Comparative genomic hybridization (CGH) was used to detect changes in relative chromosome copy number in 50 cases of peripheral nerve sheath tumour (PNSTs), including nine malignant peripheral nerve sheath tumours (MPNSTs), 27 neurofibromas (with three plexiform neurofibromas) and 14 schwannomas. Chromosome imbalances were frequently detected in benign as well as malignant PNSTs. In both NF1-associated and sporadic MPNSTs, the number of gains was higher than the number of losses, suggesting proto-oncogene activation during MPNST progression. NF1-asociated MPNSTs exhibited gains of chromosomes 17q and X (2/4 cases each), whereas sporadic MPNSTs showed gains of chromosome 4q (3/5 cases). On the other hand, in benign neurofibromas and schwannomas, the number of losses was higher than the number of gains, suggesting a predominant role of tumour suppressor genes in tumourigenesis. Both sporadic and NF1-associated neurofibromas exhibited losses at chromosome 22q in more than 50% of cases. These chromosomal regions may contain common chromosomal abnormalities characteristic of both types of neurofibromas. In NF1-associated neurofibromas, most frequent losses were found in chromosomes 17 [17p11.2-p13 in nine cases (60%); 17q24-25 in 6 cases (40%)] and 19 [19p13.2 in eight cases (53%); 19q13.2-qter in eight cases (53%)], whereas in sporadic neurofibromas and schwannomas losses of chromosomes 17 and 19 were detected in less than 50% of cases. Since this 17p11.2-p13 region is known to contain the tumour suppressor gene TP53, patients with NF1 may be at high risk of malignant neoplasms including MPNSTs. Gains were more frequently detected in plexiform neurofibromas (2/3 cases) than other benign tumours, suggesting proto-oncogene activation in tumourigenesis of plexiform neurofibroma. The significance of the losses of chromosome 19 in these cases is not clear at present, but in NF1-associated neurofibromas, the presence of some as yet unknown tumour suppressor genes on chromosome 19 cannot be ruled out.

We show that all the parameters which destabilize the weak scale can be taken around the weak scale in the MSSM without conflicting with the SM Higgs mass bound set by LEP experiment. The essential point is that if the lightest CP-even Higgs h in the MSSM has only a small coupling to Z boson, g ZZh , LEP cannot generate the Higgs sufficiently. In the scenario, the SM Higgs mass bound constrains the mass of the heaviest CP-even Higgs H which has the SM like g ZZH coupling. However, it is easier to make the heaviest Higgs heavy by the effect of off-diagonal elements of the mass matrix of the CP-even Higgs because the larger eigenvalue of 2 × 2 matrix becomes larger by introducing off-diagonal elements. Thus, the smaller stop masses can be consistent with the LEP constraints. Moreover, the two excesses observed at LEP Higgs search can naturally be explained as the signals of the MSSM Higgs h and H in this scenario.One of the most interesting results in the scenario is that all the Higgs in the MSSM have the weak scale masses. For example, the charged Higgs mass should be around 130 GeV. This looks inconsistent with the lower bound obtained by the b → sγ process as m H ± > 350 GeV. However, we show that the amplitude induced by the charged Higgs can naturally be compensated by that of the chargino if we take the mass parameters by which the little hierarchy problem can be solved. The point is that the both amplitudes have the same order of magnitudes when all the fields in the both loops have the same order of masses.a

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Three cases of infantile digital fibromatosis were studied by electron microscopy, enzyme histochemistry, and tissue culture. The tumors were made up equally of myofibroblasts containing electron-dense inclusions which were composed chiefly of microfilaments measuring about 5 to 7 nm. Dense bodies usually observable in the smooth muscle cells were found in the bundles of these microfilaments and in the process of the inclusions, suggesting that these inclusions may represent an abnormal accumulation of contractile protein in the cytoplasm of tumor cells. Two cell lines were established from culture of the tumor cells, and the cultured cells also contained inclusion bodies showing the same morphologic characteristics as those of the original tumor cells. Lysosomal enzymes were abundant in the cultured cells, but they were scant in the cells of the fresh tissue specimens. Cocultivation of the cultured cells with human embryonic lung cells yielded no cytopathic effect.