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Talkpoeder kan veilig worden ingezet om mensen te verlossen van vocht achter de longen. Voorwaarde is wel dat de poederdeeltjes niet te klein zijn, aldus hoofdonderzoeker dr. J.P. Janssen, longarts in het Canisius-Wilhelmina Ziekenhuis in Nijmegen. Vocht achter de longen komt o.a. voor bij mensen met longvlieskanker (mesothelioom). Met de talkpoedertechniek laat men de longvliezen verkleven met de binnenkant van de borstwand, zodat er geen ruimte meer is voor het vocht. Bron: Janssen, J.P. et al. (2007). Safety of pleurodesis with talc poudrage in malignant pleural effusion: a prospective cohort study. Lancet, may 5.369(9572):1535-9.
Janssen JP, Collier G, Astoul P, Tassi GF, Noppen M, Rodriguez-Panadero F, Loddenkemper R, Herth FJ, Gasparini S, Marquette CH, Becke B, Froudarakis ME, Driesen P, Bolliger CT, Tschopp JM., (2007). Safety of pleurodesis with talc poudrage in malignant pleural effusion: a prospective cohort study. Lancet. 2007 May 5.369(9572):1535-9.

ABSTRACT

BACKGROUND: Talc is the most effective chemical pleurodesis agent for patients with malignant pleural effusion. However, concerns have arisen about the safety of intrapleural application of talc, after reports of development of acute respiratory distress syndrome in 1-9% of treated patients. Our aim was to establish whether use of large-particle-size talc is safe in patients with malignant pleural effusion.

METHODS: We did a multicentre, open-label, prospective cohort study of 558 patients with malignant pleural effusion who underwent thoracoscopy and talc poudrage with 4 g of calibrated French large-particle talc in 13 European hospitals, and one in South Africa. The primary endpoint was the occurrence of acute respiratory distress syndrome after talc pleurodesis.

FINDINGS: No patients developed acute respiratory distress syndrome (frequency 0%, one-sided 95% CI 0-0.54%). 11 (2%) patients died within 30 days. Additionally, seven patients had non-fatal post-thoracoscopy complications (1.2%), including one case of respiratory failure due to unexplained bilateral pneumothorax.

INTERPRETATION: Use of large-particle talc for pleurodesis in malignant pleural effusion is safe, and not associated with the development of acute respiratory distress syndrome.

De hoeveelheid anti-oxidant enzym gluthatione in eendenkroos neemt af bij contact met chrysotiel (wit) asbest. De asbest was afkomstig uit een asbestcementfabriek. Meting van de hoeveelheid anti-oxidanten in waterplanten als eendenkroos kan een methode zijn om de milieuschade van blootstelling aan asbest te meten. Bron: Trivedi, A.K., et. al. (2007). Environmental Contamination of Chrysotile Asbestos and Its Toxic Effects on Antioxidative System of Lemna gibba. Archives of Environmental Contamination and Toxicology 52, 355-362.
Trivedi, A.K., et. al. (2007). Environmental Contamination of Chrysotile Asbestos and Its Toxic Effects on Antioxidative System of Lemna gibba. Archives of Environmental Contamination and Toxicology 52, 355-362.

Abstract.

Asbestos was monitored in various plant samples around an asbestos cement factory. Asbestos residue was found on the surface of all plant samples monitored. Based on asbestos concentration found in different plant samples during monitoring and on the property of asbestos to cause reactive oxygen species-mediated oxidative stress in animal models, laboratory experiments were conducted to assess the toxicity of chrysotile asbestos on an aquatic macrophyte, duckweed

(Lemna gibba.). L. gibba plants were exposed to four concentrations (0.5, 1.0, 2.0, and 5.0 lg/mL) of chrysotile asbestos under laboratory conditions, and alterations in the glutathione and ascorbate antioxidative system were estimated at postexposure days 7, 14, 21, and 28 in order to assess changes in their level as suitable biomarkers of chrysotile contamination. Chrysotile exposure caused a decrease in total and reduced glutathione and an enhancement in the oxidized glutathione as well as the reduced/oxidized glutathione ratio. An increase in ascorbate pool size, and reduced as well as oxidized ascorbate was found to be accompanied by a decrease in the ratio of reduced/oxidized ascorbate. Alteration in the glutathione and ascorbate level might be considered as a biomarker of exposure to an unsafe environment because these are essential compounds of the general antioxidative strategy to overcome oxidative stress due to environmental constraints. Because an increase in the oxidation rate of antioxidants weakens cellular defenses and indicates a precarious state, they could constitute

indicators of toxicity.

