Disease Information

General Information of the Disease (ID: DIS00337)

• Name: Endometriosis
• ICD: ICD-11: GA10

Type(s) of Resistant Mechanism of This Disease

  UAPP: Unusual Activation of Pro-survival Pathway

Drug Resistance Data Categorized by Drug

Approved Drug(s) 1 drug(s) in total

Fotemustine

Drug Resistance Data Categorized by Their Corresponding Mechanisms

Unusual Activation of Pro-survival Pathway (UAPP)

Key Molecule: Prostaglandin G/H synthase 2 (PTGS2) [1]

• Resistant Disease: Endometriosis [ICD-11: GA10.0]
• Molecule Alteration: Expression; Up-regulation
• Resistant Drug: Fotemustine
• Experimental Note: Discovered Using In-vivo Testing Model
• Cell Pathway Regulation: MAPK signaling pathway; Activation; hsa04010
• In Vivo Model: Female Sprague-Dawley rats model; Rattus norvegicus
• Experiment for Molecule Alteration: Western blotting analysis
• Mechanism Description: Fotemustine and dexamethasone administration had anti-apoptotic activity, restoring the impaired mechanism (TUNEL assay and Western blot analysis of Bax and Bcl-2). Moreover, no gastric disfunction was detected (histological analysis of stomachs). Thus, our data showed that the combined therapy of fotemustine and dexamethasone reduced endometriosis-induced inflammation, hyperproliferation and apoptosis resistance.

Key Molecule: DNA-binding factor KBF1 (p105) (NFKB1) [1]

• Resistant Disease: Endometriosis [ICD-11: GA10.0]
• Molecule Alteration: Expression; Up-regulation
• Resistant Drug: Fotemustine
• Experimental Note: Discovered Using In-vivo Testing Model
• Cell Pathway Regulation: MAPK signaling pathway; Activation; hsa04010
• In Vivo Model: Female Sprague-Dawley rats model; Rattus norvegicus
• Experiment for Molecule Alteration: Western blotting analysis
• Mechanism Description: Fotemustine and dexamethasone administration had anti-apoptotic activity, restoring the impaired mechanism (TUNEL assay and Western blot analysis of Bax and Bcl-2). Moreover, no gastric disfunction was detected (histological analysis of stomachs). Thus, our data showed that the combined therapy of fotemustine and dexamethasone reduced endometriosis-induced inflammation, hyperproliferation and apoptosis resistance.

Key Molecule: Prostaglandin E2 receptor EP3 subtype (PE2R3) [1]

• Resistant Disease: Endometriosis [ICD-11: GA10.0]
• Molecule Alteration: Expression; Up-regulation
• Resistant Drug: Fotemustine
• Experimental Note: Discovered Using In-vivo Testing Model
• Cell Pathway Regulation: MAPK signaling pathway; Activation; hsa04010
• In Vivo Model: Female Sprague-Dawley rats model; Rattus norvegicus
• Experiment for Molecule Alteration: Western blotting analysis
• Mechanism Description: Fotemustine and dexamethasone administration had anti-apoptotic activity, restoring the impaired mechanism (TUNEL assay and Western blot analysis of Bax and Bcl-2). Moreover, no gastric disfunction was detected (histological analysis of stomachs). Thus, our data showed that the combined therapy of fotemustine and dexamethasone reduced endometriosis-induced inflammation, hyperproliferation and apoptosis resistance.

References

• Ref 1: Regulation of Inflammatory and Proliferative Pathways by Fotemustine and Dexamethasone in Endometriosis .Int J Mol Sci. 2021 Jun 1;22(11):5998. doi: 10.3390/ijms22115998. 10.3390/ijms22115998