Biology 2e
2nd Edition
ISBN: 9781947172517
Author: Matthew Douglas, Jung Choi, Mary Ann Clark
Publisher: OpenStax
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Textbook Question
Chapter 9, Problem 19RQ
A scientist notices that a cancer cell line fails to die when he adds an inducer of apoptosis to his culture of cells. Which hypothesis could explain why the cells fail to die?
- The cells have a mutation that prevents the initiation of apoptosis signaling.
- The cells have lost expression of the receptor for the apoptosis-inducing ligand.
- The cells overexpress a growth factor pathway that inhibits apoptosis.
- All of the above.
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How is apoptosis involved in cancer? Describe the role of apoptosis in cancer and identify what molecules are involved. Cite your references.
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RAS is a signal transducer that acts as a switch for turning on cell division. Drag the descriptions below to their proper places on the
figure to show the sequence of events.
When growth factor
binds to the receptor,
the intracellular domain
activates RAS by
facilitating exchange of
GDP for GTP.
When no growth factor
is bound to the
extracellular receptor,
RAS is bound to GDP
and is inactive.
RAS activates the
first of three
sequential kinase
proteins termed the
MAP kinase cascade.
Cell proliferation
proceeds as the
machinery for cell
division is set in
motion.
The end result of the
MAP kinase cascade
is activation of a
transcription factor.
Receptor
1
Ras
GDP
2
4
5
Growth factor
Ras
GTP
TNF and Fas ligand bind cell-surface receptors to trigger cell death. Although the death signal is generated external to the cell, why do we consider the death induced by these molecules to be apoptotic rather than necrotic?
Chapter 9 Solutions
Biology 2e
Ch. 9 - Figure 9.8 HER2 is a receptor tyrosine kinase. In...Ch. 9 - Figure 9.10 In certain cancers, the GTPase...Ch. 9 - Figure 9.17 Which of the following statements...Ch. 9 - Figure 9.18 What advantage might biofilm...Ch. 9 - What property prevents the ligands of cell-surface...Ch. 9 - The secretion of hormones by the pituitary gland...Ch. 9 - Why are ion channels necessary to transport ions...Ch. 9 - Endocrine signals are transmitted more slowly than...Ch. 9 - A scientist notices that when she adds a small,...Ch. 9 - Where do DAG and IP3 originate? They are formed by...
Ch. 9 - What property enables the residues of the amino...Ch. 9 - Histamine binds to the H1 G-protein-linked...Ch. 9 - A scientist observes a mutation in the...Ch. 9 - What is the function of a phosphatase? A...Ch. 9 - How does NF-kB induce gene expression? A small,...Ch. 9 - Apoptosis can occur in a cell when the cell is...Ch. 9 - What is the effect of an inhibitor binding an...Ch. 9 - How does PKC’s signaling role change in response...Ch. 9 - A scientist notices that a cancer cell line fails...Ch. 9 - Which type of molecule acts as a signaling...Ch. 9 - Quorum sensing is triggered to begin when...Ch. 9 - A doctor is researching new ways to treat biofilms...Ch. 9 - What is the difference between intracellular...Ch. 9 - How are the effects of paracrine signaling limited...Ch. 9 - What are the differences between internal...Ch. 9 - Cells grown in the laboratory are mixed with a dye...Ch. 9 - Insulin is a hormone that regulates blood sugar by...Ch. 9 - The same second messengers are used in many...Ch. 9 - What would happen if the intracellular domain of a...Ch. 9 - If a cell developed a mutation in its MAP2K1 gene...Ch. 9 - What is a possible result of a mutation in a...Ch. 9 - How does the extracellular matrix control the...Ch. 9 - A scientist notices that a cancer cell line shows...Ch. 9 - What characteristics make yeasts a good model for...Ch. 9 - Why is signaling in multicellular organisms more...Ch. 9 - Pseudomonas infections are very common in hospital...
