Development of Drug-Resistant Models
The observation that tumors are capable of developing resistance to anticancer agents is a well-established fact in the clinic. In order to explain this phenomenon in the laboratory, fluctuation analysis has been used in a number of studies involving tumor cell lines (1 –3 ), although it was first used by Luria and Delbruck (4 ) in the study of bacterial cultures. Subsequently, work by Goldie and Coldman (5 ) using fluctuation analysis focused on the genetic instability of tumor cells as pivotal to the emergence of drug-resistant cells. The hypothesis suggested that a drug-resistant cell emerged from the clonal expansion of spontaneously mutated cells and not from changes in cellular function induced by drugs. The methodology used in fluctuation analysis is described elsewhere (3 ) and can be used to assess the mutation rate of drug treated tumor cells.
- Mutational Screening of hMLH1 and hMSH2 that Confer Inherited Colorectal Cancer Susceptibility Using Denature Gradient Gel Elect
- Detection of K-ras and p53 Mutations by Mutant-Enriched PCR-RFLP
- Isolation of Circulating MicroRNAs from Microvesicles Found in Human Plasma
- c-myb Antisense Oligonucleotide Therapeutics for Hematologic Malignancies
- Immunophenotyping of Plasma Cells in Multiple Myeloma
- 17 Direct Sequencing for Peutz-Jeghers Gene LKB1 (STK11) Mutations
- Analysis of Alterations in a Base-Excision Repair Gene in Lung Cancer
- Assessment of Insulin-Like Growth Factors and Mutagen Sensitivity as Predictors of Lung Cancer Risk
- 肾癌的survivin mRNA 基因序列
- Expression Cloning of Human B Cell Immunoglobulins