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2. Loss of enteric neuronal Ndrg4 promotes colorectal cancer via increased release of Nid1 and Fbln2

3. Lack of evidence for a causal role of CALR3 in monogenic cardiomyopathy

4. Loss of LMOD1 impairs smooth muscle cytocontractility and causes megacystis microcolon intestinal hypoperistalsis syndrome in humans and mice

5. The long Filamin-A isoform is required for intestinal development and motility:implications for chronic intestinal pseudo-obstruction

6. The long Filamin-A isoform is required for intestinal development and motility: implications for chronic intestinal pseudo-obstruction

7. TFAP2B Haploinsufficiency Impacts Gastrointestinal Function and Leads to Pediatric Intestinal Pseudo-obstruction

11. Corrigendum: TALPID3/KIAA0586 Regulates Multiple Aspects of Neuromuscular Patterning During Gastrointestinal Development in Animal Models and Human

13. TALPID3/KIAA0586 Regulates Multiple Aspects of Neuromuscular Patterning During Gastrointestinal Development in Animal Models and Human

14. The Somatic Mutation Paradigm in Congenital Malformations: Hirschsprung Disease as a Model

16. New Target Genes in Endometrial Tumors Show a Role for the Estrogen-Receptor Pathway in Microsatellite-Unstable Cancers

18. Re: Role of the Oxidative DNA Damage Repair Gene OGG1 in Colorectal Tumorigenesis

19. Size matters: Large copy number losses in Hirschsprung disease patients reveal genes involved in enteric nervous system development

21. MUTYH and the mismatch repair system: partners in crime?

24. The Human Leukocyte Antigen Region and Colorectal Cancer Risk

28. Candidate driver genes in microsatellite-unstable colorectal cancer

36. Goldberg–Shprintzen syndrome is determined by the absence, or reduced expression levels, of KIFBP

38. Infantile hypertrophic pyloric stenosis in patients with esophageal atresia

45. Exome chip association study excluded the involvement of rare coding variants with large effect sizes in the etiology of anorectal malformations

50. Three-step site-directed mutagenesis screen identifies pathogenic MLH1 variants associated with Lynch syndrome.

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