Between the paired primary tumour and distant metastatic lesions, 94% and 93% of samples had concordant HER-2 status when analysed by IHC or FISH, respectively. These results do not support routine determination of HER-2 on metastatic sites, particularly when FISH results from the primary tumour are available.

Overexpression and amplification of the HER-2 oncogene in patients with breast cancer has correlated with early onset of metastasis, resistance to hormonal therapy and some forms of chemotherapy, and shortened survival. Therefore, evaluation of this putative prognostic or predictive factor seems critical. Because different antibodies are used for the detection of the 185-kd HER-2 oncoprotein, we studied the sensitivity of 3 frequently used antibodies. Immunohistochemistry results were correlated with gene amplification level as assessed by fluorescence in situ hybridization. Protein overexpression was found in 17.2% and 12.5% of cases using antibodies against the external (TAB250) and internal (CB11) domains of the protein, respectively, and in 38.0% of cases using a rabbit polyclonal antibody. Fluorescence in situ hybridization was successful in all 160 tumors, and amplification was found in 37 tumors (23.1%). The monoclonal antibody TAB250 had the lowest misclassification rate, 9.6% (sensitivity, 67%; specificity, 97.5%).

No abstract

The MaTu interval (MN)/carbonic anhydrase (CA) IX tumour‐associated antigen is a protein that is normally expressed in the gut and belongs to the carbonic anhydrase enzyme family (CA IX). It has been detected in tumour cell lines and in some solid tumours including cervical, oesophageal and clear cell renal carcinoma. This study determined MN/CA IX expression in 65 primary non‐small cell lung cancer resected with curative intent and in 38 bronchial preneoplastic lesions, carcinoma in situ or microinvasive carcinoma as well as in normal bronchial tissue. The presence of MN/CA IX was detected using immunohistochemistry and Western blot analysis, whenever frozen material was available. Immunostaining was positive in 52/65 (80%) of the tumour samples. The staining was more often focal than diffuse. The percentage of stained cells in positive tumours was highly variable, ranging 1–85%. The pattern of immunostaining was predominantly cytoplasmic with a membranous reinforcement (87%). The intensity was mainly strong (69%). The presence of the protein in the tumour was confirmed by Western blot analysis in the eight samples tested. All the morphologically normal epithelia, except in close vicinity of tumours in some cases, as well as the preneoplastic bronchial lesions (basal cell hyperplasia, metaplasia and dysplasia) were immunonegative for MN/CA IX expression. In contrast, carcinoma in situ and microinvasive epithelioma showed the presence of MN‐immunopositive tumoural cells in 5/7 and 4/5 of the samples, respectively. These data suggest that MN/CA IX is a useful marker for the differentiation between preneoplastic lesions and bronchial non‐small cell lung cancer in the lung.

Cytogenetic study of five biphasic and five monophasic synovial sarcomas revealed the specific abnormality t(X;18) (p11;q11) in eight cases and t(X;15;18) (p11;q15;q11) and t(X;7) (q11-12;q32) in one case each. Additional, secondary aberrations were present in eight of these tumors. By combining our data with information on previously published cytogenetically abnormal synovial sarcomas, we were able to evaluate 32 tumor samples from 29 patients. The modal chromosome number was pseudodiploid or near diploid in 26 of the 32 tumors. A t(X;18) was present in 21 of 29 cases (72%). Complex translocations involving chromosomes X and 18 and another autosome were present in five cases, and one displayed a t(5;18). There was no visible rearrangement of chromosome bands Xp11 or 18q11 in only 2 of the 32 synovial sarcomas. Half of the primary tumors (6 of 12) had the X;18-translocation as the sole abnormality. Of the remaining 20 specimens from recurrent or metastatic tumors (in three cases two tumors could be analyzed), only one had t(X;18) as the sole change. The secondary aberrations in cases exhibiting clonal evolution were also generally more extensive in the metastatic and recurrent than in the primary sarcomas (five additional aberrations per case, compared with two). Chromosomes 1 and 12 were the chromosomes most frequently (one fourth of the cases) involved in additional structural changes, but with several different breakpoints. No differences were identified between the karyotypic profiles of monophasic and biphasic synovial sarcomas.