Endometrial carcinoma is a rare iatrogenic complication due to the adverse estrogenic like effect of Tamoxifen on the uterine mucosa. We report the delayed case of an endometrial carcinoma after an unusual twleve year long daily administration of Tamoxifen (cumulative dose = 131 g). Endovaginal contrast ultrasound examination (Levovist, Schering, Germany) and MRI appearances are described.

Burkitt Lymphoma (LB), a very progressive malignant lymphoma, can now be cured by chemotherapy. However, protocols used currently by developed countries are costly and can cause problems of tolerance for underprivileged children.

We have previously shown that microtubule disruption results in an increase in cell adhesion to ECM proteins. In this work we show that this enhanced cell attachment was completely abolished by specific inhibitors of tyrosine-kinases, PI3-K and PKCs. Microtubule depolymerisation was associated with an important increased in tyrosine phosphorylation of FAK and paxilline, as well as with subcellular localisation of PKCgamma, delta and epsilon. We also observed significant alterations in actin cytoskeleton leading to reduced cell spreading. Thus, microtubule depolymerisation appears to activate various intracellular kinases that lead to actin cytoskeletal changes and to an increase of integrin-dependent adhesion. Whether this enhanced attachment is due to intracellular events resulting in changes in integrin affinity or avidity remains to be determined.

Gemcitabine is a nucleoside analog used in solid tumors since 1987. The main side effect is myelosuppression. Acute renal failure with thrombotic microangiopathy has also been reported. We report a new case and suggest to screen for this complication.

Treatment of malignant tumors can delay some opportunistic infections. In this paper, we report three cases of alveolo-interstitial pneumonia among HIV negative patients who received chemotherapy.

Endothelial and smooth muscle cells interact with each other to form new blood vessels. In this review, the cellular and molecular mechanism underlying the formation of the primary vascular plexus (vasculogenesis), the sprouting of further blood vessels (angiogenesis) and their maturation via recruitment of smooth muscle cells (arteriogenesis) during physiological and pathological conditions are summarized.

The aim of this work was to quantify by flow cytometry the main adhesion receptors on CD34+ cells. These cells were isolated from bone marrow (BM) or mobilized peripheral blood (PB). The proportions of CD34+/CD49d+ and CD34+/CD49e+ are weaker on PB cells, without quantitative expression variation. This phenotypic variation may induce CD34+ cells exist from BM into circulation, promoting the mobilization. The homing to the BM implicate the CD62L receptor, which expression was found more frequently and stronger on PB cells than on BM. The CD11b, CD18 and CD54 receptors are implicated in CD34+ cells adhesion to BM micro-environment. No significant variation in CD34+/CD11b+ and CD34+/CD18+ cells frequency was noted. Moreover, CD54 receptor was more frequently expressed on PB cells. Quantitative analysis revealed that CD18 was more strongly expressed on BM than on PB cells. This quantitative variation could promote progenitor adhesion by interacting with stromal cells. Finally, quantitative expression of the main receptors on CD34+ cells provides an original option for studying CD34+ cells during the mobilization, the homing or the adhesion to BM micro-environment.

Local treatment with intra vesical BCG for bladder carcinoma have few complications. Pulmonary side effects are rare, like interstitial pneumonitis. We report a case of a 77-year-old man, treated with BCG for bladder carcinoma who developed illness and tumoral chest-X-ray opacity. Mycobacterium tuberculosis bovis was isolated in culture and 2 years after in sputum. Physio pathologic mechanism of pulmonary features remains controversial, however this case suggest that lung lesions can be result of an infection process.

RISKS RELATED TO HANDLING: Cytostatic drugs (CS) destroy malignant cells. However, they also have deleterious effects on healthy cells. Manufacturing staff and nurses may suffer from side effects when handling these molecules. WHAT TYPE OF RISKS?: Laboratory staff and nurses handling these molecules are exposed to sub-therapeutic concentrations of these products, which induce little known biological effects. Cytostatics can provoke allergies, mutations and probably have carcinogenic and teratogenic effects.

Methotrexate elimination may be delayed by different drugs. Such a delay may produce severe toxic complications.

Drug administration may be responsible for side effects including hemolytic anemia. The list of drugs which can be associated with hemolysis is long, but real responsibility has only been established for about 30 different classes of drugs. Methyldopa and antibiotics were first identified as inducers of auto-immune hemolytic anemia. More recently, diclofenac, second and third generation cephalosporins were recognized as drugs which can produce immune hemolytic anemia. Fludarabine treatment was frequently associated to hemolytic anemia in patients with chronic lymphocytic leukemia. Hemolytic-uremic syndrome can be provoked by different drugs including immunodulators but the mechanism provoking hemolysis remains unclear.

