loading...| Preferred Name |
Ovarian Cancer |
|
| Synonyms |
PathwayType: signaling CellType: cancer cell PMID: 21347793 PMID: 19461510 CellType: epithelial cell PMID: 19221485 Tissue: epithelium PMID: 22987944 Organ: ovary Organ_System: reproductive system PMID: 17204312 PMID: 18317228 NodeType: Pathway PMID: 22525820 Link: https://mammal-profservices.pathwaystudio.com/app/sd?urn=urn:agi-pathway:uuid-4bf6545c-9f11-4bf6-806b-b7edb940b1d2 Description: Ovarian cancer (OC) is the most common cause of cancer death. Pathway is built manually using published studies. Pathway_Author: M. Zharkova ORCID:0000-0001-8706-9411 Source: Diseases Notes: Headnote: Ovarian cancer is the second most common malignancy among the gynecological cancers and the most common cause of cancer death, yet the etiology of ovarian malignant transformation remains poorly understood. Different types of ovarian cancer include serous, mucinous, endometrioid, clear cell, undifferentiated, and unclassifiable. Serous epithelial ovarian carcinoma is the most common type of ovarian cancer. High-grade and low-grade serous ovarian carcinomas are considered to have a different origin. The crucial pathogenic processes involved in the emergence of ovarian tumors, regardless of hyperestrogenism, are hormone-independent cell proliferation, block of apoptosis, cell invasion, dysfunction of DNA repair, and loss of cell differentiation. Signaling description: Different histotypes of ovarian cancer are formed by common mechanisms of malignization, but have different causes. According to genetic classification, there exist two groups of ovarian tumors. Tumors of the first type which include variable mucinous, endometrioid, clear cell carcinoma, and low-grade serous carcinoma are rather genetically stable and characterized by mutations in the KRAS, HRAS, BRAF, PTEN, and ARID1A genes. Tumors of the second type are biologically aggressive; their prototype is high-grade serous carcinoma which displays distinct genetic instability and mutations in TP53, BRCA1, and BRCA2 genes. Ovarian cancer is characterized by overexpressed EGFRs, VEGFRs, TGFBR1, PDGFRs, MET, IGF1R, LPAR2/3, NTRK2, WNT7A, and NOTCH3. Outcome effects: The overexpression of growth factor receptors causes the constitutive activation of AKT1 and mitogen-activated protein kinase (MAPK) signaling cascades leading to block of apoptosis, loss of differentiation, hyperplastic growth, and migration of ovarian epithelial cells. Specifically, the overexpression of TGFBR1 activates SMAD2/3/4 complex involved in cell proliferation. The constitutive activation of NOTCH signaling leads to loss of differentiation and hyperplastic growth of ovarian epithelial cells. The overexpression of WNT triggers the constitutive activation of WNT/CTNNB1 signaling pathway resulting in loss of differentiation, redundant cell proliferation, and migration. Mutations in the BRCA1 and BRCA2 genes lead to block of DNA repair. Mutations in the BRAF, HRAS, and KRAS genes result in the activation of ERK (MAPK1/3) signaling pathway inducing genes involved in cell proliferation and migration. Mutations in PTEN cause the activation of AKT1 signaling, and mutations in ARID1A result in the dysfunction of chromatin remodeling. Highlighted proteins: Proteins with increased expression or activity are highlighted in red. Mutated genes: Mutated genes are shown in white-out style. |
|
| ID |
urn:agi-pathway:uuid-4bf6545c-9f11-4bf6-806b-b7edb940b1d2 |
|
| database_cross_reference |
PS:PathwayType PS:Description PS:Tissue PS:Pathway_Author PS:Link PS:CellType PS:Organ_System PS:PMID PS:NodeType PS:Notes PS:Organ PS:Source |
|
| has_exact_synonym |
PathwayType: signaling CellType: cancer cell PMID: 21347793 PMID: 19461510 CellType: epithelial cell PMID: 19221485 Tissue: epithelium PMID: 22987944 Organ: ovary Organ_System: reproductive system PMID: 17204312 PMID: 18317228 NodeType: Pathway PMID: 22525820 Description: Ovarian cancer (OC) is the most common cause of cancer death. Pathway is built manually using published studies. Pathway_Author: M. Zharkova ORCID:0000-0001-8706-9411 Source: Diseases Notes: Headnote: Ovarian cancer is the second most common malignancy among the gynecological cancers and the most common cause of cancer death, yet the etiology of ovarian malignant transformation remains poorly understood. Different types of ovarian cancer include serous, mucinous, endometrioid, clear cell, undifferentiated, and unclassifiable. Serous epithelial ovarian carcinoma is the most common type of ovarian cancer. High-grade and low-grade serous ovarian carcinomas are considered to have a different origin. The crucial pathogenic processes involved in the emergence of ovarian tumors, regardless of hyperestrogenism, are hormone-independent cell proliferation, block of apoptosis, cell invasion, dysfunction of DNA repair, and loss of cell differentiation. Signaling description: Different histotypes of ovarian cancer are formed by common mechanisms of malignization, but have different causes. According to genetic classification, there exist two groups of ovarian tumors. Tumors of the first type which include variable mucinous, endometrioid, clear cell carcinoma, and low-grade serous carcinoma are rather genetically stable and characterized by mutations in the KRAS, HRAS, BRAF, PTEN, and ARID1A genes. Tumors of the second type are biologically aggressive; their prototype is high-grade serous carcinoma which displays distinct genetic instability and mutations in TP53, BRCA1, and BRCA2 genes. Ovarian cancer is characterized by overexpressed EGFRs, VEGFRs, TGFBR1, PDGFRs, MET, IGF1R, LPAR2/3, NTRK2, WNT7A, and NOTCH3. Outcome effects: The overexpression of growth factor receptors causes the constitutive activation of AKT1 and mitogen-activated protein kinase (MAPK) signaling cascades leading to block of apoptosis, loss of differentiation, hyperplastic growth, and migration of ovarian epithelial cells. Specifically, the overexpression of TGFBR1 activates SMAD2/3/4 complex involved in cell proliferation. The constitutive activation of NOTCH signaling leads to loss of differentiation and hyperplastic growth of ovarian epithelial cells. The overexpression of WNT triggers the constitutive activation of WNT/CTNNB1 signaling pathway resulting in loss of differentiation, redundant cell proliferation, and migration. Mutations in the BRCA1 and BRCA2 genes lead to block of DNA repair. Mutations in the BRAF, HRAS, and KRAS genes result in the activation of ERK (MAPK1/3) signaling pathway inducing genes involved in cell proliferation and migration. Mutations in PTEN cause the activation of AKT1 signaling, and mutations in ARID1A result in the dysfunction of chromatin remodeling. Highlighted proteins: Proteins with increased expression or activity are highlighted in red. Mutated genes: Mutated genes are shown in white-out style. |
|
| id |
urn:agi-pathway:uuid-4bf6545c-9f11-4bf6-806b-b7edb940b1d2 |
|
| label |
Ovarian Cancer |
|
| notation |
uuid-4bf6545c-9f11-4bf6-806b-b7edb940b1d2 |
|
| prefLabel |
Ovarian Cancer |
|
| treeView |
urn:agi-folder:reproductive_system urn:agi-folder:o urn:agi-folder:ovarian_cancer urn:agi-folder:epithelium |
|
| subClassOf |
urn:agi-folder:reproductive_system urn:agi-folder:o urn:agi-folder:ovarian_cancer urn:agi-folder:epithelium |