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  1. De novo interstitial deletion of 1q32.2-q32.3 including the entire IRF6 gene in a patient with oral cleft and other dysmorphic features
    Salahshourifar I, Halim AS, Sulaiman WA, Ariffin R, Naili Muhamad Nor N, Zilfalil BA
    Cytogenet Genome Res, 2011;134(2):83-7.
    PMID: 21447942 DOI: 10.1159/000325541
    Microdeletion of the Van der Woude syndrome (VWS) critical region is a relatively rare event, and only a few cases have been reported in the medical literature. The extent of the deletion and the genotype-phenotype correlation are 2 crucial issues.
    Matched MeSH terms: Cysts/genetics
  2. Fulltext Assessment of fragile histidine triad expression in ameloblastoma, odontogenic keratocyst and dentigerous cyst
    Haragannavar VC, Tegginamani AS, Raju S, Kudva S, Peter CD, Shruthi DK
    Indian J Pathol Microbiol, 2019 2 2;62(1):3-6.
    PMID: 30706851 DOI: 10.4103/IJPM.IJPM_403_18
    Background: FHIT (Fragile histidine triad) a member of tumor suppressor family, has been extensively studied in many solid tumors including head and neck squamous cell carcinoma. Among all head and neck cyst and tumors odontogenic lesions account approximately 3%-9%. The molecular pathogenesis of these lesions is less explored. Defects in cell cycle regulators and tumor suppressor genes could result in the development of odontogenic cyst and tumors. Hence, we aimed to determine the significant role of a tumor suppressor gene FHIT in most commonly occurring odontogenic lesions mainly ameloblastoma, odontogenic keratocyst and dentigerous cyst.

    Subjects and Methods: Immunohistochemical analysis of FHIT was done in ameloblastoma, odontogenic keratocyst, dentigerous cyst and dental follicle. Interpretation of the stained slides were done using standard scoring criteria by two pathologist. The results were subjected for statistical analysis.

    Results: Expression of FHIT varied among the groups, with highest negative expression in ameloblastoma 44.4% followed by odontogenic keratocyst 14% and 100%positive expression was seen in dentigerous cyst. The expression levels between the groups were statistically insignificant.

    Conclusion: The varied expression or negative expression of FHIT could be considered as an indicator for aggressive behavior and transformation of preneoplastic/cystic epithelium.

    Matched MeSH terms: Odontogenic Cysts/genetics*
  3. Fulltext The JCR:LA-cp rat: a novel rodent model of cystic medial necrosis
    Pung YF, Chilian WM, Bennett MR, Figg N, Kamarulzaman MH
    Am J Physiol Heart Circ Physiol, 2017 Mar 01;312(3):H541-H545.
    PMID: 27986661 DOI: 10.1152/ajpheart.00653.2016
    Although there are multiple rodent models of the metabolic syndrome, very few develop vascular complications. In contrast, the JCR:LA-cp rat develops both metabolic syndrome and early atherosclerosis in predisposed areas. However, the pathology of the normal vessel wall has not been described. We examined JCR:LA control (+/+) or cp/cp rats fed normal chow diet for 6 or 18 mo. JCR:LA-cp rats developed multiple features of advanced cystic medial necrosis including "cysts," increased collagen formation and proteoglycan deposition around cysts, apoptosis of vascular smooth muscle cells, and spotty medial calcification. These appearances began within 6 mo and were extensive by 18 mo. JCR:LA-cp rats had reduced medial cellularity, increased medial thickness, and vessel hypoxia that was most marked in the adventitia. In conclusion, the normal chow-fed JCR:LA-cp rat represents a novel rodent model of cystic medial necrosis, associated with multiple metabolic abnormalities, vascular smooth muscle cell apoptosis, and vessel hypoxia.NEW & NOTEWORTHY Triggers for cystic medial necrosis (CMN) have been difficult to study due to lack of animal models to recapitulate the pathologies seen in humans. Our study is the first description of CMN in the rat. Thus the JCR:LA-cp rat represents a useful model to investigate the underlying molecular changes leading to the development of CMN.
    Matched MeSH terms: Cysts/genetics*
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