TROP-2 can be considered a useful marker for distinguishing papillary thyroid carcinoma follicular variant cases from follicular nodular disease and follicular adenoma cases because of its high sensitivity in the identification of papillary carcinomas of the thyroid.
we compared the diagnostic value of TROP-2 expression in distinguishing between benign and malignant thyroid lesions to those of HBME-1 CK19 and galectin-3
TROP-2 membranous staining is a very sensitive and specific marker for the classic and tall cell variants of papillary thyroid carcinoma and for papillary microcarcinomas with high overall specificity for papillary thyroid carcinoma
We identified a homozygous TACSTD2 missense mutation c.551A>G p.(Tyr184Cys) in the affected family members. Both parents were heterozygous for the mutation and unaffected siblings were either heterozygous or homozygous wild-type for this allele.
findings demonstrate that a membranous TROP-2 staining pattern is highly specific for PTC which may serve as a potential diagnostic marker aiding in the accurate classification of morphologically equivocal thyroid follicular-patterned lesions
The amino acid exchange resulting from 4461T[C does not appear to alter binding of HO-3 suggesting that treatment with catumaxomab can be offered to patients regardless of their TACSTD1-genotype.
Two novel mutations of TACSTD2 are found in three Japanese gelatinous drop-like corneal dystrophy families with their aberrant subcellular localization.
Genetic analysis revealed that all the patients possessed a homozygous Q118X mutation in TACSTD2 a major founder mutation in Japanese gelatinous drop-like corneal dystrophy.
The chimeric mRNA is a bicistronic transcript of post transcriptional origin that independently translates the Cyclin D1 and Trop-2 proteins in cancer cells.
Although mutations in TACSTD2 among Iranian patients with GDLD were heterogeneous E227K was found to be a common mutation. It is suggested that E227K may be a founder mutation in this population
It is concluded that Gelatinous Drop-like Corneal Dystrophy (GDLD) in the pedigree is probably not caused by mutations in TACSTD2 supporting evidence for the existence of at least one other locus for GDLD.
study reports two novel mutations in two gelatinous drop-like corneal dystrophy families and expands the spectrum of mutations in TACSTD2 gene that may cause pathological corneal amyloidosis
Newly identified mutation is predicted to generate shortened protein product thereby completely altering COOH-terminal region and deleting transmembrane domain required for anchoring at cell membranes and phosphatidylinosyol2-binding site.
The affected members had compound heterozygous mutations consisting of a nonsense change at codon 84 (K84X) and a missense mutation resulting in a substitution of arginine for cysteine at codon 108 (C108R).
Because the compound heterozygote mutations Q118X and Y184C cosegregated with the phenotype they are likely the cause of GDLD (gelatinous droplike corneal dystrophy) in this patient.
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