Een studie bij aan asbest blootgestelde muizen laat zien dat het sv-40 virus de ontwikkeling van mesothelioom stimuleert. De manier waarop is nog niet duidelijk. Het lijkt erop dat het virus de werking van het p-53 gen stopt: een gen dat de ontwikkeling van tumoren onderdrukt. Bron: Pietruska, J.R. & Kane, A.B., (2007). SV40 Oncoproteins Enhance Asbestos-Induced DNA Double-Strand Breaks and Abrogate Senescence in Murine Mesothelial Cells. Cancer Res, 67 (8), april 15, 3637-45.
Pietruska, J.R. & Kane, A.B., (2007). SV40 Oncoproteins Enhance Asbestos-Induced DNA Double-Strand Breaks and Abrogate Senescence in Murine Mesothelial Cells. Cancer Res, 67 (8), april 15, 3637-45.

Abstract

SV40 virus has emerged as a potential cofactor with asbestos in the development of diffuse malignant mesothelioma, but its precise role in the pathogenesis of this tumor is unclear. SV40

large T antigen is known to inactivate cellular proteins involved in DNA damage and senescence, including p53 and pRb. We hypothesize that SV40 oncoproteins will sensitize mesothelial cells to DNA damage induced by asbestos or chemotherapeutic agents. SV40 oncoprotein expression in murine mesothelial cell lines enhanced spontaneous and asbestos-induced double-strand breaks, indicated by .-H2AX foci, and potentiated micronucleus formation. Mesothelial cells exposed to asbestos or bleomycin for 96 h acquired senescent-like morphology and displayed elevated senescence associated

B-galactosidase activity, reduced bromodeoxyuridine (BrdUrd) incorporation, and reduced colony formation. SV40 oncoprotein expression abrogated the senescent phenotype,

and transfected cell lines showed an increase in both BrdUrd incorporation and colony formation after prolonged DNA damage. Murine mesothelial cell lines lacking wild-type p53 due to a point mutation or gene rearrangement also failed to senesce in response to asbestos or chemotherapeutic agents. In addition, stress-induced senescence in human mesothelial cell lines was impaired by SV40 oncoprotein

expression (MeT-5A), p53 small interfering RNA, or spontaneous p53 mutation (REN). These studies suggest that exposure to DNA-damaging agents can induce senescence in both murine and human mesothelioma cell lines and suggest a major, although not exclusive, role for p53 in this response.

SV40 virus may contribute to mesothelioma progression by impairing stress-induced senescence, in part through p53 inactivation, thereby favoring survival and proliferation of

mesothelial cells that have sustained DNA damage. [Cancer Res 2007.67(8):3637-45

Amerikaanse onderzoekers hebben een virus gevonden dat bij muizen de groei van een mesothelioomgezwel afremt. Virustherapie is erop gericht virussen te vinden die zich alleen in tumorcellen vermenigvuldigen en de normale cellen sparen. Bron: mesothelioma applied research foundation, 25 april 2007. Meer www.marf.orf

Asbestvezels kunnen de eierstokken bereiken. Dat constateerden Noorse onderzoekers bij een groep vrouwen die in een papier- en pulpfabriek hadden gewerkt. Meer onderzoek is nodig om te bepalen of de asbest in de eierstokken ook eierstokkanker kunnen veroorzaken. Bron: Langseth, H. et al. (2007). Asbestos fibers in ovarian tissue from Norwegian pulp and paper workers. International Journal of Gynecological Cancer 17, 44-49.

