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von Hippel-Lindau disease is an inherited multisystemic familial cancer syndrome caused by mutations of the VHL gene. The spectrum of clinical manifestations is broad and includes central nervous system hemangioblastomas and visual benign and malignant tumors. The various manifestations can be demonstrated by means of different imaging techniques such as magnetic resonance imaging, computed tomography, and fluorescein retinal hemangiography. A systematic approach must be followed for repeated screening in patients at risk, since many lesions in VHL disease are treatable.

Identify the bacteria responsible for cutaneous infections observed in private practice and test their sensitivity to currently used antibiotics.The patients were examined by dermatologists. A bacteriological sample was taken and sent to a central laboratory for identification of the germ and antibiograms were performed and the minimal inhibiting concentrations (MIC) determined.Folliculitis, impetigo and furuncles were the three most frequent primary infections. Four hundred and forty-three patients were included and 442 samples were placed in culture. Cultures were positive in 265 cases (a single bacterial strain in 231 cases). Staphylococcus aureus was isolated in 208 cases, streptococci in 11 and enterobacteria in 3; occasionally several germs were present. Eight strains of staphylococci were meti-R (4 p. 100). All the strains were sensitive to pristinamycin and mupirocin and 90 p. 100 were sensitive to fusidic acid.The occurrence and diffusion of resistant strains is a daily concern in hospitals. In general practice, although care must be taken, the problem rarely occurs and the antibiotics used remain effective.

In France, immediate breast reconstruction (IBR) for infiltrating carcinoma remains controversial. Many teams advocate the possible event of a post mastectomy radiotherapy and its negative effect on IBR. In our Institute we do not exclude infiltrating breast cancer patient from IBR. In the poor prognostic patients who wish IBR, we recommend autologous IBR to obtain the best aesthetic result with minimum revision procedures and best tolerance to adjuvant radiotherapy. From January 1993 to December 1997, we performed 687 IBR with myocutaneous flap for infiltrating carcinomas. In this group only 68 patients needed postoperative chest wall radiotherapy (45 Gy): 27 TRAM flap, 41 latissimus flap. Only one of the TRAM but 39 of latissimus flaps were associated with a prosthesis. The mean follow-up was 24 months. Fourteen patients developed metastatic disease, and ten were dead at the time of the chart revue. The autogenous TRAM flap tolerate radiation quite well and remain soft and mobile. The latissimus flap associated with a prosthesis developed capsular contracture (BAKER II or III) in 71% of cases. In all cases the cosmetic impairment was not important and the result after capsulectomy remained soft. We concluded that IBR could be offered to motivated patients in all stages of the disease regardless of the subsequent chest wall radiotherapy, and we recommend its use for possible autologous reconstruction.

The genotype-phenotype relationship of Lynch syndrome displays many enigmatic features which cannot be explained satisfactorily by the prevailing concepts of carcinogenesis and genetic predisposition to cancer. We propose here a new model of carcinogenesis divided into two and only two evolutive phases: a) a preliminary phase starting with the counter-selective loss of mismatch repair function, in which most clones with the RER mutator phenotype are eliminated through apoptosis or an accelerated ageing process; b) an explosive phase that is initiated only if mutations blocking apoptosis and senescence, rapidly acquired during the short life span of the non-transformed RER+ clones, eventually rescue one mismatch repair-deficient cell that gives rise to the malignant clone. Carcinogenesis is proposed here to progress irreversibly and very rapidly once initiated. We shall show how this model provides a meaningful etiologic and pathogenic interpretation of all the curious features of Lynch syndrome.

Serum antibodies reacting with the tumor suppressor protein p53 have been detected previously in cancer patients with a variety of neoplasms. Two initial (although insufficient) prerequisites for a B-cell response to occur have been proposed: p53 protein accumulation in the tumor or a mutant p53 gene, or both. We have examined 65 esophageal cancer cases (42 from Guangzhou and Shenyang, People's Republic of China, and 23 from Paris, France) to obtain a prevalence estimate of anti-p53 antibodies for this type of cancer and to define the relationship of p53 tumor status to B-cell immune response. Sera were analyzed in a triplicate assay (enzyme-linked immunoassay, immunoprecipitation, and immunoblot) for anti-p53 antibodies. Tumor DNA was screened for mutations in exons 5-8, and tumor tissue was examined by immunohistochemistry for abnormal p53 protein accumulation. p53 mutations were found in 36 (58%) of 62 cases analyzed. Sixteen patients (25%) had circulating antibodies to the tumor suppressor protein. All but two (88%) of the tumors from seropositive cases had a mutation in the DNA binding region of the p53 gene, and with one exception, these tumors also showed nuclear accumulation of the p53 protein. In contrast, tumor mutations were found in just 22 (46%) of the 48 individuals in whom we did not detect anti-p53 antibodies. Among the 22 seronegative cases for which we found no tumor mutations, 11 revealed p53 protein accumulation by immunohistochemical analysis. Thus, circulating anti-p53 antibodies may be present in one-fourth of esophageal cancer patients, most of whom also would be expected to have a p53 gene mutation in their tumors. Patients without such mutations appear considerably less likely to mount a B-cell response to the p53 tumor suppressor protein than those that do (P0.01).

The prevalence of antibodies to 13 Legionella antigens was compared in three populations: 583 blood donors, 140 tuberculosis patients and 66 patients with acute non-legionellosis pneumonia. Antibody levels were determined by indirect immunofluorescence (IFA) using formalin-fixed antigens prepared from bacteria developed in embryonated hen yolk sac. The very weak prevalence of anti-L. pneumophila antibodies in a healthy population [almost 0 for serogroups (SG) 2, 3, 4 and 5; 1.5% for SG 6 and a maximum of 2.5% for SG 1 at a titer of 1: 16] confirms the criteria that have been recommended by the Centers for Disease control, USA. For the other legionellae studied, these criteria cannot be applied due to a higher prevalence in healthy populations (14.5% with levels of 1: 16-32 and 1% with levels of 1: 64-128 for L. bozemanii and progressively decreasing by as much as 2% for the other species: L. micdadei, L. longbeachae, L. gormanii, L. dumoffii and L. jordanis), in tuberculosis patients (12.1% with a level at 1: 64-128 for L. bozemanii, and for the same titer, 9.2% for L. gormanii, 5.7% for L. micdadei, 5% for L. longbeachae 2), and also in acute pneumonia (2 to 3.3% with levels of 1: 64-128 for L. longbeachae 1 and 2, L. jordanis, L. dumoffii, L. micdadei and L. bozemanii). Although the significance of these prevalences remains to be discussed, with formalin-fixed antigens, it seems reasonable for these species to assign a threshold of 1: 256 for the presumptive serodiagnosis following seroconversion.