Advances in Understanding Genetic Changes in Cancer Impact on Diagnosis and Treatment Decisions in the 1990s (1992) / Chapter Skim
Currently Skimming:
1. Introduction
1. Introduction
Pages 1-7
The Chapter Skim interface presents what we've algorithmically identified as the most significant single chunk of text within every page in the chapter.
Select key terms on the right to highlight them within pages of the chapter.
From page 1... ...
Many of the genetic changes that underlie malignant transformation of cells and/or distinguish malignant clones can be used as markers to diagnose, monitor, or characterize various forms of cancer. The purpose of this report is to assess the current status of genetic testing in cancer management both from the standpoint of those tests and genetic markers that are presently available and from the perspective of genetic approaches to cancer testing that are likely to have an impact on cancer management in the near future.
|
From page 2... ...
DNA replication occurs by separation of the two strands in a DNA molecule, followed by synthesis of two new daughter strands having nucleotide sequences based on the template provided by the two parent strands. The result is a doubling of the DNA, with each molecule containing a parental strand and a new daughter strand complementary to the parent strand.
|
From page 3... ...
Abundant, pure DNA fragments generated by cloning have been invaluable for the structural and functional analyses of nucleotide sequences in DNA and for the production of reagents used in diagnosis. _A^_ rim JAA I ~ ~~~j5~11~ MU Brief Overview of Cancer Genetics Recognition of the basic role of mutation in the genesis of cancer required the identification of unique genetic changes associated with particular tumors.
|
From page 4... ...
Breaks occur in bands q34 and qll of chromosomes 9 and 22, respectively, followed by a reciprocal exchange of chromosomal material. This rearrangement results in the translocation of the ABL oncogene, normally located at 9q34, adjacent to the BCR gene on chromosome 22, giving rise to a chimeric BCR-ABL gene, whose protein product plays a role in the transformation of myeloid cells.
|
From page 5... ...
While genetic heterogeneity due to the appearance of subclones during growth and progression of the tumor may complicate this picture, those changes that are directly responsible for the malignant phenotype are likely to be maintained throughout the entire population of cells. Such changes constitute a specific marker that can be exploited to distinguish malignant from normal cells.
|
From page 6... ...
The precise manner in which this occurs is still being defined, but many of these genes seem to regulate the entrance of resting cells into the cell cycle, an event necessary for cell proliferation. For this reason, mutations involving tumor suppressor genes usually abolish the function of the protein and result in increased proliferative potential.
|
From page 7... ...
INTROD UCTION ciple, is that the presence of the viral genomes in the cell acts as a cofactor in malignant transformation by stimulating the cell to divide, and that more rapid replication of cellular DNA predisposes the cell to mutation. Regardless of the mechanism of oncogenesis, the presence of viral genomes and virus-specific proteins produces changes in the genotype and phenotype of the host cell, and in some circumstances, these changes can serve as tumorspecific markers.
|
Key Terms
This material may be derived from roughly machine-read images, and so is provided only to facilitate research.
More
information on Chapter Skim is available.