Langseth, H., Johansen B.V., Nesland, J.M. & Kjaerheim, K. (2007). Asbestos fibers in ovarian tissue from Norwegian pulp and paper workers

Abstract

An elevated risk of ovarian cancer has been observed in Norwegian pulp and paper workers who were possibly occupationally exposed to asbestos. The present study was initiated to investigate if the increased risk could be associated with asbestos fibers in ovarian tissue from workers in this industry. Normal ovarian tissue specimens from three groups of women were included in the study. The case group included specimens from 46 women diagnosed with ovarian cancer in the period 1953-2000, and who had been working in one or more pulp and paper mills between 1920 and 1993. Normal ovarian tissue specimens from two control groups without occupational history from pulp and paper work were selected from the

Cancer Registry database. Tissue blocks were digested and prepared for transmission electron microscopy. Number of fibers per gram wet weight was calculated. Asbestos fibers were found in normal ovarian tissue from two subjects in the case group, while no fibers were found in the control groups. The two asbestos positive cases had been working as paper sorter/packer and chlorine plant worker, respectively. Both were possibly secondary exposed to asbestos from family members working as insulators. We conclude that the findings in this study did not allow drawing any firm conclusion about an association between occupational exposure to asbestos and ovarian cancer in Norwegian pulp and paper workers. Our study confirms that asbestos fibers may reach the ovaries and demonstrates that the applied method is appropriate for identification of the fiber.

Knoflook werkt als een anti-occidant en vermindert daardoor de schadelijke werking van chrysotiel asbest in het bloed. Dit constateerden Indiase en Duitse onderzoekers in een in-vitro studie. Het ging om een reageerbuis-experiment met menselijk bloed. Bron: Yadav, S. (2006). Modulatory Effects of Fresh Garlic Extract on Chrysotile Asbestos Induced Genotoxicity: An In Vitro Study. Bulletin Environmental Contamination and Toxicology 77: 477-483.

De invloed van blootstelling aan asbest in het milieu op het risico op longkanker bij mensen die nooit gerookt hebben is onduidelijk. Longkanker heeft bij mensen die nooit gerookt hebben andere moleculaire en biologische kenmerken dan bij rokers. Twee recente overzichtsstudies beschrijven dat niet-rokende vrouwen vaker longkanker krijgen dan niet-rokende mannen: tussen de 15 en 25% van de vrouwelijke longkankerpatiënten heeft nooit gerookt, bij mannelijke longkankerpatiënten is dat tussen de 5 en 10%. Bron: Wakelee H.A. et al. (2007). Lung cancer incidence in never smokers. Journal of Clinical Oncology, Feb 10.25(5):469-71. Subramanian, J. & Govindan, R. (2007). Lung cancer in never smokers: a review. Journal of Clinical Oncology feb 10. 25(5), 561-70.
Wakelee H.A., Chang ET, Gomez SL, Keegan TH, Feskanich D, Clarke CA, Holmberg L, Yong LC, Kolonel LN, Gould MK, West DW (2007). Lung cancer incidence in never smokers. Journal of Clinical Oncology, Feb 10.25(5):469-71.

PURPOSE: Lung cancer is a leading cause of cancer death worldwide. Although smoking remains the predominant cause of lung cancer, lung cancer in never smokers is an increasingly prominent public health issue. However, data on this topic, particularly lung cancer incidence rates in never smokers, are limited. METHODS: We reviewed the existing literature on lung cancer incidence and mortality rates among never smokers and present new data regarding rates in never smokers from the following large, prospective cohorts: Nurses’ Health Study. Health Professionals Follow-Up Study. California Teachers Study. Multiethnic Cohort Study. Swedish Lung Cancer Register in the Uppsala/Orebro region. and First National Health and Nutrition Examination Survey Epidemiologic Follow-Up Study. RESULTS: Truncated age-adjusted incidence rates of lung cancer among never smokers age 40 to 79 years in these six cohorts ranged from 14.4 to 20.8 per 100,000 person-years in women and 4.8 to 13.7 per 100,000 person-years in men, supporting earlier observations that women are more likely than men to have non-smoking-associated lung cancer. The distinct biology of lung cancer in never smokers is apparent in differential responses to epidermal growth factor receptor inhibitors and an increased prevalence of adenocarcinoma histology in never smokers. CONCLUSION: Lung cancer in never smokers is an important public health issue, and further exploration of its incidence patterns, etiology, and biology is needed.

