Abstract. Global miRNA expression arrays were used for analysis of 836 miRNAs in formalin-fixed paraffin-embedded samples from 21 tongue cancer patients and 8 controls. Samples had been stored for one to eleven years. Results separated tumour samples from controls, however, the largest variation was correlated to sample storage time, detectable already after one year. With the use of a linear regression model we could adjust for the storage-dependent effect, leading to the identification of 54 differentially expressed miRNAs in tongue cancer, compared to 16 when using standard normalization, including up-regulation of a novel miRNA, miR-424.
Background p53 mutation influences breast cancer cell growth and patient prognosis. However, different p53 mutations impart specific functions to the mutant protein, including dominant negative or gain of function effects. Mutant p53 molecules R273H and R175H are commonly found in primary breast cancers and are present in the MDA-MB-468 and SKBR3 cell lines, respectively. To compare the direct effects of these two mutations in vivo in an identical cellular background, H1299 (p53-null) cells were constructed to express R273H or R175H p53 mutants. Methods Thirty female SCID mice were injected subcutaneously with 106 H1299 (p53-null), H1299/R273H or H1299/R175H cells in DMEM + Matrigel (50:50) suspension. Some mice were treated with an Hsp90 inhibitor, which is required for correct folding of many oncogenic proteins. Results Xenografts bearing R175H showed a mean lag phase (time between cell injection and tumors at exponential growth) of 21 days and a doubling time of 5 days, whereas tumors bearing H1299 (p53-null) or R273H mutation had a lag phase of 31 days with a doubling time of 7 days. Immunohistochemical examination demonstrated a highly heterogeneous pattern of p53 protein expression in the more aggressive R175H expressing cells compared with R273H expressing cells. Hsp90 inhibitor treatment reduced the growth of H1299 and R273H cells, but not R175H cells. Conclusions The specific p53 mutations directly influence the rate of tumor growth and the p53 protein staining pattern on immunohistochemistry. The differential effects of specific p53 mutations should be considered when interpreting clinical data involving p53 mutation such as in the EORTC 10994 trial, with implications for prognostic determination of individual breast cancer patients. Citation Information: Cancer Res 2010;70(24 Suppl):Abstract nr P1-03-07.
Summary The Blood Transfusion Service introduced screening for Hepatitis C antibody (HCV) in September 1991. This is done by second generation enzyme linked immunosorbent assay (ELISA) tests. We present a case of post‐transfusion hepatitis C hepatitis in a patient with myeloma. Infection was acquired before screening was introduced. Both the patient and the infected blood donor were diagnosed using ELISA assays and the polymerase chain reaction (PCR). In this way we prevented the blood donor from spreading the virus via subsequent blood donations. There were some interesting discrepancies in the HCV assays. Blood samples, when tested by different methods, gave both positive and negative results. The results also varied according to when the blood samples to be tested were taken. The case illustrates the importance of confirming positive results and that no single laboratory test is entirely satisfactory in diagnosing HCV infection.
Summary Recent research suggests that over expression of P‐glycoprotein is involved in the resistance of some malignancies to structurally unrelated cytotoxic agents (Pastan & Gottesman, 1987; Kaye & Kerr 1991). It is postulated that P‐glycoprotein decreases intracellular concentrations of cytotoxic agents by promoting their active efflux across the cell membrane (Musto et al. 1991). Modulating agents such as cyclosporin A and its analogues, (Sonneveld & Nooter 1990), verapamil, quinidine, the newer cephalosporines and torenifene have been put forward to inhibit resistance, by inhibiting active drug efflux. We report a case of acute myeloid leukaemia which was resistant to standard induction therapy. In vitro tests showed cyclosporin A to increase the sensitivity of the patient's myeloblasts to daunorubicin by threefold. Remission was successfully induced when cyclosporin A was combined with daunorubicin, cytosine, arabinoside and etoposide.
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