To review:
The reason for the failure of a transcriptionally active fusion gene to cause chronic myelogenous leukemia (CML) in healthy individuals.
Introduction:
Chronic myelogenous leukemia is a type of cancer of the white blood cells (WBCs). In this form of leukemia, an increased and unregulated growth of the immature myeloid cells occurs in the bone marrow. This is followed by the accumulation of these proliferated cells in the blood and spleen. The characteristic genetic change responsible for this disease is a chromosomal translocation that leads to the formation of Philadelphia chromosome that contains the Breakpoint cluster region (BCR) and Abelson murine leukemia (ABL) genes to form a fusion protein, this protein is responsible for the failure of cell cycle control.
Want to see the full answer?
Check out a sample textbook solutionChapter 16 Solutions
Essentials of Genetics (9th Edition) - Standalone book
- The diosgenin drug (DSG) has been tested on human cholangiocarcinoma cells (bile duct cancer cells). To this aim, the human cholangiocarcinoma cell lines HuCCT1, QBC939, SK-ChA-1, HuH28, RBE, and Mz-ChA-1 have been subjected to different conditions of treatment with DSG, then assessed for their viability using a MTS assay, and their cell cycle progression using flow cytometry (FCM).Note: The MTS assay is based on the reduction of the MTS tetrazolium compound by viable cells to generate a colored formazan dye that is soluble in cell culture media. This conversion is thoughtto be carried out by NAD(P)H-dependent dehydrogenase enzymes in metabolically active cells.The formazan dye is quantified by measuring its absorbance at 490-500 nm. Question : To which kind of biological molecule does this DSG drug resemble? To which kind of properties do you expect for DSG?arrow_forwardThe following chromosomal aberration is found in nearly 90-95% of all patients who have chronic myelogenous leukemia. This is because the change brings the BCR and ABL genes in close proximity. BCR is responsible for cell growth, and ABL is a proto-oncogene... this favors uncontrolled growth. Which is the most accurate description of the aberration... chio moso me 9 Philad elphia chromosome chromosome 22 BCR ABL 22q11.2 (BCR) 9934 1 (ABL) Deletion Translocation Inversion Duplication DELL O O O Carrow_forwardBased on the sensitivity of DNA to DNase I, as illustrated in Figure , which type of chicken hemoglobin (embryonic or adult) is likely to be produced in the highest quantity in the following tissues and developmental stages? Q. Erythroblasts at day 5arrow_forward
- Based on the sensitivity of DNA to DNase I, as illustrated in Figure, which type of chicken hemoglobin (embryonic or adult) is likely to be produced in the highest quantity in the following tissues and developmental stages? Q.Erythroblasts during the first 24 hoursarrow_forwardBriefly describe the effects of colchicine treatment on cells. What are the genetic implications of such effects?arrow_forwardBelow is a figure (here called Figure 1) from “Prognostic Significance of CpG Island Methylator Phenotype and Microsatellite Instability in Gastric Carcinoma,” by An et al., published in Clinical Cancer Research in 2005. The authors look at five microsatellite loci (BAT 25, BAT 26, D2S123, D5S346, and D17S250) in normal (N) and tumor (T) tissue from patients with Gastric Carcinoma. They amplify the loci by PCR and then instead of using standard agarose gel electrophoresis, they run the PCR products through capillary gel electrophoresis and detect bands as they pass a laser near the positive charge terminal. The x-axis in these plots is the time at which the band passed the laser (aka size of the PCR product) and the intensity of the peaks represents the amount of DNA in that band A. Which patient- 18, 30, or 1- shows the most microsatellite instability? Which patient shows the least? How do you know? B. In which repair pathway is it most likely that you will find the driver mutations…arrow_forward
