Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0035412 (rhabdomyosarcoma)
 6,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antineoplastic therapy causes developmental disturbances in the dental enamel and root if children are treated during tooth development. Increased caries activity has also been reported. The effect of anticancer therapy on the function of the masticatory system (i.e. jaws, dentition, masticatory muscles) is not well known. A case report of a 9-year-old girl with right auricular rhabdomyosarcoma is presented. She received irradiation of 50 Gy to the right auricular area and chemotherapy. A year and a half after cessation of cancer therapy, she was disease free and the clinical stomatognathic examination combined with electromyogram (EMG) registration of the masseter and temporal muscles and magnetic resonance imaging (MRI) examination of the temporomandibular joints (TMJ) revealed a strongly restricted mouth opening capacity, painful right TMJ, and flattened head of the right mandibular condyle. Muscle atrophy in the right masseter muscle was clearly visible but EMG activities of the masseter and temporal muscles, however, were higher on the right than on the left. More severe developmental defects, and worse gingival and cariological health were observed on the right side than on the left side. She developed 12 carious lesions and all the lesions were on the right maxilla or mandible or on anterior teeth. The left side was not affected. Intensive prophylactic dental care after cancer treatment is important in order to prevent caries and gingival inflammation. Stomatognathic treatment (i.e. management of occlusal and dysfunctional problems) may improve the mouth opening capacity and relieve pain.
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PMID:Influence of antineoplastic therapy on function of the masticatory system, tooth development, and cariogenic status: a case report. 864 17

We report two unrelated patients with infantile spinal muscular atrophy (SMA) types II and IIIa who developed alveolar rhabdomyosarcoma (ARMS) at 15 and 19 years, respectively. The tumours were located in the forearm, within severely atrophic flexor muscles. They displayed a similar histology and shared the most common translocation, t(2;13)(q35;14) in ARMS. Since cell proliferation is increased in de- and regenerating muscle and the PAX3/FKHR fusion protein activates myogenic transcription, it is tempting to speculate whether severe muscle atrophy in SMA might predispose to malignant transformation in long-standing disease.
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PMID:Alveolar rhabdomyosarcoma in infantile spinal muscular atrophy: coincidence or predisposition? 1563 20

Myoblast differentiation is fundamental to skeletal muscle development and regeneration after injury and defects in this process are implicated in muscle atrophy associated with aging or pathological conditions. MyoD family transcription factors function as mater regulators in induction of muscle-specific genes during myoblast differentiation. We have identified bakuchiol, a prenylated phenolic monoterpene, as an inducer of MyoD-mediated transcription and myogenic differentiation. C2C12 myoblasts treated with bakuchiol exhibit enhanced muscle-specific gene expression and myotube formation. A key promyogenic kinase p38MAPK is activated dramatically by bakuchiol which in turn induced the formation of MyoD/E protein active transcription complexes. Consistently, the recruitment of MyoD and Baf60c to the Myogenin promoter is enhanced in bakuchiol-treated myoblasts. Furthermore, bakuchiol rescues defective p38MAPK activation and myogenic differentiation caused by Cdo-depletion or in RD rhabdomyosarcoma cells. Taken together, these results indicate that bakuchiol enhances myogenic differentiation through p38MAPK and MyoD activation. Thus bakuchiol can be developed into a potential agent to improve muscular regeneration and repair to treat muscular atrophy.
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PMID:Bakuchiol augments MyoD activation leading to enhanced myoblast differentiation. 2690 38