration of the GSK3i peptide potently suppressed LPS-mediated endotoxin shock. CONCLUSION: Collectively, we present a rational strategy for the development of a therapeutic GSK3i peptide. This peptide may serve as a novel template for the design of non-ATP competitive GSK3 inhibitors.
Animals ; Cytokines ; Glycogen Synthase Kinase 3 ; Glycogen Synthase Kinases ; Interleukin-12 Subunit p40 ; Interleukin-6 ; Interleukins ; Macrophages ; Mice ; Peptides ; Phosphorylation ; Phosphotransferases ; Protein Kinases ; Rodentia ; Serine ; Shock ; Shock, Septic