- For the following diseases, describe the best technique for diagnosing them. Please make sure you include how you would tell someone with the disease from someone without the disease. B. Factor V Leiden thrombophilia is caused by a point mutation at position 1691 in exon 10 of the Factor V clotting factor gene that changes an arginine into a glutamine. This change removes one of the cleavage sites for activated protein C and leads to an increased tendency to clot.arrow_forwardWhat is the Philadelphia chromosome? Briefly describe how it causes chronic myeloid leukemia.arrow_forwardUse the sequence provided here to identify the tag and tag location for the encoded DHFR fusion protein: ATATGCATCACCATCACCATCACATGGTTGGTTCGCTAAACTGCATCGTCGCTGTGTCCCAGAACATGGGCATCGGCAAGAACGGGGACCTGCCCTGGCCACCGCTCAGGAATGAATTCAGATATTTCCAGAGAATGACCACAACCTCTTCAGTAGAAGGTAAACAGAATCTGGTGATTATGGGTAAGAAGACCTGGTTCTCCATTCCTGAGAAGAATCGACCTTTAAAGGGTAGAATTAATTTAGTTCTCAGCAGAGAACTCAAGGAACCTCCACAAGGAGCTCATTTTCTTTCCAGAAGTCTAGATGATGCCTTAAAACTTACTGAACAACCAGAATTAGCAAATAAAGTAGACATGGTCTGGATAGTTGGTGGCAGTTCTGTTTATAAGGAAGCCATGAATCACCCAGGCCATCTTAAACTATTTGTGACAAGGATCATGCAAGACTTTGAAAGTGACACGTTTTTTCCAGAAATTGATTTGGAGAAATATAAACTTCTGCCAGAATACCCAGGTGTTCTCTCTGATGTCCAGGAGGAGAAAGGCATTAAGTACAAATTTGAAGTATATGAGAAGAATGATTAAarrow_forward
- A wild-type mouse that is heterozygous for two immunoglobulin heavy chain alleles (IgHa/b) generates the population of B cells shown on the left of the figure below. A mouse strain, also IgHa/b, carries an inactivating mutation in the VpreB gene. In addition to producing fewer mature B cells than the wild-type mice, the VpreB-deficient mice generate B cells as shown on the right. What is the explanation of the difference seen between the wild-type and the VpreB-mutant B cells?arrow_forwardBased on the sensitivity of DNA to DNase I, as illustrated in Figure , which type of chicken hemoglobin (embryonic or adult) is likely to be produced in the highest quantity in the following tissues and developmental stages? Q. Brain cells throughout developmentarrow_forward. Mutations in an autosomal gene in humans cause aform of hemophilia called von Willebrand disease(vWD). This gene specifies a blood plasma proteincleverly called von Willebrand factor (vWF). vWFstabilizes factor VIII, a blood plasma protein specified by the wild-type hemophilia A gene. Factor VIIIis needed to form blood clots. Thus, factor VIII is rapidly destroyed in the absence of vWF.Which of the following might successfully be employed in the treatment of bleeding episodes in hemophiliac patients? Would the treatments workimmediately or only after some delay needed forprotein synthesis? Would the treatments have only ashort-term or a prolonged effect? Assume that allmutations are null (that is, the mutations result in thecomplete absence of the protein encoded by the gene)and that the plasma is cell-free.a. transfusion of plasma from normal blood into avWD patientb. transfusion of plasma from a vWD patient into adifferent vWD patientc. transfusion of plasma from a hemophilia A…arrow_forward
- Human Anatomy & Physiology (11th Edition)BiologyISBN:9780134580999Author:Elaine N. Marieb, Katja N. HoehnPublisher:PEARSONBiology 2eBiologyISBN:9781947172517Author:Matthew Douglas, Jung Choi, Mary Ann ClarkPublisher:OpenStaxAnatomy & PhysiologyBiologyISBN:9781259398629Author:McKinley, Michael P., O'loughlin, Valerie Dean, Bidle, Theresa StouterPublisher:Mcgraw Hill Education,
- Molecular Biology of the Cell (Sixth Edition)BiologyISBN:9780815344322Author:Bruce Alberts, Alexander D. Johnson, Julian Lewis, David Morgan, Martin Raff, Keith Roberts, Peter WalterPublisher:W. W. Norton & CompanyLaboratory Manual For Human Anatomy & PhysiologyBiologyISBN:9781260159363Author:Martin, Terry R., Prentice-craver, CynthiaPublisher:McGraw-Hill Publishing Co.Inquiry Into Life (16th Edition)BiologyISBN:9781260231700Author:Sylvia S. Mader, Michael WindelspechtPublisher:McGraw Hill Education