Disease relevance of MYP2

• Refinement of the region by transmission disequilibrium testing suggests that a candidate gene (or genes) for this locus named myopia 2 (MYP2) is likely in an interval between markers D18S63 and D18S52 [1].
• Verteporfin therapy of subfoveal choroidal neovascularization in pathologic myopia: 2-year results of a randomized clinical trial--VIP report no. 3 [2].
• A preliminary study of photodynamic therapy using verteporfin for choroidal neovascularization in pathologic myopia, ocular histoplasmosis syndrome, angioid streaks, and idiopathic causes [3].
• Two hundred nine macular holes of both pathologic myopia and idiopathic senile type were statistically analyzed to find out which factors cause retinal detachment in eyes with macular holes [4].
• Macular retinoschisis with stellate foveal appearance may rarely be associated with pathologic myopia [5].

High impact information on MYP2

• The purpose of this study was to determine whether DNA sequence variants in the human TGIF gene are causally related to MYP2-associated high myopia [6].
• METHODS: The protein coding regions and intron-exon boundaries of the human TGIF gene were sequenced using genomic DNA samples from MYP2 individuals (affected, unaffected) and external control subjects [6].
• Although LPIN2 gene was excluded as a candidate for MYP2, the SNPs detected in this study will aid in future mapping and association studies involving this gene [1].
• Visudyne (verteporfin for injection), Novartis Ophthalmics, is FDA approved for the treatment of patients with predominantly classic subfoveal choroidal neovascularization due to age-related macular degeneration, pathologic myopia or presumed ocular histoplasmosis [7].
• Physiologic vs pathologic myopia: genetics vs environment [8].

Biological context of MYP2

• Recently, the transforming growth beta-induced factor (TGIF) gene was reported to be a candidate gene for MYP2-associated high myopia in single-nucleotide polymorphism studies [6].
• Mutation analysis of the encoded TGIF gene for MYP2 autosomal dominant high myopia did not identify sequence alterations associated with the disease phenotype [6].
• A genomic interval of 2.2 centiMorgans (cM) was defined on chromosome band 18p11.31 using 7 families diagnosed with autosomal dominant high myopia and was designated the MYP2 locus [9].
• Further refinement of the MYP2 locus for autosomal dominant high myopia by linkage disequilibrium analysis [10].
• METHODS: A physical map of a contracted MYP2 interval was compiled, and gene expression studies in ocular tissues using complementary DNA library screens, microarray matches, and reverse-transcription techniques aided in prioritizing gene selection for screening [11].

Anatomical context of MYP2

• BACKGROUND: Lacquer crack lesion (LCL) is a complication of human pathologic myopia, accompanied by loss of retinal pigment epithelium (RPE) and break of Bruch's membrane [12].
• Four of the patients with pathologic myopia had corneal dystrophy that was bilaterally manifest as white opacities in the posterior stroma near Descemet's membrane in an axial distribution; 1 of these 4 patients also had a tilted disc [13].
• CONCLUSIONS: Peripapillary detachment in pathologic myopia is an asymptomatic, yellow-orange peripapillary detachment of the retinal pigment epithelium and retina in pathologic myopia [14].
• RESULTS: With these methods, retrobulbar vessels could be observed in the eyes of these patients with pathologic myopia and thin sclera [15].
• RESULTS: Choroidal neovascular membranes were removed at 3 days (presumed ocular histoplasmosis), 29 days (punctate inner choroiditis), 63 days (AMD, pathologic myopia), 66 days (AMD), 107 days (pathologic myopia), 116 days (AMD), and 152 days (idiopathic) after verteporfin ocular photodynamic therapy [16].

Associations of MYP2 with chemical compounds

• METHOD: In the setting of a tertiary referral center, patients with pathologic myopia in whom fluorescein and conventional ICG angiography demonstrated distinct CNV vessels supplying the subfoveal neovascular complex were submitted to focal ingrowth site treatment using a new therapeutic modality termed ICG-mediated photothrombosis [17].
• The authors performed a prospective study of 36 eyes affected by pathologic myopia with macular subretinal neovascularization (SRNV) successfully treated with either argon green, dye orange (590 nm), or krypton red lasers [18].

Other interactions of MYP2

• Photodynamic Therapy vs Limited Macular Translocation in the Management of Subfoveal Choroidal Neovascularization in Pathologic Myopia: A Two-year Study [19].
• Prolidase deficiency associated with pathologic myopia [20].
• Outer retinal diseases include age-related macular degeneration, pathologic myopia, and retinitis pigmentosa [21].

Analytical, diagnostic and therapeutic context of MYP2

• Laser photocoagulation for choroidal neovascularisation in pathologic myopia [22].
• Optical coherence tomography after photodynamic therapy for patients with pathologic myopia [23].
• PATIENTS AND METHODS: The angiograms of all consecutive patients with pathologic myopia photographed with confocal indocyanine green angiography using a scanning infrared laser or ophthalmoscope from March 1997 to December 1999 were reviewed [24].
• Although the exact mechanism of the upper eyelid retraction in these two cases is unclear, previous retinal surgery that involves superiorly placed implants must be considered in the differential diagnosis of unilateral upper eyelid retraction, especially when the patient has a history of pathologic myopia [25].
• OBJECTIVE: A retrospective study was performed to establish the incidence of retinal detachment among 107 patients (165 eyes) with pathologic myopia who underwent clear-lens extraction [26].

References