Cancer is driven by alterations in the expression of critical genes, namely tumour suppressors, which play a growth-regulatory role, and proto-oncogenes, which promote the growth and survival of the cell. For both classes of cancer-related gene, suggest a likely mechanism of alteration and sketch the consequence for the gene and protein. Tumour suppressor gene (i.e. TP53, PTEN or APC) Oncogene (i.e. RAS, MYC)

Cancer is driven by alterations in the expression of critical genes, namely tumour suppressors, which play a growth-regulatory role, and proto-oncogenes, which promote the growth and survival of the cell. For both classes of cancer-related gene, suggest a likely mechanism of alteration and sketch the consequence for the gene and protein. Tumour suppressor gene (i.e. TP53, PTEN or APC) Oncogene (i.e. RAS, MYC)

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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Which 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 genes
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.
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.
Out of these 8 hallmarks ( sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, deregulating cellular energetics and metabolism, and avoiding immune destruction). Rank them from least important to most for cancer development. Explain in 2-3 sentences how.
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?
"In the cellular regulatory pathways that control cell growth and proliferation, the products of oncogenes are stimulatory components and the products of tumor suppressor genes are inhibitory components" is true or false.
Explain how mutations in tumor-suppressor genes can be recessive at the level of the cell but cause dominantly inherited predispositions to cancer.
Hereditary retinoblastoma generally affects children in both eyes, while spontaneous retinoblastoma usually occurs during adulthood only in one eye. Explain the genetic basis for the epidemiological distinction between these two forms of retinoblastoma. Explain the apparent paradox: loss-of-function mutations in tumor-suppressor genes act recessively, yet hereditary retinoblastoma is inherited as an autosomal dominant.
Explain the following characteristics of an ideal tumor marker • Specificity for a single type of cancer • High sensitivity and specificity for cancerous growth • Correlation of marker level with tumor size • Homogeneous (i.e., minimal post-translational modifications) • Short half-life in circulation
EXPLAIN BRIEFLY: Explain the molecular mechanisms of cancers caused by a P53 gene mutation.
Which of the following is true of tumor suppressor genes? Group of answer choices a) If this gene is overactive, it becomes an oncogene b) If one of the alleles is mutated, there is usually little effect. Two inactivating mutations are usually required for loss of function (recessive mutation). c) If one copy is lost, the gene no longer functions (dominant mutation) d) Tumor suppressors genes usually cause mitosis or cell growth e) Tumor suppressor genes decrease apoptosis
Describe the general process of cell signalling pathways: what events take place for a signal to cause cellular changes? Provide examples and how perturbation of these events can result in “cancer pathways”. In addition, describe in detail a typical cancer pathway and its strategy to activate gene expression. What is the origin of many cancer pathways, i.e., during which stage of an organism’s live process(es) are they physiologically activated? Why is this important for cancer development?