Subramanian, J. & Govindan, R. (2007). Lung cancer in never smokers: a review. Journal of Clinical Oncology feb 10. 25(5), 561-70.

ABSTRACT

Lung cancer is the leading cause of cancer-related death in the United States. Although tobacco smoking accounts for the majority of lung cancer, approximately 10% of patients with lung cancer in the United States are lifelong never smokers. Lung cancer in the never smokers (LCINS) affects women disproportionately more often than men. Only limited data are available on the etiopathogenesis, molecular abnormalities, and prognosis of LCINS. Several etiologic factors have been proposed for the development of LCINS, including exposure to radon, cooking fumes, asbestos, heavy metals, and environmental tobacco smoke, human papillomavirus infection, and inherited genetic susceptibility. However, the relative significance of these individual factors among different ethnic populations in the development of LCINS has not been well-characterized. Adenocarcinoma is the predominant histologic subtype reported with LCINS. Striking differences in response rates and outcomes are seen when patients with advanced non-small-cell lung cancer (NSCLC) who are lifelong never smokers are treated with epidermal growth factor receptor tyrosine kinase (EGFR-TK) inhibitors such as gefitinib or erlotinib compared with the outcomes with these agents in patients with tobacco-associated lung cancer. Interestingly, the activating mutations in the EGFR-TK inhibitors have been reported significantly more frequently in LCINS than in patients with tobacco-related NSCLC. This review will summarize available data on the epidemiology, risk factors, molecular genetics, management options, and outcomes of LCINS.

Volgens patholoog Gibb en collega’s is de in 1997 in Helsinki overeengekomen methode om de relatie tussen asbestblootstelling en longkanker vast te stellen aan de hand van een schatting van de asbestblootstellingsfrequentie, intensiteit en het aantal vezeljaren niet nauwkeurig. Het samengaan met asbestose, een andere asbestziekte, lijkt op dit moment nog het meest betrouwbare criterium om vast te stellen dat longkanker door asbestblootstelling is veroorzaakt. Sorgdrager schrijft dat de invloed van roken de causaliteitsvraag nog moeilijker maakt. Sinds 1975 worden bijna 3000 intensief aan blauw asbest blootgestelde ex-werknemers uit het Australische Wittenoom periodiek gevolgd. In deze populatie blijkt het asbesteffect op het risico op longkanker tussen rokers en niet-rokers niet significant verschillend. Andere specifieke populatiekenmerken lijken van groter belang. Dit is opmerkelijk omdat inmiddels in de wetenschap steeds meer aangenomen wordt dat roken en asbest samen het risico op longkanker vergroten. Bron: Gibbs, A. et al. (2007). The “Helsinki Criteria” for attribution of lung cancer to asbestos exposure. How robust are the Criteria. Editorial. Arch Pathol Lab Med 131, february, 181-184. Sorgdrager, B. (2007). Longkanker en asbest, hoe zit het met de rol van sigaretten? Referaat. TBV 15, 2, 88-89.

Het Amerikaanse “National Institute for Occupational Safety and Health (NIOSH)” heeft in een beleidsdocument geadviseerd nieuw onderzoek te doen naar welke asbestkenmerken gezondheidsrisico’s veroorzaken bij beroepsmatige blootstelling. Het document vermeldt een aantal vragen waarop op dit moment wetenschappelijk nog geen eenduidig antwoord te geven is. Het instituut wil hiermee de publieke dialoog op gang brengen. Bron: Niosh, 12 maart 2007. Meer www.cdc.gov

De Amerikaanse “Food and Drug Administration” heeft de Mesomark bloedtest goedgekeurd als middel in het onderzoek naar mesothelioom. Met deze test wordt de hoeveelheid mesotheline in het bloed gemeten, die aanwijzingen geeft over de grootte van een mesothelioom gezwel. De test kan gebruikt worden om te meten hoeveel effect een behandeling op een patiënt heeft. De Mesomark test, waarvoor alleen een bloedmonster nodig is, kan daarom misschien een alternatief zijn voor andere belastende en kostbare testmethodes die gebruikt worden. In Europa wordt de test momenteel beoordeeld voor klinisch gebruik. Bron: Mesothelioma Applied Research Foundation, 25 januari 2007. Meer www.marf.org