Immunoexpression of SALL4 in Wilms Tumors and Developing Kidney
暂无分享,去创建一个
[1] Yan Peng,et al. Diagnostic Utility of Novel Stem Cell Markers SALL4, OCT4, NANOG, SOX2, UTF1, and TCL1 in Primary Mediastinal Germ Cell Tumors , 2010, The American journal of surgical pathology.
[2] M. Fukayama,et al. SALL4 Represents Fetal Gut Differentiation of Gastric Cancer, and is Diagnostically Useful in Distinguishing Hepatoid Gastric Carcinoma From Hepatocellular Carcinoma , 2010, The American journal of surgical pathology.
[3] D. Rakheja,et al. Diagnostic utility of SALL4 in primary germ cell tumors of the central nervous system: a study of 77 cases , 2009, Modern Pathology.
[4] T. Shen,et al. Overexpression of the novel oncogene SALL4 and activation of the Wnt/beta-catenin pathway in myelodysplastic syndromes. , 2009, Cancer genetics and cytogenetics.
[5] D. Rakheja,et al. Diagnostic Utility of SALL4 in Extragonadal Yolk Sac Tumors: An Immunohistochemical Study of 59 Cases With Comparison to Placental-like Alkaline Phosphatase, Alpha-fetoprotein, and Glypican-3 , 2009, The American journal of surgical pathology.
[6] H. Ben‐Hur,et al. Expression of Stem Cell Markers in the Human Fetal Kidney , 2009, PloS one.
[7] N. Amariglio,et al. Developmental tumourigenesis: NCAM as a putative marker for the malignant renal stem/progenitor cell population , 2009, Journal of cellular and molecular medicine.
[8] P. Humphrey,et al. SALL4 Is a Novel Diagnostic Marker for Testicular Germ Cell Tumors , 2009, The American journal of surgical pathology.
[9] P. Humphrey,et al. SALL4 is a novel sensitive and specific marker for metastatic germ cell tumors, with particular utility in detection of metastatic yolk sac tumors , 2009, Cancer.
[10] Yan Peng,et al. SALL4 Is a Novel Sensitive and Specific Marker of Ovarian Primitive Germ Cell Tumors and Is Particularly Useful in Distinguishing Yolk Sac Tumor From Clear Cell Carcinoma , 2009, The American journal of surgical pathology.
[11] Ha-won Jeong,et al. Stem Cell Factor SALL4 Represses the Transcriptions of PTEN and SALL1 through an Epigenetic Repressor Complex , 2009, PloS one.
[12] Li Chai,et al. Genome-wide analysis reveals Sall4 to be a major regulator of pluripotency in murine-embryonic stem cells , 2008, Proceedings of the National Academy of Sciences.
[13] L. Fink,et al. SALL4 is a key regulator of survival and apoptosis in human leukemic cells. , 2008, Blood.
[14] G. Rechavi,et al. Accumulation of Malignant Renal Stem Cells Is Associated with Epigenetic Changes in Normal Renal Progenitor Genes , 2008, Stem cells.
[15] I. Paradisi,et al. IVIC syndrome Is caused by a c.2607delA mutation in the SALL4 locus , 2007, American journal of medical genetics. Part A.
[16] Yupo Ma,et al. Differential expression of the novel oncogene, SALL4, in lymphoma, plasma cell myeloma, and acute lymphoblastic leukemia , 2006, Modern Pathology.
[17] J. Ritz,et al. SALL4, a novel oncogene, is constitutively expressed in human acute myeloid leukemia (AML) and induces AML in transgenic mice. , 2006, Blood.
[18] Li Chai,et al. Sall4 modulates embryonic stem cell pluripotency and early embryonic development by the transcriptional regulation of Pou5f1 , 2006, Nature Cell Biology.
[19] H. Aburatani,et al. The murine homolog of SALL4, a causative gene in Okihiro syndrome, is essential for embryonic stem cell proliferation, and cooperates with Sall1 in anorectal, heart, brain and kidney development , 2006, Development.
[20] Yupo Ma,et al. Transcriptional Activation of the SALL1 by the Human SIX1 Homeodomain during Kidney Development* , 2006, Journal of Biological Chemistry.
[21] J. Kohlhase,et al. A family with features overlapping Okihiro syndrome, hemifacial microsomia and isolated Duane anomaly caused by a novel SALL4 mutation , 2006, American journal of medical genetics. Part A.
[22] A. Amoroso,et al. A SALL4 zinc finger missense mutation predicted to result in increased DNA binding affinity is associated with cranial midline defects and mild features of Okihiro syndrome , 2006, Human Genetics.
[23] D. Chitayat,et al. SALL4 mutations in Okihiro syndrome (Duane‐radial ray syndrome), acro‐renal‐ocular syndrome, and related disorders , 2005, Human mutation.
[24] W. Reardon,et al. SALL4 deletions are a common cause of Okihiro and acro-renal-ocular syndromes and confirm haploinsufficiency as the pathogenic mechanism , 2004, Journal of Medical Genetics.
[25] R. Hennekam,et al. Novel mutations in the gene SALL4 provide further evidence for acro-renal-ocular and Okihiro syndromes being allelic entities, and extend the phenotypic spectrum , 2004, Journal of Medical Genetics.
[26] W. Reardon,et al. Mutations at the SALL4 locus on chromosome 20 result in a range of clinically overlapping phenotypes, including Okihiro syndrome, Holt-Oram syndrome, acro-renal-ocular syndrome, and patients previously reported to represent thalidomide embryopathy , 2003, Journal of medical genetics.
[27] W. Reardon,et al. Okihiro syndrome is caused by SALL4 mutations. , 2002, Human molecular genetics.
[28] C. St. Hilaire,et al. Duane radial ray syndrome (Okihiro syndrome) maps to 20q13 and results from mutations in SALL4, a new member of the SAL family. , 2002, American journal of human genetics.
[29] Yupo Ma,et al. Hsal 1 is related to kidney and gonad development and is expressed in Wilms tumor , 2001, Pediatric Nephrology.
[30] W. Reardon,et al. Molecular analysis of SALL1 mutations in Townes-Brocks syndrome. , 1999, American journal of human genetics.
[31] H. Jäckle,et al. spalt encodes an evolutionarily conserved zinc finger protein of novel structure which provides homeotic gene function in the head and tail region of the Drosophila embryo. , 1994, The EMBO journal.
[32] K. Nakano,et al. Duane Syndrome and Congenital Upper-Limb Anomalies: A Familial Occurrence , 1977 .
[33] W. Engel,et al. Mutations in the SALL1 putative transcription factor gene cause Townes-Brocks syndrome , 1998, Nature Genetics.