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Cancer ppt C. 11.15-11.18 & C. 8.9-8.10

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© 2015 Pearson Education, Inc.

Cancer

– unregulated cell growth

https://www.youtube.com/watch?v=46Xh7OFkkCE

Detecting & Treating https://www.youtube.com/watch?v=

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© 2015 Pearson Education, Inc.

Cancer – uncontrolled cell division

Normal Cell

• Anchorage dependence

• Contact inhibition

• Checkpoints observed

• Tumor suppressor & proto-oncogenes

functioning properly

• Set life span (# of divisions) - apoptosis

Cancer Cell

• Can metastasize

• Invades surrounding tissue

• Angiogenesis

• Ignores checkpoints

• Mutations in tumor suppressor & proto-oncogenes (become oncogenes)

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© 2015 Pearson Education, Inc.

11.15 Cancer results from mutations in genes

that control cell division

• Cancer is a set of diseases in which the control

mechanisms that normally limit cellular growth have malfunctioned.

Scientists have learned that such malfunction is

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© 2015 Pearson Education, Inc.

11.15 Cancer results from mutations in genes

that control cell division

• The genes that a cancer-causing virus inserts into

a host cell can make the cell cancerous.

• Such a gene is called an oncogene (from the Greek onco, tumor).

https://www.youtube.com/watch?v=2wIVwZksIt4

• Over the last century, researchers have identified a number of viruses that harbor cancer-causing

genes.

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© 2015 Pearson Education, Inc.

11.15 Cancer results from mutations in genes that control cell division

• Mutations in two types of genes can cause cancer.

1. Oncogenes

Proto-oncogenes are normal genes that promote cell division.

• Mutations to proto-oncogenes create cancer-causing oncogenes that often stimulate cell division.

2. Tumor-suppressor genes

Tumor-suppressor genes normally inhibit cell division or function in the repair of DNA damage.

http://goo.gl/XoOzBQ

• Mutations inactivate the genes and allow uncontrolled division to occur.

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© 2015 Pearson Education, Inc. Figure 11.15a

Proto-oncogene

(for a protein that stimulates cell division) DNA

A mutation within the gene

Oncogene

Hyperactive growth-stimulating protein in a normal amount

Multiple copies of the gene

Normal growth-stimulating protein

in excess

The gene is moved to a new DNA locus,

under new controls

New promoter

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© 2015 Pearson Education, Inc. Figure 11.15b

Tumor-suppressor gene

Mutated tumor-suppressor gene

Normal growth-inhibiting protein

Defective,

nonfunctioning protein

Cell division under control

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© 2015 Pearson Education, Inc.

8.9 CONNECTION: Growing out of control,

cancer cells produce malignant tumors

• Cancer currently claims the lives of 20% of the

people in the United States.

• Cancer cells escape controls on the cell cycle.

Cancer cells divide excessively and invade other

tissues of the body.

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© 2015 Pearson Education, Inc.

8.9 CONNECTION: Growing out of control,

cancer cells produce malignant tumors

• A tumor is a mass of abnormally growing cells within otherwise normal tissue.

Benign tumors remain at the original site but may disrupt certain organs if they grow in size.

Malignant tumors can spread to other locations in a process called metastasis.

• An individual with a malignant tumor is said to have

cancer.

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© 2015 Pearson Education, Inc.

Figure 8.9

Tumor

Glandular tissue

Tumor growth Invasion Metastasis

Lymph vessels Blood vessel

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© 2015 Pearson Education, Inc.

8.9 CONNECTION: Growing out of control,

cancer cells produce malignant tumors

• Cancers are named according to the organ or

tissue in which they originate.

• Carcinomas originate in external or internal body coverings.

• Leukemia originates from immature white blood cells within the blood or bone marrow.

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© 2015 Pearson Education, Inc.

8.9 CONNECTION: Growing out of control,

cancer cells produce malignant tumors

• Localized tumors can be

• removed surgically and/or

• treated with concentrated beams of high-energy radiation.

https://goo.gl/siIvVx

Metastatic tumors are treated with chemotherapy.

http://goo.gl/dyg9YQ

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© 2015 Pearson Education, Inc.

