Either Kras activation or Pten loss similarly enhance the dominant-stable CTNNB1-induced genetic program to promote granulosa cell tumor development in the ovary and testis.
about
Insights into granulosa cell tumors using spontaneous or genetically engineered mouse modelsUbiquitin E3 ligase CRL4(CDT2/DCAF2) as a potential chemotherapeutic target for ovarian surface epithelial cancerConstitutively active transforming growth factor β receptor 1 in the mouse ovary promotes tumorigenesisFOXO1/3 and PTEN Depletion in Granulosa Cells Promotes Ovarian Granulosa Cell Tumor Development.YAP regulates cell proliferation, migration, and steroidogenesis in adult granulosa cell tumors.Transforming growth factor alpha (TGFα) regulates granulosa cell tumor (GCT) cell proliferation and migration through activation of multiple pathways.Minireview: animal models and mechanisms of ovarian cancer development.Consequences of RAS and MAPK activation in the ovary: the good, the bad and the ugly.The Müllerian inhibiting substance type 2 receptor suppresses tumorigenesis in testes with sustained β-catenin signalingTechnical challenges and limitations of current mouse models of ovarian cancer.Long non-coding RNA profiling links subgroup classification of endometrioid endometrial carcinomas with trithorax and polycomb complex aberrations.MicroRNAs and Recent Insights into Pediatric Ovarian Cancers.SMAD3 Activation: A Converging Point of Dysregulated TGF-Beta Superfamily Signaling and Genetic Aberrations in Granulosa Cell Tumor Development?Proteomic analysis of exosomes from mutant KRAS colon cancer cells identifies intercellular transfer of mutant KRAS.Understanding follicle growth in vitro: Are we getting closer to obtaining mature oocytes from in vitro-grown follicles in human?β-Catenin directs the transformation of testis Sertoli cells to ovarian granulosa-like cells by inducing Foxl2 expression.MicroRNA 17-92 cluster regulates proliferation and differentiation of bovine granulosa cells by targeting PTEN and BMPR2 genes.Endogenous c-Jun N-terminal kinase (JNK) activity marks the boundary between normal and malignant granulosa cells.
P2860
Q26751012-01048FFA-8895-49C3-9FDF-081E44027BC5Q28674964-FD98B9E9-BEB1-47B7-B27D-80125AB69BB6Q30354729-924D6AEE-D7A1-493A-A717-9C2A8C71AE95Q30358011-5D8FAE17-1D8C-435E-9654-4C4913F4BEA4Q34463878-D686E000-7258-4201-9EF6-DA9144F6F53AQ34478979-1B285BA0-4CE7-4303-A362-01AB24F32B20Q35872732-8672088C-0D95-4F4E-94B1-5D67602D37DAQ35892495-205A5C2E-2960-4C78-B146-1DA87B170706Q36435768-143C6796-787B-4CE6-B655-69987BDCCF08Q36510070-C9D961BE-91F9-4596-B345-ACDF93EC7178Q36545494-8E3F34D0-3B91-45F3-BB0A-E900B36A6ED5Q36804155-CD60FD65-555F-4B7F-94A8-6EB71A43F703Q38967398-D273F6C0-9365-44BB-80C7-7912237D2EC8Q39242962-0CD9D51B-3804-4106-B151-36FD87FB41CFQ39269056-5D9E756E-C8C8-4439-A1BA-DAABDA3FBCE6Q47642166-113EF03F-73C4-4839-9CBD-30AAC3BBCE20Q50509742-FF6E3DB2-0AB8-4FEC-B905-F1953086CF16Q51739092-3F31EF6B-90F7-42AA-9514-C00BC3E29DAA
P2860
Either Kras activation or Pten loss similarly enhance the dominant-stable CTNNB1-induced genetic program to promote granulosa cell tumor development in the ovary and testis.
description
2011 nî lūn-bûn
@nan
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
2011年论文
@zh
2011年论文
@zh-cn
name
Either Kras activation or Pten ...... pment in the ovary and testis.
@ast
Either Kras activation or Pten ...... pment in the ovary and testis.
@en
type
label
Either Kras activation or Pten ...... pment in the ovary and testis.
@ast
Either Kras activation or Pten ...... pment in the ovary and testis.
@en
prefLabel
Either Kras activation or Pten ...... pment in the ovary and testis.
@ast
Either Kras activation or Pten ...... pment in the ovary and testis.
@en
P2093
P2860
P356
P1433
P1476
Either Kras activation or Pten ...... pment in the ovary and testis.
@en
P2093
D Boerboom
J S Richards
P2860
P2888
P304
P356
10.1038/ONC.2011.341
P407
P577
2011-08-22T00:00:00Z
P5875
P6179
1040691307