[New influenza A (H1N1) pandemia and cancer patients: what do we do?]. / Nouvelle pandémie de grippe A (H1N1) : que faire pour les patients atteints d'un cancer ?

The new swine-origin influenza A (H1N1) strain (S-OIV) pandemia may expose immunodepressed cancer patients under chemotherapy to an increased risk of mortality. Here, we put into perspective available antiviral treatments and influenza vaccination efficacy in cancer patients and consider that recommendations for seasonal influenza vaccination for these patients are applicable for the upcoming S-OIV vaccines. We recommend a triple vaccination in cancer patients (seasonal influenza, S-OIV, streptococus pneumoniae), if possible at least two weeks before beginning chemotherapy. In case of an influenza-like illness under chemotherapy, the care will depend on the neutrophilic level. If neutrophil count is under 500 units/mm3, hospital admission is recommended with adapted isolation measures and the prescription of an antiviral treatment with oseltamivir 75 mg twice a day for 5 days, if the onset of symptoms occurred within 48 hours. In case of a sign of severity, antiviral treatment should be started regardless of time of the onset of symptoms. Probabilistic antibiotics should also be introduced. In the absence of neutropenia, home care should be favored, by explaining recommended hygienic measures and by starting an antiviral treatment with the same modalities as described previously. Hospital admission is indicated if a sign of severity is present. Patients under chemotherapy, if not vaccinated, who have had a contact with an infected person should receive a prophylactic antiviral treatment with oseltamivir 75 mg once a day for 10 days.

A histopathologic investigation of PGE(2) pathways as predictors of proliferation and invasion in urothelial carcinomas of the bladder.

INTRODUCTION AND OBJECTIVES: The pattern of arachidonate acid (AA) transformation in tumor cells has been shown to play a role in determining tumor cell invasiveness. AA is released from membrane phospholipids by cPLA(2). Then it is metabolized into prostaglandins and PGE(2) especially via cyclooxygenase pathways. PGE(2) production seems to be necessary for rendering the cells invasive. We aimed to characterize cPLA(2), cyclooxygenase 2 (COX2) and prostaglandine E synthase (PGES) expression in human transitional carcinoma (TCC) of the urinary bladder and correlate with the Ki-67 proliferating marker. METHODS: Formalin-fixed human TCC tissues (n=54) obtained from TURB or cystectomies were evaluated for cPLA(2), COX2, PGES and Ki-67 expression using specific antibodies. There were 6 CIS, 9 pTaG1, 9 pTaG3, 10 pT1G3 and 10 pT2G3. 10 normal bladder tissues were also evaluated. Control slides were incubated without primary antibodies and treated in a similar way. RESULTS: cPLA(2), COX2 and PGES were not expressed in the 10 normal tissues. In the same normal tissues, Ki-67 expression was observed only in 1% of the cells. However, cPLA(2) was expressed in 1/6 CIS, 1/9 pTaG1, 3/9 pTaG3, 6/10 pT1G3 and 2/10 pT2G3. COX2 was expressed in 0/6 CIS, 0/10 pTaG1, 2/9 pTaG3, 3/10 pT1G3 and 1/10 pT2G3. PGES was expressed in 4/6 CIS, 0/9 pTaG1, 4/9 pTaG3, 2/10 pT1G3 and 5/10 pT2G3. Ki-67 expression was 39.5% for CIS, 6.5% in pTaG1, 37% in pTaG3, 34.5% in pT1G3 and 55% in pT2G3. If we consider it a positive result when at least one enzyme was expressed, there were 5/6 CIS positive, 1/9 pTaG1 positive, 9/9 pTaG3 positive, 10/10 pT1G3 positive and 10/10 pT2G3 positive. Also the Ki-67 is more often expressed in cells with high grade tumor. CONCLUSIONS: These results suggest that (i). not only COX2 is involved in the tumorogenesis of the TCC but also cPLA(2) and PGES, (ii). there is relationship between the AA metabolic PGE(2) pathway expression and the aggressiveness of the TCC of the urinary bladder.