Treatment modalities for allergic reactions in pigmented tattoos.

Decorative tattoos have become very popular. As a result, a higher number of hypersensitivity reactions are seen, caused by the mostly undeclared tattoo dyes. If local and intralesional therapy with corticosteroids is not effective, total excision was formerly considered the best approach. Selective laser therapy offers an alternative approach for removing the offending pigment. Case reports are used to illustrate the individual treatment options for removal of tattoos.

Hereditary lattice corneal dystrophy is associated with corneal amyloid deposits enclosing C-terminal fragments of keratoepithelin.

PURPOSE: To investigate the molecular basis of hereditary lattice corneal dystrophy (LCD) type IIIA associated with corneal amyloid deposits afflicting several members of a four-generation family. METHODS: Histologic, immunohistochemical and biochemical studies were performed on corneal tissue samples obtained after perforating keratoplasty. DNA was extracted from peripheral blood leukocytes. All exons of the keratoepithelin-encoding TGFBI gene were amplified and sequenced. The presence of a mutation was confirmed by digestion of the isolated PCR product with the restriction enzyme AlwNI. RESULTS: The cornea of the index patient (II-1) contained large patchy deposits of amyloid, which were immunoreactive for the C terminus of keratoepithelin. Western blot analysis of the polypeptide chains extracted from the amyloid deposits of paraffin-embedded tissue revealed that these represented mainly fragments of the full-length protein. The smallest fragments were 6.5 and 6.9 kDa. DNA analyses of the TGFBI gene revealed a heterozygous T-->C transition at the second position of codon 540 in exon 12, indicating that replacement of phenylalanine by serine (Phe540Ser) leads to dominant disease. The mutation creates a new restriction site for the enzyme AlwNI. Five of the examined family members carried this mutation. Three of them (aged >/=41 years) had the disease, two family members (aged <20 years) do not yet show any clinical symptoms. An additional inconsequential single-nucleotide polymorphism (T1667C) was found at the third position of the same codon (Phe540Phe) in three unaffected family members. CONCLUSIONS: This is the first report of a single-nucleotide mutation at codon 540 of TGFBI leading to LCD, and the first to demonstrate that the amyloid deposits in LCD contain proteolytic fragments of keratoepithelin.

HER2 protein overexpression and gene amplification in upper urinary tract transitional cell carcinoma: systematic analysis applying tissue microarray technique.

OBJECTIVES: To investigate HER2 (c-erbB-2) protein overexpression and HER2 gene amplification in upper urinary tract transitional cell carcinoma (TCC) with respect to its association with tumor grade and stage, as well as the prognostic significance. METHODS: A total of 53 consecutive TCC specimens were analyzed immunohistochemically (HercepTest) and with fluorescence in situ hybridization applying a tissue microarray technique. RESULTS: Overall, HER2 immunoreactivity (expression) was detected in 28 of 53 TCC specimens and tended to be stronger in high-stage (8 [36%] of 22 pT1 versus 20 [65%] of 31 pT2-T3; P = 0.06) and high-grade (11 [39%] of 28 low-grade versus 17 [68%] of 25 high-grade; P = 0.054) tumors. Weak overexpression (HercepTest score 2+) was seen in 9 cases (17%) and was associated with angioinvasion (P = 0.02) and had independent prognostic significance with respect to metastasis-free survival (risk ratio 9.6; P = 0.03). Low HER2 amplification was present in four TCC specimens (9%), with HER2/chromosome 17 ratios of 2.03, 2.77, 2.91, and 3.39, and polysomy of chromosome 17 was present in another 3 cases (7%). HER2 amplification and/or polysomy of chromosome 17 prevailed in high-stage (0 [0%] of 20 pT1 versus 7 [27%] of 26 pT2-T3; P = 0.01) and high-grade (1 [4%] of 24 low-grade versus 6 [27%] of 22 high-grade; P = 0.04) tumors, but lacked independent prognostic significance. Of nine TCC specimens with weak HER2 overexpression (HercepTest score 2+), 3 (33%) showed low HER2 amplification and two others had polysomy of chromosome 17. CONCLUSIONS: HER2 overexpression and HER2 gene amplification were infrequent in our series. Thus, only a small number of patients with upper urinary tract TCC might benefit from HER2-targeted (Herceptin) cancer therapy.

HER2 status in non-small cell lung cancer: results from patient screening for enrollment to a phase II study of herceptin.

PURPOSE: For the first time a large number (563) of non-small cell lung cancer (NSCLC) samples was used to compare three different technologies for the assessment of HER2 status. Fluorescence in situ hybridization (FISH) and immunohistochemistry (IHC) were used for tumor tissue samples, and ELISA for serum samples. The results were compared with other tumor entities, mainly breast. EXPERIMENTAL DESIGN: Samples (563) from patients suffering from primary advanced or metastatic NSCLC were evaluated. RESULTS: HER2 overexpression was demonstrated using IHC in 20% (83 of 410) of the specimens, whereas 2% (7 of 378) were positive by FISH and 6% (31 of 511) showed elevated serum HER2 levels (>15 ng/ml) by ELISA. Sixty-six specimens were positive by IHC only and 13 by ELISA only, whereas none of the specimens was positive only by FISH. Concordance between all of the techniques was seen for only 3 specimens. Of 7 IHC 3+ specimens, 4 showed gene amplification by FISH, and 3 were positive by ELISA (>15 ng/ml), whereas of 76 IHC 2+ cases only 2 were amplified by FISH, and 4 were positive by ELISA. HER2 positivity by at least one of the three techniques was most common in adenocarcinomas, at 29% (42 of 143). CONCLUSION: Gene amplification and HER2 protein overexpression at the 3+ level appear to be uncommon in NSCLC. The concordance between FISH and IHC 3+ disease was good in this study, in addition, ELISA would have detected several patients without IHC/FISH-positive disease.