Tamoxifen--a non steroidal triphenylethyl compound--in addition to having antiestrogenic properties may provoke weak estrogenic effects, the well known "paradoxical effects" on the female genital tractus. Concern has been raised about prolonged tamoxifen treatment and subsequent occurrence of endometrial adenocarcinoma; subsequent attention has been drawn through high risk histologic subtypes including poorly differentiated patterns and uterine sarcomas.

The objective of the study was to estimate the cost of first line chemotherapy in metastatic colorectal cancer treated in the Gustave-Roussy Institute. Patients were randomized in the study FFCD 9601 with four schedules of treatment: Tomudex(R), 5FU weekly, LV5FU2 with low dose of folinic acid and LV5FU2 with high dose of folinic acid.

Oxaliplatin is a new platinum compound with a 1,2-diaminocyclohexane (DACH) carrier ligand. It has recently been developed in metastatic colorectal cancer treatment, where it is generally combined with 5FU and leucovorin. Safety data in this indication concern over 1,700 patients, who received 12,500 cycles during clinical trials. Oxaliplatin appears to be relatively well tolerated and easy to handle, even on an outpatient basis. Gastrointestinal toxicity is common, but controllable and rarely severe or long-lasting. Haematological and mucosal tolerance is satisfactory, and oxaliplatin does not seem to have renal toxicity. Neurological side effects are the drug's limiting toxicity and can present as acute neurotoxicity (dysesthesiae), which is rapidly reversible, or sometimes as a longer-lasting effect, correlated in this case with the cumulative dose and leading to functional impairment in 10 to 20% of patients after 6 cycles or more. Neurological symptoms improve in the vast majority of cases after treatment is stopped. In this situation, it is even possible to restart oxaliplatin treatment. Good patient information and dose adjustments should allow us to manage the majority of neurological toxicity associated with oxaliplatin administration.

The three platinum derivatives currently available share many pharmacokinetic and pharmacodynamic (PK-PD) properties but present also some distinct characteristics, due to their structural differences. They result in different systemic PK-PD and metabolic behaviour and toxicity profile. Oxaliplatin is quickly transformed into dach-platinum, the active metabolite, by loosing oxalate chain. Eighty to eighty-eight per cent of platinum are bound to proteins, as for cisplatin, whereas carboplatin is less reactive. Cisplatin and oxaliplatin active metabolites, i.e. monoaquo platin and dach-platin quickly react with small proteins with sulfhydryl groups, such as glutathione, cysteine and methionine, and then with high molecular weight proteins, such as albumin and gammaglobulins through covalent link. Thus, their terminal half lives are long, about ten days, but no platinum accumulation has been reported in plasma with oxaliplatin, whereas after cisplatin administration, both total and ultrafiltrable platinum progressively accumulate in plasma. This difference may play a role in the lack of oxaliplatin nephrotoxicity and its more delayed and reversible neurotoxicity. On the other hand, carboplatin is more stable, less bound to proteins and is largely excreted inchanged in urine. This can explain that it passes more easily through the blood brain barrier. Erythrocytes represent an important deep compartment, especially for oxaliplatin, a little bit less for cisplatin. Oxaliplatin is trapped in erythrocytes through a covalent binding to globin. There, its half life is identical to that of erythrocytes. According to certain authors, this trapping would be involved in the incidence of anemia. On the contrary, carboplatin is quickly extruded from erythrocytes. The three derivatives kinetics in plasma present a wide interindividual variability, resulting in differences in term of toxicity and efficacy. For the three of them, plasma clearance is correlated to creatinine clearance, but only carboplatin dosage can be individually adjusted, based on creatinine clearance measurement, thanks to its simple renal excretion, due to exclusive glomerular filtration, and after Calvert's, Egorin's and Chatelut's population kinetics studies. Cisplatin renal excretion is more complex, combining reabsorption and secretion processes. Therefore, individual dosage adjustment needs platinum concentration measurement in plasma, but there is no general agreement on the platinum species to measure, ultrafiltrable or bound. Oxaliplatin is too recent in clinical practice and still lacks of PK-PD data. These characteristics can help us for a better knowledge of the three platinum derivatives clinical properties, both in term of kinetics, behaviour and toxicity.