In this report we have investigated the effects of BAX in enhancing apoptosis in two primary non-small cell lung cancer cell lines. A count of the apoptotic cells by TUNEL staining revealed that almost 70% of BAX over-expressing cells died, while very few apoptotic cells were detectable in the wildtype cells or in the cells transfected with an empty vector. These findings suggest that de-regulated expression of BAX may provide a novel mechanism for initiating cell death in non-small cell lung cancer cells. Further studies are needed to better define the involvement of this protein in the complex mechanism of lung carcinogenesis and to definitely demonstrate the therapeutic utility of targeting this pathway.

A case of benign, cystic intrapulmonary teratoma occurring in the right lobe of a 22-year old female is described with grossly and microscopically findings. The connection between the tumor and the segmental bronchus, together with the absence of germ cell neoplasms in other locations, clearly established the true intrapulmonary nature of the lesion. The unusual finding of thymic tissue within the wall supports the possible origin from the third pharyngeal pouch.

The purpose of this article is to review the findings from research directed at understanding the effects of volatile anesthetics on the respiratory surface known as pulmonary surfactant. Anesthetics have long been known to have a disruptive effect on biological membranes. This review will highlight the interactions of volatile anesthetics with pulmonary surfactant. This paper has emphasized the interaction of volatile anesthetics with the pulmonary surfactant monolayer versus the lipid bilayer. The goal of this review is to uncover to what extent this understanding has progressed in forty years. Although the goal is quite broad, the information gathered and the advice given is specific. Theories of anesthesia and surfactant structure and function are summarized and discussed in light of early physico-chemical approaches and extend to an era where powerful new three-dimensional structural techniques can be used to answer this question.

The first cyclin dependent kinase inhibitor to be discovered was the p21 cdk interacting protein (a.k.a., WAF1, Cip1, CAP20, Sdi1, mda6). p21 expression may or may not be dependent on p53. This pathway also inhibits DNA replication by merit of p21's interaction with PCNA, but it has also been shown that this same inhibitory interaction with p21 does not affect PCNA DNA repair abilities. We assessed the immunohistochemical expression of p21 protein in 60 curative surgical resected non small cell lung cancers relating it to the expression of PCNA to clarify the contribution of the p21/PCNA pathway to the development of NSCLC. We did not find any relationship between PCNA and p21 expression. This last result may indicate that the mechanism by which PCNA controls the DNA repair is the most important activity of this protein during lung cancer progression and development, compared to its contribution to cell proliferation. In fact, this last event is strongly counteracted by p21 expression, which in this last case works as an inhibitor of PCNA expression. In conclusion this study highlighted the important role of the p21/PCNA pathway in lung carcinogenesis, pointing out the contribution of PCNA to the response to lung aggression and not only it's role as a proliferation index. Therefore, these results offer a background to further study to evaluate potential novel therapeutic approaches to lung cancer treatment.

A case of rare primary adenocarcinoma of the bulbomembranous portion of the male urethra is presented The histological and immunohistochemical characteristics of this tumor are identical to those of colon adenocarcinomas. The pathogenesis can be explained either by neoplastic degeneration of globet cells found in the urethral epithelium or by malignant degeneration of persistent glandular elements that are embryonal residues. The patient was successfully treated with transurethral prostatectomy and with a high dose of radiation therapy.

The field of gene therapy has been in rapid expansion since the first submissions of gene therapy trials in the early 1990s which provided encouraging results. Since then, many gene therapy protocols have been approved for phase I clinical trials for the treatment of inherited genetic diseases and cancer The possibility of employing gene transfer technology to treat AIDS and neurologic diseases is currently under evaluation. Many gene delivery systems have been developed for in vivo studies and therapy. The efficiency of in vivo gene transfer however, still needs to be optimized, even though significant advances have recently been achieved in improving gene delivery, gene regulation and avoidance of immune responses. This review provides a general outline focusing on the description of the most common gene delivery systems and on their current applications in therapeutics.

Cancer of the lung is the most frequent cancer in the world, but with wide geographical variation in risk. It is most spread among males of all races worldwide, the only exception being its incidence among Chinese women aged 70 years and older. When comparing the different ethnic groups we have to consider that besides inhaling cigarette smoke actively or as a passive smoker the exposure to occupational carcinogens varies considerably according to different work places. In our study we compared 10 years of data from African-Americans in Howard University Hospital, Washington D.C. with 20 years of data from the white population in the University Hospital of Vienna, Austria. Ethnic patterns are generally consistent within each group in terms of both incidence and mortality. The difference in susceptibility between the sexes, the three major racial groups and already proven differences in genetic variations indicate the difference between individuals concerning the initiation and progression of lung cancer.

Lung cancer claimed about 153 000 lives in 1994 in the United States. Despite research overall lung cancer survival has still not improved during the last 20 years, with 5-year relative survival remaining about 13% (1). In addition several epidemiologic and molecular studies showed a difference in the incidence of lung cancer in the three major races. The aim of our study was to investigate the variations of race in lung cancer patients, in order to identify potential risk factors linked to the different racial status. In this light we compared a 10 years lung cancer data of black population from Howard University Hospital Washington D.C., U.S.A. and a 20 years data of white population from the Vienna University Hospital Austria. Our results did not show any significant difference in mean age or tumor localization in both groups, but highlighted a remarkable difference in the incidence of the lung cancel histological types also according to the sex. In this respect it could be more successful to consider carcinogenesis like a protracted process of gene function deregulation in response to cell injury from exposure to genotoxic substances with individual specificity.

Lung cancers still represent an incurable group of malignancies, where we have to admit that therapy, be it surgery, chemotherapy or radiation, still fails. The emphasis in research has centered on exogenous factors causing the initiation and progression of the different types of lung cancer, especially exposure to tobacco smoke. But so far we have learned that endogenous factors play an equal, if not a more important role, in the onset of this group of diseases. Cancer arising spontaneously never appears to be due to one specific factor, but experimental cancers have been shown to do so. In this light, recent advances in molecular biology have pointed out the relevance of the role of oncogenes and tumor suppressor genes in the pathogenesis of lung cancers. It is the purpose of this paper to review these latest findings, especially from a genetic point of view.