China
Africa
Explore chapters and articles related to this topic
Prostate Development: Mechanisms for Opposite Effects of Low and High Doses of Estrogenic Chemicals
Published in Rajesh K. Naz, Endocrine Disruptors, 2004
Catherine A. Richter, Barry G. Timms, Frederick S. vom Saal
Development of the prostate begins with outgrowths (glandular buds) of the urothelium lining the lumen of the UGS. The first detectable molecular event in prostate development is the expression of the homeobox gene Nkx3.1 in UGS epithelium, which precedes formation of epithelial buds. Nkx3.1 expression is dependent on activity of the sonic hedgehog (Shh) gene. The homeobox transcription factors HoxA10, HoxA13, and HoxD13 are also required for prostate development.21
Embryology of the Female Urogenital System and Clinical Applications
Published in Linda Cardozo, Staskin David, Textbook of Female Urology and Urogynecology - Two-Volume Set, 2017
trAnscription fActors PAx2, PAx8, Lim1, emx2, HoxA13, And DAch1 plAy A mAjor role in MülleriAn development. In Lim1null mice, ovAriAn development still occurs but the femAle neonAtes lAck uteri And fAllopiAn tubes [13]. other signAling molecules Are postulAted to be required for normAl MülleriAn development such As Wnt9b And Wnt4, which Act viA A pArAcrine mechAnism [14] And retinoic Acid [15]. Despite these findings in murine models, A study of 25 women Affected by the MAyer–rokitAnsky–Kuster–HAuser syndrome, chArActerized by vArying degrees of uterine duplicAtion or Agenesis And renAl findings, fAiled to support the role of Wnt4 And the retinoic Acid receptor pAthwAys [16]. These discrepAncies between experimentAl And clinicAl observAtions Are not surprising, becAuse the genetic deletion in the mouse often tArgets the first step in A long complex cAscAde, whereAs clinicAl syndromes mAy hAve defects much fArther Along in the sAme pAthwAys. by week 6, the MülleriAn ducts form from the intermediAte mesoderm locAted lAterAlly to the WolffiAn ducts And develop Along the Anterior–posterior Axis of the embryo. LineAge trAcing experiments in chicks And mice reveAl thAt these ducts Are All derived from different populAtions of coelomic epithelium without Any direct cellulAr contribution from the AdjAcent WolffiAn ducts [17]. Although cells derived from the WolffiAn duct do not contribute to the MülleriAn duct, cell–cell signAling between these ducts mediAted by Wnt9b And Wnt4 induces MülleriAn development. Indeed, close contAct with the WolffiAn duct is necessAry for MülleriAn duct elongAtion [18]. The MülleriAn ducts begin As solid cords thAt likely tubulArize on the bAsis of Apoptosis during their differentiAtion. ProximAl pArts of these ducts form the fAllopiAn tubes; distAlly, they fuse in the midline producing the uterus, cervix, And proximAl two-thirds of the vAginA [19]. by week 7, the cAudAl ends of the MülleriAn ducts migrAte through the urorectAl septum to penetrAte the posterior Aspect of the urethrA [20] At the MülleriAn tubercle between the two openings of the WolffiAn ducts (Figure 22.5A) [19]. The urethrA And MülleriAn structures
Current and emerging bladder cancer biomarkers with an emphasis on urine biomarkers
Published in Expert Review of Molecular Diagnostics, 2020
Antonio Lopez-Beltran, Liang Cheng, Thomas Gevaert, Ana Blanca, Alessia Cimadamore, Matteo Santoni, Francesco Massari, Marina Scarpelli, Maria R. Raspollini, Rodolfo Montironi
Cxbladder is a family of noninvasive molecular diagnostic laboratory tests optimized to assess the probability of having bladder cancer through urine analysis [105]. The test is messenger RNA based and predicts a patient’s probability of bladder cancer by measuring the following five genetic biomarkers related to bladder cancer: MDK, which affects migration and angiogenesis in cancer cellsHOXA13, which affects cell differentiationCDC2 (CDK1), which is essential to complete the cell cycle and cell proliferationIGFBP5, which inhibits apoptosisCXCR2 which is relevant to avoid inflammation related false positives.
Mutational landscape of patients with acute myeloid leukemia or myelodysplastic syndromes in the context of RUNX1 mutation
Published in Hematology, 2020
Kai Wang, Feng Zhou, Xiaohui Cai, Hongying Chao, Ri Zhang, Suning Chen
The cDNA synthesis and multiple RT–PCR were conducted by using SureFireRTTM Kit (Promega, USA) (AIBOJIN, Cat#06-104) and Leukemia Related Fusion Gene Detection Kit (YUANQI BIO), respectively. Multiple RT–PCR amplification was performed as 8 parallel multiplex reactions on 7500 Real-time PCR System (Applied Biosystems). Leukemia Related Fusion Gene Detection Kit included 41 gene fusions (BCR-ABL, SIL-TAL1, E2A-HIF, TEL-AML1, MLL-AF4, E2A-PBX1, AML1-ETO, MLL-AF9, PML-RARα, MLL-(AF6, AF10, ELL, ENL), PLZF-RARα, STAT5b-RARα, NPM-MLF1, TEL-PDGFRB, PIP1L1-PDGFRA, AML-MDS1/EVI1, AML1-MTG16, CBFβ-MYH11, DEK-CAN, TEL-ABL, ETV6-PDGFRA, NUP98-(HoxA13, HoxC11, HoxD13, HoxA9, HoxA11, PMX1), TEL-JAK2, MLL-(AF17, AF1q, AF1p, AFX, SEPT6), (NPM, FIP1L1, PRKAR1A, NUMA1)-RARα).
Competing endogenous RNA networks in cervical cancer: function, mechanism and perspective
Published in Journal of Drug Targeting, 2019
lncRNA XLOC_006390 was also called lncRNA HOXA13 [33]. LncXLOC_006390 was proved to increase in cervical cancer tissues and patients with high XLOC_006390 expression was associated with advanced FIGO stages, lymphatic metastasis and distant metastasis. And then, they tested the expression of SET8 in cervical cancer tissues. SET8 also called PR-Set7/9, KMT5A or SETD8, is one of the SET domain-containing methyltransferases that specifically targets histone H4 lysine 20 (H4K20) for monomethylation, and which exerts diverse biological processes, including activation or silencing of gene transcription, maintaining chromosome structure and stability, regulating the cell cycle and preventing premature chromatin compaction in the S phase, and rescuing and degrading DNA damage. The results indicated SET8 was also increased in cervical cancer tissues and its expression was positively associated with XLOC_006390. The experiments in vitro suggested that lncRNA XLOC_006390 promotes cervical cancer cell growth and metastasis through the regulation of SET8 [34].