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asu biology

asu biology

Description

School: Arizona State University
Department: OTHER
Course: Cancer--Mother of All Diseases
Term: Spring 2019
Tags: #exam, #bio302, and #studyguide
Cost: 50
Name: Exam 1 Study Guide
Description: This study guide covers what is going to be on our first exam.
Uploaded: 02/04/2019
12 Pages 11 Views 9 Unlocks
Reviews

cjameson2015 (Rating: )

Some errors sprinkled in. Good overview though. :)



Cancer- Mother of All Diseases Exam 1 Study Guide 


Why study cancer?



Dr. Compton

Lecture 1 & 2: Why Study Cancer 

1. Why study cancer

a. It’s important in the scheme of human life

b. The leading cause of death in US: 595,930 deaths per year

c. Top two killers: cancer and heart disease

d. Progress is being made

i. Death rates are dropping for some cancer types: lung, breast, colon, and prostate

e. Cancer is a global problem

i. Cancer is the second leading cause of death worldwide

ii. Ischemic heart disease and stroke are the leading cause

2. What is Cancer?

a. A condition ingrained in the very nature of evolution and selection in all living organisms

b. Mutation: a permanent change in the nucleotide sequence of DNA

i. May change form and/or function

ii. Types

1. Substitution

2. Addition of a single nucleotide

3. Addition of a nucleotide sequence


Who discovered cancer?



4. Deletion of a nucleotide

5. Deletion of a nucleotide sequence

6. Rearrangement of entire segments of chromosomes

c. Mutation and Cancer

i. Development of cancer requires the loss, malfunctions or overriding of normal mutation control mechanisms

ii. The loss of control is ITSELF caused by mutation in the elements of systems that constitute the control mechanisms

d. Cancer: The Most Difficult Biomedical Problem

i. We are evolved to be susceptible to cancer (mutation and selection drive evolution)

ii. Goal for war on cancer: die of something else

e. Mutation and Biology

i. Mutations are significant when they change cell functions and behaviors f. Rapid Proliferation, Diversification, and Darwinian Selection in Cancer i. Cancer has deficient mutation correction/elimination

ii. More rapid diversification that any known eukaryotic cell type g. Hallmarks of Cancer: Abnormal Form and Function


When Does Apoptosis Occur?



i. Abnormal form: basis for screening and diagnosis

ii. Abnormal function: hallmarks of cancerDon't forget about the age old question of a network is a communications system created by linking two or more devices and establishing a standard methodology by which they can communicate.
If you want to learn more check out math 21c

3. The Cellular Basis of Cancer

a. Cancer Refers to a Group of Diseases in Which Abnormal Cells:

i. Divide continuously without control

ii. Invade and destroy other tissues without control

iii. Travel to other parts of the body through the blood and lymph systems and divide and invade without control

b. Types of Cell Growth

i. Normal

1. Physiological response, repair, reversible

ii. Abnormal

1. Pathological

2. Not reversible

c. Principles of Histopathology

i. As genetic alterations accumulate, cells begin to look different from their normal counterparts

d. Dysplasia: Pre-Cancer

4. The Language of Cancer

a. Basic Terminology

i. Cancer: nonspecific term for malignant neoplasm

ii. Neoplasm: new tissue

iii. Tumor: mass

iv. Benign neoplasm: lacks the capacity to metastasize

v. Malignant neoplasm: has the capacity to metastasize= “cancer” If you want to learn more check out mac 1105 final exam review

vi. Carcinoma: cancer arising from epithelial cells

vii. Sarcoma: cancer arising from connective tissue cells

viii. Lymphoma: arise from immune system cell precursors in bone marrow or lymph nodes

ix. Leukemia: arises from blood forming cells in bone marrow

x. Melanoma: arise from pigment-producing cells in epithelia

5. The Bottom Line

a. Take Home Messages

i. Cancer is a group of diseases characterized by the uncontrolled growth of abnormal cells

ii. Carcinogenesis is a multi-stage molecular process involving:

1. Initiation

2. Promotion

3. Progression

iii. Only malignant neoplasms can metastasize

iv. The earlier the cancer is found and treated, the better the outcome

v. Cancer cells may become more resistant to therapy with new mutations, a process driven by therapy itself

Lecture 3 & 4: Who Gets Cancer and Why? 

1. Causes of Cancer

a. All cancer is caused by mutation in cellular DNA

b. Cancer causation is related to both environmental and genetic factors c. Carcinogenesis in Context

i. Cancer is primarily an environmental disease

1. 90-95% of cases attributed to environmental factors

d. Bottom Line

i. “Proof” in the absolute sense that an agent is a human carcinogen may be impossible to obtain

ii. However, causal inference may be quite strong or even overwhelming e. Carcinogenesis

i. Usually causal for specific cancer, not all cancer Don't forget about the age old question of What is the meaning of hindsight bias?

ii. No carcinogen causes cancer predictably, all the time, in any individual, under any circumstances

f. Carcinogenesis in Cigarette Smoke

i. Cigarette smoke contains 250 known harmful chemicals

g. Risk Factors for Cancer That Cannot Be Altered

i. Age, genetics, family history, personal history, world region h. Risk Factors for Cancer That Can Be Altered

i. smoking/tobacco, obesity. Alcohol, nutrition/diet, physical activity, viral infection, exposures to carcinogens

i. Risk Factors For Cancer That Can Be Treated: Opportunities For Cancer Prevention

i. Chronic inflammation, viral infections, bacterial infection, dietary deficiencies, diabetes, hormonal status

