Wait times from presentation to treatment for colorectal cancer: a population-based study.

BACKGROUND: The wait time from cancer diagnosis to treatment has been a recent focus of cancer care in Canada. OBJECTIVE: To examine the trends in wait times from patient presentation to treatment (overall health system wait time [OWT]) for colorectal cancer (CRC). METHODS: Patients with colorectal adenocarcinomas, diagnosed between 2001 and 2005, and their first definitive treatments were identified from the population-based Manitoba Cancer Registry (Winnipeg, Manitoba). By linkage to Manitoba Health and Healthy Living's administrative databases, a patient's first gastrointestinal investigation (abdominal radiological imaging, lower gastrointestinal endoscopy or fecal occult blood test) before CRC diagnosis was identified. The index contact with the health care system was estimated from the date of the visit with the physician who ordered the first gastroenterological investigation. The OWT was defined as the time from the index contact to the first treatment, while diagnostic delay was defined as the time from the index contact to the diagnosis of CRC. Multivariate Cox regression analysis was performed to determine independent predictors of OWT. RESULTS: The OWT was estimated for 2552 cases of CRC over the five years that were examined. The median OWT increased from 61 days in 2001 to 95 days in 2005 (P<0.001). Most of the increase was in diagnostic wait times (median of 44 days in 2001 versus 64 days in 2005 [P<0.001]). Year of diagnosis, older age, urban residence and diagnosis at a teaching facility were independent predictors of OWT. CONCLUSIONS: The OWT from presentation to treatment of CRC in Manitoba steadily increased between 2001 and 2005, mostly due to diagnostic delays.

Low doses of ultraviolet A radiation stimulate adhesion of human dermal fibroblasts by integrins in a protein kinase C-dependent pathway.

In this work, we have studied the modulation of fibroblast-extracellular matrix interactions by physiological doses of ultraviolet A (UV-A) radiation using an adhesion assay on collagen. We have shown that low doses of UV-A (20 kJ/m2) stimulate fibroblast adhesion while higher doses (100 and 200 kJ/m2) inhibit it. By measurement of the thiobarbituric acid reactive substances (TBARS) and use of the chain-breaking antioxidant vitamin E, no role of lipid peroxidation can be detected in these effects. By incubating fibroblasts with a specific protein kinase C (PKC) inhibitor, GF109203X, we have demonstrated that the stimulation of the adhesion by low doses of UV-A involves, at least in part, a PKC-dependent mechanism. In addition, using function-blocking antibodies of alpha 1, alpha 2 or alpha 5 integrin chains involved in extracellular matrix anchorage, we have shown that they decrease the stimulation of adhesion following low doses of UV-A radiation, demonstrating the involvement of these three integrin chains in this UV-A effect. In parallel, 20 kJ/M2 of UV-A are found to rapidly stimulate membrane expression of alpha 1, alpha 2 and alpha 5 integrin chains. This work, which underlines the involvement of integrins in UV-A effects, contributes to the evaluation of the mechanisms by which cell-matrix interactions modulate cell behaviour.

Atypical mycobacteriosis as a complication of talc pneumoconiosis.

A 57 year old man, receiving compensation for talc pneumoconiosis since 1977, was admitted to hospital for the first time in 1987, with symptoms of weight loss, fever, dyspnoea and productive cough. A chest roentgenogram showed bilateral cavitation. Two years later, Mycobacterium xenopi was found in sputum cultures. Despite specific oral antibiotherapy, the patient's health deteriorated and he died in 1990. To the best of our knowledge, this is the first reported case of an association of talcosis with a M. xenopi pneumonia. The relative timing of the two diseases suggests that talc pneumoconiosis predisposed to the infection by M. xenopi.