Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0184567 (acute pain)
3,962 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Women with breast cancer have many adverse symptoms, of which some are specific to premenopausal patients. Management of these common symptoms include non-hormonal drugs, such as antidepressants and antiseizure compounds to alleviate hot flushes. Non-oestrogenic vaginal lubricants seem to moderately decrease occurrence of vaginal dryness and dyspareunia. Transdermal testosterone alone has not been shown to improve libido in these women. Options for fertility preservation include cryopreservation of embryos or oocytes before chemotherapy. Exercise is the one evidenced-based intervention shown to positively affect cancer-related fatigue. However, effective prevention and treatments for peripheral neuropathy and paclitaxel acute pain syndrome remain elusive. Weight-bearing exercise helps to maintain bone strength with adequate intake of calcium and vitamin D. Use of bisphosphonates in women taking aromatase inhibitors (combined with ovarian suppression in premenopausal women) to prevent bone fractures has not been substantiated, although it should be considered in women with osteoporosis. No specific drug has been shown to prevent radiation-induced dermatitis alone. Although some effective treatments can counteract symptoms related to cancer or treatments, research is needed to expand evidence-based care in premenopausal survivors of breast cancer.
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PMID:Symptom management in premenopausal patients with breast cancer. 1907 Dec 56

Aromatase is a key enzyme responsible for the biosynthesis of estrogen from testosterone. Although recent evidence indicates that spinal cord aromatase participates in nociceptive processing, the mechanisms underlying its regulation and its involvement in nociception remain unclear. The present study focuses on the potential role of astrocyte aromatase in formalin-induced acute pain and begins to uncover one mechanism by which spinal aromatase activation is controlled. Following intraplantar formalin injection, nociceptive responses were quantified and immunohistochemistry/co-immunoprecipitation assays were used to investigate the changes in spinal Fos expression and the phospho-serine levels of spinal aromatase. Intrathecal (i.t.) injection of letrozole (an aromatase inhibitor) mitigated both the late phase formalin-induced nociceptive responses and formalin-induced spinal Fos expression. Furthermore, formalin-injected mice showed significantly reduced phospho-serine levels of aromatase, which is associated with the rapid activation of this enzyme. However, sigma-1 receptor inhibition with i.t. BD1047 blocked the dephosphorylation of aromatase and potentiated the pharmacological effect of letrozole on formalin-induced nociceptive responses. In addition, i.t. administration of a sub-effective dose of BD1047 potentiated the pharmacological effect of cyclosporin A (a calcineurin inhibitor) on both the formalin-induced reduction in phospho-serine levels of aromatase and nociceptive behavior. These results suggest that dephosphorylation is an important regulatory mechanism involved in the rapid activation of aromatase and that spinal sigma-1 receptors mediate this dephosphorylation of aromatase through an intrinsic calcineurin pathway.
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PMID:Spinal Sigma-1 Receptor-mediated Dephosphorylation of Astrocytic Aromatase Plays a Key Role in Formalin-induced Inflammatory Nociception. 2928 21