2. Smoking

a. Cigarettes cause 16 types of cancer

3. Obesity

a. Obesity linked to 13 types of cancer

b. Obesity is associated with substantial metabolic and endocrine abnormalities c. Obesity is an epidemic: The USA is getting fatter not fitter If you want to learn more check out the spiritual dimension: sexual decision making

4. Alcohol

a. Heavy or regular alcohol consumption increases the risk of:

i. 7 types of cancer

5. Diet

a. Fruits and vegetables lower the risk of many cancers: strong evidence 6. Physical Activity

a. Physical Activity and Cancer

i. Strong associated with lowered risk of colon, breast, and endometrial cancer

b. Exercise Lowers the Risk Of At Least 10 Types of Cancer

7. Infection

a. Viruses Associated With Human Cancers

i. HBV, HCV, HPV, EBV, HTLV-1, HIV

8. Radiation Exposure

a. Sun exposure increases chances for cancer

9. Industrial Exposure

a. Many occupational carcinogens increase risk for cancers

10. Big Take Home Message

a. Most Cancer Can Be Prevented Through Behavior Change

b. Preventing Cancer

i. Avoiding carcinogen exposures

ii. Blocking development of cancer (reducing risk)

c. A causal factor is a determining element of a disease

Lecture 5: Hallmarks of Cancer 1 

1. There are multiple hallmarks of cancer Don't forget about the age old question of cs 1331 gatech

2. Control, Balance And Stability Are Lost

a. Cancers do not invent NEW biology, they draw on and distort normal biological capabilities

b. No cancer has a normal genome

3. Cell Profileration

a. The normal body cell mass of 40 trillion cells is maintained throughout adult life by stem cell division balancing continual cell loss

b. Cell is a tightly regulated process to ensure homeostasis

c. Cancer cells exhibit a loss of proliferation control

i. Sustained proliferative signaling

ii. Evasion of growth suppression

4. Evading Growth Suppressors

a. Pro- and anti- cell division signals are highly coordinated in normal cells b. Cell cycle

i. The series of events that occur during cell division

c. Cancer cells deactivate “stop” signals for proliferation

5. Two Classes of Tumor Suppressor Genes

a. Gatekeepers: act through cell cycle to stop proliferation

i. Ex: p53

b. Caretakers: function in DNA repair and chromosome sorting

i. Ex: BRCA1, MLH1

6. DNA Damage Checkpoints

a. Cancer cells lose cell cycle checkpoint control

7. Gatekeepers

a. P53 is the master controller

i. TP53 gene encodes p53 protein

ii. Single most commonly mutated gene in cancer

8. Take Home Messages

a. Cancer cells utilize normal biological processes in abnormal ways

b. Inability to repair defects in DNA and cell cycle checkpoints leads to instability of the genome and gives rise to other hallmarks

c. Altered expression or function of tumor suppressor genes allows cancer cells to circumvent anti-proliferative control

d. Different mutations arise among different populations of cells within a tumor leading to heterogeneity and challenges for “targeted therapy”

Lecture 6: Hallmarks of Cancer 2 

1. Many Types of Programmed Cell Death

a. Built-in mechanisms to eliminate old, damaged, or infected cells

2. Unregulated Cell Death

a. Called Necrosis

3. When Does Apoptosis Occur?

a. Maintenance of the organism

b. Immune response

c. Cell stress or damage

d. Biological remodeling

4. Mutations in Apoptosis and Disease

a. Mutations affecting apoptosis can contribute to the development

i. Alzheimer’s

ii. Parkinson’s

iii. Huntington’s disease

iv. Stroke

v. AIDS

vi. Cancer

5. Apoptosis: Regulated Form of Death

a. Initiated either from inside or outside the cell

b. Mediated by multiple factors

c. Outcome:

i. Disassembly of the cell components

ii. Formation of a dense cell corpse or multiple cell fragments

6. DNA Damage and Checkpoint Loss: Corollary for Chemotherapy

a. Chemotherapy damages DNA

i. DNA damage leads to apoptosis in cells with functional p53

ii. If p53 is mutated, therapy won’t work

7. Aging and Telomere Shortening

a. Telomeres

i. End caps of chromosomes consisting of multiple copies of short, repearing non-coding DNA sequences

1. Protect the useful information from being lost

2. Not replicated by DNA polymerase

3. Replication requires a unique enzyme: telomerase

8. Telomerase and Cancer

a. Telomerase is expressed in ~90 % of tumors

b. TERT mutations

i. Most common non-coding mutation in cancer

9. Cancer Metabolism

a. Warburg Hypothesis (1924)

i. Aberrant metabolism in cancer cells

ii. Preferential use of anaerobic metabolism, even in the presence of oxygen iii. Cancer are avid sugar consumers

iv. More glycolysis, more lactate

10. Another Source of Cancer Heterogeneity

a. Some tumors can have two populations of cells:

i. One more hypoxic that uses glycolysis and secretes lactate

ii. Another, better, oxygenated that important lactate and uses it as an energy source in oxidative phosphorylation

11. Metabolic Pathways in Cancer

a. Additional pathways are also utilized by cancer cells

b. The choice of pathway can depend on the cell environment

c. This creates an even greater heterogeneity in cancers

12. Angiogenesis

a. The stimulation of new blood vessels

b. Normally occurs during development of the circulatory system in fetal life, wound healing, and the final reproductive cycle

c. Angiogenic Switch

i. Key factors: vascular endothelial growth factor (VEGF) and fibroblast growth factor (FGF)

a. Highly expressed in many cancers ***END OF STUDY GUIDE***

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