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排序方式: 共有327条查询结果,搜索用时 15 毫秒
31.
32.
Correlation of P-glycoprotein expression and function in childhood acute leukemia: a children's cancer group study 总被引:7,自引:0,他引:7
Clinical drug resistance may be attributed to the simultaneous selection and expression of genes modulating the uptake and metabolism of chemotherapeutic agents. P-glycoprotein (P-gp) functions as a membrane-associated drug efflux pump whose increased expression results in resistance to anthracyclines, epipodophyllotoxins, vinca alkaloids, and some alkylating agents. This type of resistance occurs as both de novo and acquired resistance to therapy for leukemia. We have studied P- gp expression and function in childhood acute leukemias by developing a series of doxorubicin- and vincristine-selected CEM, T-cell lymphoblastoid cell lines that recapitulate the low levels of expression and resistance seen clinically. These cell lines have been used to develop flow cytometric assays for the semiquantitative measurements of P-gp expression with the MRK16 monoclonal antibody and P-gp function using the enhanced retention of rhodamine 123 in the presence of verapamil, a resistance modulator. Kolmogorov-Smirnov statistics, represented by the D measurement, are used to determine the difference in level of P-gp expression by comparing MRK16 staining to an IgG2a isotype control. When D is > 0.09, there is an excellent correlation (R = 0.82) between P-gp expression and function. The evaluation of 107 bone marrow specimens from 84 children with lymphoblastic or myelogenous leukemia showed a statistically significant (P = .004) increase in P-gp function at relapse. P-gp expression at relapse, however, approached but did not reach a significant level (P = .097). Using this methodology, we can identify patients with levels of P-gp expression and function that we can define clinically, as well as children with discordant multidrug resistance phenotypes. This study supports the role of P-gp-mediated drug resistance in childhood leukemia and confirms that P-gp expression and function are measurable in their leukemic blasts. These assays provide the means for the in vitro testing of resistance modulators and the monitoring of in vivo response to treatment with these agents. 相似文献
33.
Teerenhovi L; Knuutila S; Ekblom M; Rossi L; Borgstrom GH; Tallman JK; Andersson L; de la Chapelle A 《Blood》1984,64(5):1116-1122
A major problem in the cytogenetic analysis of hematologic neoplasms has been an inability to identify the cell from which the chromosomes were obtained. We describe a procedure that allows simultaneous analysis of karyotype and cell cytology in mitotic cells. The method differs from conventional cytogenetic analysis in that after mild hypotonic treatment, the cells are cytocentrifuged onto glass slides. In mitotic cells, this procedure often results in adequate spread of the chromosomes within the intact cell membrane. The cytoplasmic structure also remains intact, so that cytologic preparations are of good quality. Morphologic and immunologic identification of mitotic cells can be done using routine hematologic stains, such as Giemsa or Sudan black B, and various antisera using immunofluorescence techniques. The chromosomes can be simultaneously analyzed either without banding on slides stained with Giemsa or with Q-banding on slides stained with immunofluorescence techniques. Identification of numerical and structural karyotype aberrations thus is possible in morphologically identified cells. 相似文献
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39.
Women worried about their familial breast cancer risk--a study on genetic advice in general practice
de Bock GH; Perk DC; Oosterwijk JC; Hageman GC; Kievit J; Springer MP 《Family practice》1997,14(1):40-43
AIMS: To ascertain whether women who consulted their GP because they
perceived themselves as at increased risk of familial breast cancer were
indeed at increased risk, and to evaluate potential strategies for
assessing genetic risk of breast cancer in general practice. METHODS:
Sixty-seven out of 81 women who had consulted their GP for advice about
their possible increased risk of developing breast cancer due to breast
cancer in the family were interviewed. Familial breast cancer risk was
assessed by a clinical geneticist. This assessment was compared with two
recent guidelines for referral for genetic counselling. RESULTS: More than
half (52%; n = 35) the women had a relative risk of two and over for
developing breast cancer, while another half of these 35 (25%; n = 17) had
a relative risk of three and over. All the women (n = 17) with a relative
risk of three and over were identified by means of the two current
guidelines for referral for genetic counselling, while more than half of
the women (61%; n = 11) with a relative risk between two and three were
identified. CONCLUSIONS: More than half the women concerned about their
familial risk of breast cancer are indeed at increased risk of breast
cancer. Current guidelines correctly identify women at high risk. However,
doubts about the health gain and feasibility of referral warrant caution,
and need further investigation.
相似文献
40.
Florian Brunner Lucas M Bachmann Ulrich Weber Alfons GH Kessels Roberto SGM Perez Johan Marinus Rudolf Kissling 《BMC musculoskeletal disorders》2008,9(1):92