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- The Bax gene, codes for a cytosolic protein that plays an important role in apoptosis. Growth factor withdrawal stimulates the pro-apoptotic protein Bax. Which of the following are true for the Bax gene? Select all that apply The Bax gene is a proto-oncogene The Bax gene is a tumor suppressor gene In cancer or transformed cells, the Bax gene mutation would be dominant, and a gain of function mutation In cancer or transformed cells, the Bax gene mutation would be recessive, and a loss of function mutationarrow_forwardIdentify which of the following statements is a lie? Select one: a. Apoptosis occurs as the body produces certain enzymes that initiate degradation of nuclear and cytoplasmic material, breaking the cell into necrosis bodies. b. Apoptosis helps maintain a healthy and normal population of cells. c. Apoptosis plays an essential role in growth, immune surveillance, and embryological development.arrow_forwardWhich is true for cancer cells: 1) Cell death occurs after a determined number of cell divisions 2) Contact with other cells reduces chance of cell division 3) Cell division occurs in the presence of stop signals.arrow_forward
- Some cancer cells are insensitive to typical chemotherapy. Research into the mechanisms underlying this insensitivity uncovered an ability by these cells to pump the treatment drug out of the cell against its concentration gradient. Additional drugs have been developed that inhibit the pump, thus trapping the chemotherapeutic agent inside to promote cancer cell destruction. The Figure shows what happens when two types of cells are treated with a 3H-labeled anti-cancer drug, paclitaxel. Which set of cells (A or B) would be described as resistant to the cancer treatment? Explain your answer. What type of transport are the resistant cells using?arrow_forwardTumor suppressor proteins can assist in slowing down the cell cycle under appropriate conditions. In humans, the TP53 gene encodes a tumor suppressor called p53. Most mutations in the TP53 gene result in a mutant form of p53 that can no longer function to slow down the cell cycle, which can lead to a cell becoming cancerous. However, some mutant forms of p53 actually possess the ability to increase a cell's resistance to anticancer treatments. Which of the following BEST describes the latter type of mutation? loss-of-function mutation gain-of-function mutation suppressor mutation reverse mutationarrow_forwardGive typing answer with explanation and conclusionarrow_forward
- The epidermal growth factor receptor (EGFR) activates a complex signaling network to increase expression of several genes and promote cell proliferation as shown in the figure below. EGF Active EGFR Inactive EGFR Inactive EGFR P- EP Inactive Ras-GDP Ras-GTP Active Raf -P NUCLEUS МЕК-F МАРК-Р Active МАРК-P C-myc gene transcribed CYTOPLASM Cell proliferation Which of the following scenarios would result in decreased expression of the c-myc gene? Select all that apply A homozygous mutation of the EGFR gene resulting in a deletion of the ligand binding domain A homozygous mutation of the ras gene so that Ras protein was not able to exchange GDP for GTP A homozygous mutation of the ras gene so that Ras protein was not able to hydrolyze GTP for GDP A homozygous mutation of the MAPK gene so that MAPK protein was always in a phosphorylated statearrow_forwardIn order for certain cancers to propagate, they require a growth factor known as Vascular Endothelial Growth Factor (VEGF). What does VEGF signal the cell to do and how does this promote the propagation of cancer cells?arrow_forwardThe epidermal growth factor receptor (EGFR) activates a complex signaling network to increase expression of several genes and promote cell proliferation as shown in the figure below. EGF Active EGFR Inactive EGFR P- Inactive EGFR Inactive Ras-GDR Ras-GTP Active Raf -P МЕК- Р NUCLEUS МАРК-Р Active МАРК-Р C-myc gene transcribed CYTOPLASM Cell proliferation Which of the following scenarios would result in increased expression of the c-myc gene? Select all that apply. A homozygous mutation of the EGFR gene resulting in a deletion of the ligand binding domain A homozygous mutation of the ras gene so that Ras protein was not able to exchange GDP for GTP A homozygous mutation of the MAPK gene so that MAPK protein was always in a phosphorylated state A homozygous mutation of the ras gene so that Ras protein was not able to hydrolyze GTP for GDParrow_forward
- A normal cell has no growth factor bound to the growth factor receptor. What do you predict about ERK in this situation? it will activate a transcription factor it will be phosphorylated it will not be phosphorylate it will not go into the nucleus Darrow_forwardMatch each of the changes that can contribute to cancer with its correct description. Loss of function of regulators that send old or damaged cells into apoptosis Hyperactivation of signalling pathways that tell the cell to grow and divide 1. Sustaining proliferative signalling Loss of function of structural proteins that anchor cells to surrounding tissue and/or activation of cell migration 2. Evading growth suppressors 3. Activating invasion and metastasis Loss of function of 4. Enabling replicative immortality regulators that stop inappropriate growth and cell division 5. Inducing angiogenesis 6. Resisting cell death Loss of function of regulators that force aging cells to exit the cell cycle and enter GO or replicative senescence 00arrow_forwardp53 gene, as is the Rb gene, is a tumor suppressor gene. p53 protein binds to DNA leading to the simulation of p21 that work together with cdk2. When p21 is defective and cannot joined to cdk2 the cell cannot pass through to the next stage of cell division. Mutated p53 cannot bind to DNA in an effective way, and therefore the p21 protein is not available to act as the 'stop signal' for cell division. Thus cells divide uncontrollably, and form tumors. Hi, can you please elaborate on this: based on the info above, what is the relationship between genetics and environment in the development of these type of cancer. Which factor (genetics or environment) is playing a larger role in the generation of these types of cancers?arrow_forward
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