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Mutations in genes that control cell growth and division are responsible for:

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Cancer

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Cancers arise when:

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critical genes are mutated, causing unregulated proliferation of cells

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rapidly dividing cells pile up on top of each other to form:

answer

a tumor

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When cells detach from the tumor and invade surrounding tissues, the tumor is ______ and may form secondary tumors at other locations in a process called _________

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malignant metastasis

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A tumor whose cells do not invade surrounding tissues is

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Benign

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Cancer cells can be obtained by:

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removing tissue from a tumor and dissociating it into its constituent cells, which can be cultured in vitro with appropriate nutrients.

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Cancer cells can be derived from cultures of normal cells by:

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treating the cells with carcinogens, which can irreversibly transform normal cells into cancerous cells

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Characteristics of Cancer Cells:

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- Unregulated growth -Formation of masses in cell culture instead of a monolayer -Disorganized skeleton -Synthesis of unusual cell surface proteins -Aneuploidy

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Transitions between different phases of the cell cycle (G1, S, G2, and M) are regulated at ___________

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checkpoints

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What is a checkpoint

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A checkpoint is a mechanism that halts progression through the cycle until a critical process is completed

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Important checkpoint proteins are the (2 proteins)

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cyclins and the cyclin-dependent kinases (CDKs)

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complexes formed between cyclins and CDKs cause

answer

the cell to advance

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The CDKs ____________ target proteins but are __________unless they are associated with a _______ protein.

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a) phosphorylate b) inactive c) cyclin

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Cell cycling requires the:

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alternate formation and degradation of cyclin/CDK complexes

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In tumor cells, cell cycle checkpoints are often ______________ due to genetic defects in the machinery that alternately raises and _________ the abundance of the cyclin/CDK complexes.

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a) deregulated b) lowers

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Define: Apoptosis

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programmed cell death; part of the normal developmental program in animals and is important in the prevention of cancer.

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What are caspases

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a family of proteolytic enzymes, are involved in apoptosis and cleave many target proteins.

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If apoptosis is impaired -

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a cell that should be killed can survive and proliferate, potentially forming a clone that could become cancerous.

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Evidence of a Genetic Basis for Cancer:

answer

- The cancerous state is clonally inherited. - Some types of viruses can induce the formation of tumors in experimental animals. - Cancer can be induced by mutagens. - Certain types of cancer tend to run in families. - Certain types of white blood cell cancers are associated with particular chromosomal abnormalities.

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What are oncogenes

answer

genes that, when mutated, actively promote cell division.

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What are Tumor Suppressor Genes

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are genes that, when mutated, fail to repress cell division.

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Define: overactivity mutation

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(gain of function) normal cell >>>> single mutation event; creates oncogene>>>>>>>activating mutation enables oncogene to stimulate cell proliferation

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Define: underactivity mutation

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(loss of function) normal cell>>>>> mutation event inactivates tumor suppressant gene; no effect of mutation in one gene copy>>>>>>second mutation event; inactivates second gene copy>>>>>two inactivated mutations eliminate tumor suppressant gene & stimulating cell proliferation

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Cancer is a group of diseases in which

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the cellular cycle of growth and division is unregulated

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What is the Rous sarcoma virus

answer

the first tumorinducing virus, contains four genes

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What are protooncogenes or normal cellular oncogenes

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proteins encoded by viral oncogenes are similar to cellular proteins with important regulatory functions

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The Transfection Test to Identify Mutant Cellular Oncogenes

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1. Isolate DNA & add red marker to each fragment 2. Transfer DNA into normal cells 3. Oncogene is integrated & daughter cell descendants are cancer cells 4. Cancer cells form a colony from culture 5. Isolate specific DNA gained by transformed cells (identified by red marker) 6. Repeat procedure to verify transforming ability

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The mutant c-H-ras protein has:

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a mutation that impairs its ability to hydrolyze GTP. This keeps the mutant protein in an active signaling mode and causes it to stimulate cell division

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The c-H-ras oncogene was identified by the:

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transfection test

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A single mutant c-ras allele is _________in its ability to bring out the cancerous state.

