UCLA FINAL bio

UCLA FINAL bio - Your Name_ ID Number_ Final Exam LS3...

Info iconThis preview shows pages 1–3. Sign up to view the full content.

View Full Document Right Arrow Icon
Your Name__________________________________ ID Number__________________________________ Final Exam LS3 Section 2, Fall 2003 December 10, 2003 175 Total Points + 20 Points for Multiple Choice Lab Questions As frequently discussed in lecture, mutations in genes involved in the regulation of cell growth and cell division frequently contribute to the development of cancers. The mutations in these “oncogenes” are often missense mutations. However, another type of mutation, called a translocation, frequently contributes to the development of leukemias, which are cancers of blood cells. Translocations involve the fusion of a portion of one chromosome to a portion of another chromosome (see figures on last page). These abnormal chromosomes can be seen under a microscope during a procedure known as karyotype analysis. Genes located at the junction between the two chromosomes are usually altered in some way. These alterations cause the leukemia. Acute lymphoblastic leukemia (ALL) is the most common type of cancer in young children. A substantial percentage of ALL samples contain an abnormal chromosome possessing a portion of chromosome 19 fused to a portion of chromosome 1, as shown on the last page of the exam. This is called a t(1;19) translocation. Cells containing this abnormal chromosome also contain one normal copy of chromosome 1 and one normal copy of chromosome 19. In 1989, David Baltimore’s laboratory at MIT cloned the gene encoding a transcription factor called E2A. During the initial characterization of the E2A gene, they isolated both cDNA and genomic clones, determined the complete DNA sequences of the clones, and prepared antibodies against the E2A protein. These reagents might be useful for answering some of the questions raised below. During this initial characterization, they found that the E2A gene was located on chromosome 19, in the vicinity of the region of this chromosome that becomes fused to chromosome 1 in the t(1;19) translocation. This observation led to the hypothesis that the E2A gene might be at the chromosome 19/chromosome 1 junction. If the E2A gene were indeed at the junction, it would likely be altered in some way and might be the primary cause of a high percentage of ALLs. To determine whether the E2A gene is located at the chromosome 19/chromosome 1 junction, the researchers established a collaboration with Michael Cleary at Stanford, a leader in the ALL field. They first performed a Southern blot with genomic DNA from normal cells and from ALL cells. Fortunately, ALL cells from some patients can be grown on tissue culture dishes, allowing the investigators to obtain large quantities of these cells. The blot was hybridized to a radiolabeled E2A cDNA probe. The Southern blot results, which confirmed that the E2A gene is indeed at the translocation junction 1
Background image of page 1

Info iconThis preview has intentionally blurred sections. Sign up to view the full version.

View Full DocumentRight Arrow Icon
Your Name__________________________________ ID Number__________________________________ and is indeed altered by the translocation, are shown on the last page. The translocation
Background image of page 2
Image of page 3
This is the end of the preview. Sign up to access the rest of the document.

Page1 / 13

UCLA FINAL bio - Your Name_ ID Number_ Final Exam LS3...

This preview shows document pages 1 - 3. Sign up to view the full document.

View Full Document Right Arrow Icon
Ask a homework question - tutors are online