Hair loss is a well-known side effect of chemotherapy; why does this side effect occur? (1) Chemotherapy targets cells undergoing division. Hair stem cells are constantly replenishing (growing) just like cancer cells. They are then also targeted by chemotherapy, causing hair loss. (2) Chemotherapy targets all cells, whether dividing or not dividing, and hair cells are collateral in the fight against cancer (3) Chemotherapy targets proteins in our cells and hair cells have an abundance of proteins

Hair loss is a well-known side effect of chemotherapy; why does this side effect occur? (1) Chemotherapy targets cells undergoing division. Hair stem cells are constantly replenishing (growing) just like cancer cells. They are then also targeted by chemotherapy, causing hair loss. (2) Chemotherapy targets all cells, whether dividing or not dividing, and hair cells are collateral in the fight against cancer (3) Chemotherapy targets proteins in our cells and hair cells have an abundance of proteins

Human Heredity: Principles and Issues (MindTap Course List)

11th Edition

ISBN:9781305251052

Author:Michael Cummings

Publisher:Michael Cummings

Chapter12: Genes And Cancer

Section: Chapter Questions

Problem 15QP: Which of the following mutations will result in cancer? a. homozygous recessive mutation in a...

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Similar questions

How can the role of epigenetics in cancer be reconciled with the idea that cancer is caused by the accumulation of genetic mutations in tumor-suppressor genes and proto-oncogenes?
Cancer-promoting mutations are likely to have different effects on the activity of proteins encoded byproto-oncogenes than they do on proteins encodedby tumor-suppressor genes. Explain.
The rb gene encodes a protein that inhibits E2F, a transcriptionfactor that activates several genes involved in cell division.Mutations in rb are associated with certain forms of cancer,such as retinoblastoma. Under each of the following conditions,would you expect the cancer to occur?A. One copy of rb is defective; both copies of E2F are functional.B. Both copies of rb are defective; both copies of E2F arefunctional.C. Both copies of rb are defective; one copy of E2F is defective.D. Both copies of rb and E2F are defective.
Is the presence of oncogenic Ras necessary for transient inflammatory stimulation to induce chronic pathologies (such as cancer) OR is chronic inflammation essential for oncogenic Ras to induce tumorigenesis?
What is a signal-transduction pathway? Why are mutations in components of signal-transduction pathways often associated with cancer?
A research study indicated that an agent in cigarette smoke caused the silencing of a tumor suppressor gene called p53. However,upon sequencing, no mutation was found in the DNA sequence for this gene. Give two possible explanations for these results.
Which of the following accurately compares tumor suppressor genes and proto-oncogenes? A. Both tumor suppressor and proto-oncogenes prevent the spread of cancer by targeting and destroying existing cancer cells. B. A person who has both tumor suppressor and proto-oncogenes will always develop cancer. C. Proto-oncogenes code for growth factors, while tumor suppressor genes inhibit cell division of damaged cells. D. When a proto-oncogene mutates, it becomes a tumor suppressor gene.
Studies suggest that the presence of oncogenic Ras is not sufficient to drive tumorigenesis. Instead, the activity of Ras needs to be amplified and sustained to induce pathological consequences. Recent studies have suggested a role for inflammatory stimuli on tumor development in the context of oncogenic Ras. Is the presence of oncogenic Ras necessary for transient inflammatory stimulation to induce chronic pathologies (such as cancer) OR is chronic inflammation essential for oncogenic Ras to induce tumorigenesis?
For each of the following situations, provide a plausible explanation for how it could lead to unrestricted cell division.(a) Colon cancer cells often contain mutations in the gene encoding the prostaglandin E2 receptor. PGE2 is a growth factor required for the division of cells in the gastrointestinal tract.(b) Kaposi sarcoma, a common tumor in people with untreated AIDS, is caused by a virus carrying a gene for a protein similar to the chemokine receptors CXCR1 and CXCR2. Chemokines are cell-specific growth factors.(c) Adenovirus, a tumor virus, carries a gene for the protein E1A, which binds to the retinoblastoma protein, pRb. (d) An important feature of many oncogenes and tumor suppressor genes is their celltype specificity. For example, mutations in the PGE2 receptor are not typically found in lung tumors. Explain this observation. (Note that PGE2 acts through a GPCR in the plasma membrane.)
Distinguish between proto-oncogenes and tumor-suppressor genes. To become cancer promoting, do proto-oncogenes and tumor-suppressor genes undergo gain-of-function or loss-of-function mutations? Classify the following genes as proto-oncogenes or tumor-suppressor genes: p53, ras, BCL-2, JUN, MDM2, and p16.
Why do cancer cells undergo EMT and MET? What are the cellular changes (expression or suppression of molecules) associated with EMT and MET? What does each change facilitate?
TGF-β1 is a protein that affects cell growth and differentiation. Scientists conducted an experiment where epithelial cells were treated with transforming growth factor beta 1 (TGF-β1) in the laboratory. At the end of the experiment, the epithelial cells had transformed through several stages from epithelial cells to embryonic stem cells (ESCs) to neural progenitor cells (NPCs), and finally to cortical neurons (CNs). The scientists observed the transformation of the cells by analyzing gene expression at certain stages (M1-M7) and determined the relative gene expression level, as shown in the graph. The graph shows the relative gene expression level for cells at different stages of differentiation. Which of the following claims could account for the differences in gene expression at each stage of cell differentiation, and how does this correlate with the distance of the genes on the chromosome? A - Cell differentiation is controlled by RNA translation, but there is no…