As you will learn later in this chapter, cancer cells from patients with Burkitt lymphoma carry a reciprocal chromosomal translocation between chromosome 8 and another chromosome, often 22. Each patient exhibits a unique pattern of chromosome breakage (“breakpoints”) and reattachment, but each cell from that patient carries the same breakpoints. From this result, what can you conclude regarding how the lymphoma arose?
To determine: The reason for the development of Burkitt lymphoma..
Introduction: The chromosomal translocation can result in the development of various types of cancers like Burkitt’s lymphoma. The starting point for all the cancers is the disturbance in the regulatory mechanism of the cell cycle. When cell cycle regulation is affected, it leads to the uncontrolled growth of the cells. The body has mechanisms for the prevention of such conditions by apoptosis and activation of the tumor suppressor gene, but failure of these mechanisms result in the development of cancer.
Explanation of Solution
The various cellular abnormalities which result in the development of the Burkitt’s lymphoma are as follows:
- It is caused by the translocation of the proto-oncogene which is called as MYC.
- This gene is normally present on the chromosome 8 but is translocated to chromosome 14.
- The region of chromosome 14 where MYC gene is translocated is a very high expression area as it is used to produce antibodies.
- The MYC gene encodes for Myc protein which acts as transcription factor for cell proliferation.
- Since MYC gene is now in the high expression region, it is also expressed along with the antibody producing genes.
- The increased concentration of the MYC gene results in the production of excess amount of MYC protein.
- The excessive amount of this transcription factor results in the excessive proliferation of the lymphocytes; thereby, causing the cancer.
Hence chromosomal abnormalities result in the development of Burkitt’s lymphoma.
Want to see more full solutions like this?
Chapter 26 Solutions
EBK BECKER'S WORLD OF THE CELL
- Why are proto-oncogenes present in non-cancerous cells? A one sentence answer is fine.arrow_forwardYOU DON'T NEED TO EXPLAIN THESE QUESTIONS JUST PROVIDE ANSWER DNA separates during ____ of mitosis. a)Prophase b)Telophase c)Metaphase d)Interphase e)Anaphase 2. What separates during mitosis? a)Single DNA strands b)Cytoplasm c)Sister chromatids d)Telomeres e)Homologous chromosomes 3. Oncogenes are associated with cancer because they Oncogenes are associated with cancer because they (select one answer) Cause cells to initiate a death pathway Fail to put a “brake” on the cell cycle Push cells through the cell cycle Divert cells into G0 phase Slow down the cell cyclearrow_forwardAlthough slow acting retroviruses lack oncogenes, retroviral infection can activate proto oncogenes leading to oncogenesis. a. Describe the mechanism of proto-oncogenes activation that can result from with infection with slow acting retroviruses. b. In what other ways can proto-oncogenes be converted to oncogenes?arrow_forward
- Which of the following effectively describes the situation of someone with an inherited predisposition to cancer such as familial adenomatous polyposis or BRCA-associated familial breast cancer? Choose all that apply a) If they get malignant cancer, somatic mutations will not have been a factor b) Their cancer will most likely arise in their germ cells, not their somatic cells c) None of the answers effectively describes the situation d) Every cell of their body contains a gain-of-function allele of an oncogene e) Most cells in their body contain multiple cancer-causing mutations f) Every cell of their body contains a defective, loss-of-function allele of a tumor suppressor genearrow_forwardThe family of a sixth-grade boy in Palo Alto, California, wasinformed by school administrators that he would have to transferout of his middle school because they believed his mutation ofthe CFTR gene, which does not produce any symptoms associatedwith cystic fibrosis, posed a risk to other students at the schoolwho have cystic fibrosis. After missing 11 days of school, a settlementwas reached to have the boy return to school. What ethicalproblems might you associate with this example?arrow_forwardWhy is the Philadelphia chromosome important to understanding & treating some cancers, especially CML?arrow_forward
- 3) Examine the graph showing the relative percentage normal and cancer cells spend in various stages of the cell cycle. Based on the information in the graphs, infer how cancer cells differ from typical, noncancerous cells. Select ALL that apply. A) Cancer cells do not replicate their DNA. B) Cancer cells replicate their DNA too quickly. C) Cancer cells do not go through interphase during their cell cycle. D) Cancer cells spend more time dividing compared to typical cells. E) Cancer cells do not always grow to the same size as typical cells. more than 1 answer. not gradedarrow_forwardHyper-IgE syndrome, also known as Job’s syndrome, is an immunodeficiency disease resulting from the lack of function of a single gene (gene ‘X’). Patients with this disease are highly susceptible to infections with extracellular bacteria and fungi, most frequently including Staphylococcus aureus infections and Candida albicans infections in the skin. Analysis of the various immune cell compartments indicates that these patients have normal numbers of each cell lineage (i.e., CD4 and CD8 T cells, B cells, monocytes, dendritic cells, NK cells, granulocytes, etc.), and normal levels of IgG, IgA, and IgM antibodies, but higher than normal levels of IgE. Given this information, name a likely component of the immune response that could be impaired in these patients.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_forward
- Please answer the following questions: 1. What is the role of MinC, MinD, and MinE in bacterial cell division? a. What would happen if MinC was deleted from the cell? (Be as specific as you can) b. What would happen if MinD was deleted from the cell? (Be as specific as you can) c. What would happen if MinE was deleted from the cell? (Be as specific as you can) 2. What would happen if SulA was deleted from a bacterial cell? 3. If a culture had 150 cells to begin with, how many cells would be present after 6 generations? 4. If a culture had 4 cells to begin with and has a generation time of 60 minutes, how long would it take to get 1,048,576 cells? (Although we didn't learn this explicitly, between you, google, and your long lost math skills, I know you can do it). 5. Describe the four phases of bacterial cell division. a. Where would horizontal gene transfer occur? b. Where would sporogenesis occur? c. If antibiotics generally target cells which are growing and dividing as fast as they…arrow_forward1. a)Proteins that stimulate/promote progression through the cell cycle are encoded by (oncogenes or tumor suppressor genes). Boldface one. b)Proteins that inhibit progression through the cell cycle are encoded by (oncogenes or tumor suppressor genes). Boldface one. c)What is the difference between a proto-oncogene and an oncogene? d)To cause cancer, proto-oncogenes require (1 or 2)allele(s) to be mutated and therefore are considered (dominant or recessive). The mutation results in a (loss or gain) of function. For each underlined pair, boldface one. e)To cause cancer, tumor suppressor genes require (1 or 2)allele(s) to be mutated and therefore are considered (dominant or recessive). The mutation results in a (loss or gain) of function. For each underlined pair, boldface one.arrow_forwardLooking at Figure 1, what did Romansik et al. (2007) find regarding the relationship between the mitotic index and tumor grades. Explain their findings in your own words. Use specific details from Figure 1. The research paper is here: https://journals.sagepub.com/doi/10.1354/vp.44-3-335arrow_forward
- Human Heredity: Principles and Issues (MindTap Co...BiologyISBN:9781305251052Author:Michael CummingsPublisher:Cengage Learning