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dominant

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What are dominant activators

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Mutations in c-ras and other oncogenes are dominant activators or uncontrolled cell growth

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Most dominant activating mutations in cellular oncogenes occur ____________ in ________ cells, not in the ________

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a) spontaneously b) somatic c) germline

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Cancer is the Result of __________ mutation(s)

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a) several

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The Philadelphia chromosome is the result of & is an example of:

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Chromosome rearrangement: a reciprocal translocation between chromosomes 9 and 22. The fusion gene created by this rearrangement encodes a tyrosine kinase that promotes cancer in white blood cells.

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Burkitt's Lymphoma is the result of ; is an examply of

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Chromosome rearrangement: The translocations juxtapose c-myc to the genes for the immunoglobulin genes, causing overexpression of c-myc in B cells. (uncontrolled growth)

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Viral oncogenes are _________________ to cellular genes (proto-oncogenes)

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homologous

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Mutations in proto-oncogenes actively _________ cell proliferation

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promote

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Many cancers involve the inactivation of genes whose products play important roles in regulating the cell cycle:

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Tumor Suppressant genes

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Many cancers involve the overexpression of certain genes or the abnormal activity of their mutant protein products:

answer

Oncogenes

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Knudson's Two-Hit Hypothesis: ( 3 points)

answer

- When tumor suppressor genes are mutated, a predisposition to develop cancer often follows a dominant pattern of inheritance. - The mutation is usually a loss-of-function mutation in the tumor suppressor gene. - Cancer develops only if a second mutation in somatic cells knocks out the function of the wild-type allele.

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The proteins encoded by tumor suppressor genes are involved in

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cell division, cell differentiation, programmed cell death, and DNA repair.

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Inherited mutations in TP53 are associated with

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Li-Fraumeni syndrome.

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Somatic mutations that inactivate both copies of TP53 are associated with

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the majority of cancers

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Most mutations in that inactivate p53 are

answer

he DNA-binding domain (DBD) and impair its ability to bind enhancer sequences in its target genes.

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p53 is :

answer

a Transcription Factor

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The Cellular Function of p53

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Expression of p53 increases in response to DNA damage due to a decrease in degradation. p53 can inhibit cell division or induce apoptosis

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pAPC mutations are associated with

answer

polyposis coli, which often leads to colorectal cancer

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pAPC regulates

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the renewal of cells in the epithelium of the large intestine.

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Loss of pAPC function results in

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the formation of polyps.

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pAPC binds to

answer

??catenin, which binds to transcription factors.

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Cells with mutations in pAPC lose

answer

their ability to control ??catenin levels.

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The phMSH2 protein is

answer

a homologue of the bacterial and yeast MutS protein, which is involved in DNA repair

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Mutations in the hMSH2 gene are associated with

answer

hereditary nonpolyposis colorectal cancer (HNPCC), a dominant autosomal condition

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Cells in HNPCC tumors exhibit

answer

genetic instability

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Mutations in the tumor suppressor genes BRCA1 and BRCA2:

answer

have been implicated in hereditary breast and ovarian cancer

question

Carriers of mutations in tumor-suppressor genes are at_____ _______ to develop tumors

answer

high risk

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Cancers develop through

answer

an accumulation of somatic mutations in proto-oncogenes and tumor suppressor genes.

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Most malignant tumors cannot be:

answer

attributed to mutation of a single gene

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Tumor formation, growth, and metastasis depend on:

answer

the accumulation of mutations in several different genes.

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The genetic pathways to cancer are:

answer

diverse and complex

question

Hallmarks of Pathways to Malignant Cancer: (6 points)

answer

1. Cancer cells acquire self-sufficiency in the signaling processes that stimulate division and growth. 2. Cancer cells are abnormally insensitive to signals that inhibit growth. 3. Cancer cells can evade programmed cell death. 4. Cancer cells acquire limitless replicate potential. 5. Cancer cells develop ways to nourish themselves. 6. Cancer cells acquire the ability to invade other tissues and colonize them.

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Somatic mutation is the basis for:

answer

the development and progression of all types of cancer

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As mutations accumulate and cells become unregulated:

answer

genetic instability increases the likelihood that the cells will develop the hallmarks of cancer

question

Factors that increase the mutation rate:

answer

increase the incidence of cancer

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Immortalized cancer cells can:

answer

divide endlessly

question

Tumors can ________ when they induce the in-growth of blood vessels to nourish their cells.

answer

a) expand

question

True or False: Cancer cells may stimulate their own growth and division

answer

True

Chapter 21: The Genetic Basis of Cancer – Flashcards

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