Introduction to Immunotherapy

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© 2015 Pearson Education, Inc.

8.10 SCIENTIFIC THINKING: Tailoring

treatment to each patient may improve

cancer therapy

• It is increasingly possible to personalize cancer

treatment by

• sequencing the genome of tumor cells and

tailoring treatment based upon the tumor’s specific

genetic profile.

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© 2015 Pearson Education, Inc.

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© 2015 Pearson Education, Inc.

11.16 Multiple genetic changes underlie the

development of cancer

• More than 100,000 Americans will be stricken by

cancer of the colon this year.

• Colon cancer is one of the best-understood types

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© 2015 Pearson Education, Inc.

11.16 Multiple genetic changes underlie the

development of cancer

• Colon cancer illustrates the gradual progression

from somatic mutation to cancer.

1. An oncogene arises or is activated, resulting in increased cell division in apparently normal cells in the colon lining.

2. Additional DNA mutations cause the growth of a small benign tumor (polyp) in the colon wall.

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© 2015 Pearson Education, Inc. Figure 11.16a-3 Colon wall 2 1 3 DNA changes: An oncogene is activated Cellular changes: Increased cell division A tumor-suppressor gene is inactivated

Growth of a polyp (benign tumor)

A second tumor-suppressor gene

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© 2015 Pearson Education, Inc. Figure 11.16b

Normal cell

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© 2015 Pearson Education, Inc.

11.17 Faulty proteins can interfere with

normal signal transduction pathways

• Proto-oncogenes and tumor-suppressor genes

often code for proteins involved in signal

transduction pathways leading to gene expression.

Two main types of signal transduction pathways

lead to the synthesis of proteins that influence cell division.

1. One pathway produces a product that stimulates

cell division.

2. A second pathway produces a product that

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© 2015 Pearson Education, Inc. Figure 11.17a-0 Normal Mutant Growth factor Target cell Normal product of

ras gene

Relay proteins Transcription factor (activated) CYTOPLASM DNA Transcription Translation Protein that stimulates cell division Normal cell division No growth factor Normal product of

ras gene

DNA Transcription Increased cell division NUCLEUS NUCLEUS Hyperactive relay protein (product of

ras oncogene) even in absence of growth factor

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© 2015 Pearson Education, Inc. Figure 11.17b-0 Normal Growth-inhibiting factor Transcription factor (activated) Mutant Receptor Relay proteins Normal product of

p53 gene

Transcription Translation Protein that inhibits cell division No cell division Transcription and translation

do not occur

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© 2015 Pearson Education, Inc.

11.18 CONNECTION: Lifestyle choices can

reduce the risk of cancer

• After heart disease, cancer is the second-leading

cause of death in most industrialized nations.

• Cancer can run in families if an individual inherits

an oncogene or a mutant allele of a

tumor-suppressor gene that makes cancer one step closer.

But most cancers cannot be associated with an

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© 2015 Pearson Education, Inc.

11.18 CONNECTION: Lifestyle choices can

reduce the risk of cancer

Carcinogens are cancer-causing agents that alter DNA.

• Most mutagens (substances that promote

mutations) are carcinogens.

• Two of the most potent carcinogens (mutagens)

are

• X-rays and

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© 2015 Pearson Education, Inc.

11.18 CONNECTION: Lifestyle choices can

reduce the risk of cancer

• The one substance known to cause more cases

and types of cancer than any other single agent is tobacco.

• More people die of lung cancer than any other form of cancer.

• Although most tobacco-related cancers come from smoking, passive inhalation of second-hand smoke is also a risk.

Tobacco use, sometimes in combination with

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© 2015 Pearson Education, Inc.

11.18 CONNECTION: Lifestyle choices can

reduce the risk of cancer

• Healthy lifestyles that reduce the risks of cancer

include

• avoiding carcinogens, including the sun and tobacco products,

• exercising adequately,

• regular medical checks for common types of cancer, and

a healthy high-fiber, low-fat diet including plenty of

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© 2015 Pearson Education, Inc.

Emperor of All Maladies

PBS Series

Conversation with Katie Couric, Ken Burns,

Siddhartha Mukherjee, and Sharon Rockefeller

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