EBK ESSENTIALS OF GENETICS
9th Edition
ISBN: 8220102741614
Author: Palladino
Publisher: YUZU
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Chapter 16, Problem 25PDQ
Summary Introduction
To review:
A new gene has been discovered during cancer research project. The gene is mutated in many metastatic tumors. It has been found that the newly discovered gene sequence resembles with some serine proteases. Determine the contribution of new gene towards the development of highly invasive cancers.
Introduction:
Cancer is a conglomeration of diseases. Abnormal cell division in the body causes cancer and the abnormal cell division is known as cancer metastasis. Invasion of cancer depends on various factors. Proteases contribute in many ways towards developing cancer.
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As part of a cancer research project, you have discovered a gene that is mutated in many metastatic tumors. After determining the DNA sequence of this gene, you compare the sequence with those of other genes in the human genome sequence database. Your gene appears to code for an amino acid sequence that resembles sequences found in some serine proteases. Conjecture how your new gene might contribute to the development of highly invasive cancers.
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Chapter 16 Solutions
EBK ESSENTIALS OF GENETICS
Ch. 16 -
CASE STUDY | I thought it was safe
A middle-aged...Ch. 16 -
CASE STUDY | I thought it was safe
A middle-aged...Ch. 16 -
CASE STUDY | I thought it was safe
A middle-aged...Ch. 16 - HOW DO WE KNOW? In this chapter, we focused on...Ch. 16 -
2. Review the Chapter Concepts list on page 307....Ch. 16 - What is the relationship between signal...Ch. 16 - Where are the major regulatory points in the cell...Ch. 16 -
5. Describe kinases and cyclins. How do they...Ch. 16 - (a) How does pRB function to keep cells at the G1...Ch. 16 - What is the difference between saying that cancer...
Ch. 16 -
8. What is apoptosis, and under what...Ch. 16 - Define tumor-suppressor genes. Why is a mutation...Ch. 16 - A genetic variant of the retinoblastoma protein,...Ch. 16 -
11. Part of the Ras protein is associated with...Ch. 16 - If a cell suffers damage to its DNA while in S...Ch. 16 - Prob. 13PDQCh. 16 - Prob. 14PDQCh. 16 - Prob. 15PDQCh. 16 - Prob. 16PDQCh. 16 - Prob. 17PDQCh. 16 - How do normal cells protect themselves from...Ch. 16 - Prob. 19PDQCh. 16 - Explain how environmental agents such as chemicals...Ch. 16 - Radiotherapy (treatment with ionizing radiation)...Ch. 16 - Genetic tests that detect mutations in the BRCA1...Ch. 16 - Prob. 23PDQCh. 16 - Prob. 24PDQCh. 16 - Prob. 25PDQCh. 16 - Prob. 26PDQCh. 16 - Prob. 27PDQCh. 16 - Prob. 28PDQ
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- Sequencing the human genome, the development of microarray technology, and personal genomics promise to improve our understanding of normal and abnormal cell behavior. How are these approaches dramatically changing our understanding and treatment of complex diseases such as cancer?arrow_forwardImagine you have used cBioportal and breast cancer patient datasets and identified a cancer-associated mutation in a particular protein. What would you do next to understand whether that mutation contributes to tumor progression (include experimental approach)?arrow_forwardMany of the mutations in cancer samples are not necessarily driver mutations, but rather passenger mutations that are along for the ride. Just because the tumors with a strong environmental component possess a higher frequency of mutations does not mean more oncogenes or more failure of tumor suppressors is occurring. Hematologic childhood cancers have a lower frequency of mutations than tumors with a strong environmental component such as lung cancers and melanoma; WHY?arrow_forward
- Unlike many other diseases, the vast majority of cancers in humans are not transmissible - meaning a person can’t ‘catch cancer’ from someone else. How does a person get cancer, then? Starting with a normal (non-cancerous) cell, describe a possible sequence of events that could eventually result in metastasized cancer, including the genes, structures or processes involved.arrow_forwardHow do normal cells protect themselves from accumulating mutations in genes that could lead to cancer? How do cancer cells differ from normal cells in these processes?arrow_forwardWhat are the biggest challenges that mutations pose to oncologists and cancer biologists who seek to find novel cures against cancers?arrow_forward
- Why are people more likely to develop cancer as they age? Why does inheriting a mutation increase cancer risk?arrow_forwardBecause cancer cells do not normally die, does this imply that if people attempted to extend their lives, it would most likely be through the employment of cancer cells? Could cancer be used as a vector to modify cells or shape it into what is desired?arrow_forwardAlthough it is well known that X-rays cause mutations, they are routinely used to diagnose medical problems, including potential tumors, broken bones, and dental cavities. Why is this done? What precautions need to be taken?arrow_forward
- One unexpected result of the sequencing of the human genome was the finding that mutations in a single gene can be responsible for multiple distinct disorders. For example, mutations in the RET gene can cause two different types of multiple endocrine neoplasias, familial medullary thyroid carcinoma, and Hirschsprung disease. How do you think mutations in a single gene can have such diverse effects?arrow_forwardWhich of the following statements about cancer is false? (a) oncogenes arise from mutations in proto-oncogenes (b) tumor suppressor genes normally interact with growth-inhibiting factors to block cell division (c) more than 120 cancer-driving genes have been discovered (d) oncogenes were first discovered in mouse models for cancer (e) the development of cancer is usually a multistep process involving both oncogenes and mutated tumor suppressor genesarrow_forwardWhat is the difference between a proto-oncogene and a tumor-suppressor gene?arrow_forward
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