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BI416 > Chapter 7 - Neoplasia > Flashcards

Chapter 7 - Neoplasia Flashcards

1
Q

Define Neoplasia

A

New growth in regards to tumour growth

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2
Q

What is malignant neoplasm?

A
  • Cancerous; associated with altered expression of cellular genes
  • Abnormal cell size/shape
  • Rapid growth
  • May not survive
  • Re-occurances
  • Poor if untreated
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3
Q

What is benign growth?

A
  • Generally easily cured
  • Typical of tissue origin
  • Slow and local
  • Rare re-occurances
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4
Q

What does -oma and -carcinoma or -sarcoma indicate?

A
  • Benign (adenoma)

- Malginant

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5
Q

Define carcinoma

A

Epithelial origin

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6
Q

Define Sarcoma

A

Mesenchymal origin

- Bone, muscles, nerve

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7
Q

Define Leukemia

A
  • Cancer of WBC

- Exception - has its own name

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8
Q

Name the exception to cancer terminology

A
  • Lymphoma
  • Hepatoma
  • Melanoma
  • All are malignant
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9
Q

What are the characteristics of the malignant phenotype

A
  • Ignores growth controlling signals

Anti-social behaviours include:

  • Proliferate despite lack of growth initiating signals from environment
  • Escape signals die and achieve a kind of immortality (unlimited replication)
  • Loss of differentiated features; poor function
  • Genetically unstable; evolve by new mutations at fast rate
  • Invade local tissue and over-run neighbours
  • Gain ability to migrate from origin and colonize at distant sites***
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10
Q

Define Epidemiology and know cancer facts

A

Epidemiology: study and analysis of patterns, causation, and effects of health and disease conditions in defined populations

Risk Factors

  • 2nd leading cause of death in US
  • Most cancer deaths occur at age 55+
  • Men 1/2 chance
  • Women 1/3 Chance
  • 5 year survival rate = 68%
  • Lung cancer is responsible for most death
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11
Q

List the most important risk factors

A
  • Tobacco
  • Nutrition
  • Obesity
  • Sun exposure
  • Sexual Exposure to HPV
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12
Q

Describe tobacco use in regards to lung cancer

A

Lung Cancer: Leading cause of death in men and women

  • Worst survival rate
  • More men die than women

Contains carcinogens

  • Initiator: causes genetic damage
  • Promotor: promotes tutor growth
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13
Q

Define carcinogen

A

A substance capable of causing cancer in living tissue

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14
Q

Nutrition and Cancer

A

Dietary factors

  • Fat
  • Fiber
  • Alcohol (liver)
  • Antioxidants

Dietary Suggestions

  • Limit calorie/alcohol intake
  • Increase fibre, fruit, and veggies
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15
Q

Define proto-oncogene

A

Enhance growth-producing pathways

- Can be transformed into oncogenes by activating mutations

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16
Q

Define tumor supressor genes

A

Inhibits cell proliferation

- cancer can arise when this gene function is lost/inhibited

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17
Q

Define oncogene

A

Proto-oncogene in its mutant over active form

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18
Q

Proto-oncogene gain-of-function mutations…

A

1) Growth Factors (Mitogens)
- Secreted into extracellular space and diffuse to nearby cells to interact with receptor and activate signalling cascade = excessive self-stimulated growth

2) Growth Factor Receptors
- Transmembrane proteins bind with mitogens which activates proliferation = excessive responsiveness (many receptors with abnormal high affinity)

3) Cytoplasmic Signalling Pathways
- numerous enzymes/chemical that transmit signals from activated receptors at cell surface to nucleus; mutant proto-oncogenes can activate this pathway even with no signal
- Ras gene: mutations lead to cancer - stimulates growth with presence of GTP but in malignant cels can be turned on without GTP

4) Transcription Factors
- Proteins must be assembled at promotor area to begin gene transcription and are normally prevented activity until appropriate signal causes release - mutations cause over production / interfere with normal functions of keeping them in check

19
Q

From Proto-oncogene to Oncogene

A

-Become activated oncogenes when mutations alter their activity so that proliferation-promoting signals are generated inappropriately

20
Q

4 general ways for proto-oncogenes activation:

A

1) Oncogenes introduced to host cell by retrovirus
2) Proto-oncogene within cell suffers a mutagenic event
3) DNA sequence may be lost/damaged and allows proto-oncogene to become abnormally active
4) Error in chromosome replication causes extra copies of proto-oncogene in the genome

21
Q

Tumor Suppressor Genes

A
  • Act as “BRAKE” to regulate cell growth & prevent mutations
  • Slow cell cycle
  • Inhibit proliferation of cells due to GFs (growth factors)
  • Stop proliferation if cells damaged
  • Tumor-Suppressor Genes are inactivated by mutations, which removes BRAKE on cell proliferation
  • Contribute to cancer only when not present
  • Both copies of tumor suppressor genes are inactivated when cancer develops
  • One can inherit a defective copy of tumor suppressor gene
    • At much higher risk for cancer development
  • Mutations can cause the gene to not function
    • Chromosome deletions
    • Point mutations
    • Nondisjunction
  • Epigenetic process
    • “Silences” the gene
    • Does not require a mutation
22
Q

Rb Genes

A
  • Normally “master brake” for the cell cycle
  • Normally blocks/stops cell division
    • Binds transcription factors
    • Inhibits these factors from transcribing genes that initiate cell cycle
  • Normally can be induced to release transcription factors when sufficiently phosphorylated
  • An inactivating mutation of the Rb gene removes restraint on cell division and replication occurs
  • Defective Rb gene
    • Common in some cancers

The Rb protein functions to bind transcription factors in the nucleus and keep them from participating in the transcription of cell cycle–related genes. pRb is induced to release its hold on the E2F transcription factors when it is sufficiently phosphorylated by cyclin-dependent kinases (Cdk). Cyclin-dependent kinases are activated by cyclin proteins that accumulate when growth factors bind to receptors and stimulate growth pathways. Other signals, such as transforming growth factor-β (TGF-β), inhibit the activity of cyclin/Cdk through activation of inhibitory proteins such as p16. A loss of pRb function removes the “major brake” on cell division. P, Phosphate group; EGF, epidermal growth factor.

23
Q

p53 Gene

A
  • Most common tumor-suppressor gene defect identified in cancer cells
  • More than ½ of all types of human tumors lack functional p53
  • Normally p53 inhibits cell cycling
  • Accumulates only after cellular (DNA) damage
  • Binds to damaged DNA and stalls division to allow DNA to repair itself
  • May direct cell to initiate apoptosis
  • Mutated or damaged p53 allows genetically damaged/unstable cells to survive and continue to replicate
  • Chemotherapy/radiation
  • Damages target/cancer cell to trigger p53-mediated cell death
  • Cancer cells that lack functional p53 may be resistant to chemotherapy/radiation
24
Q

Normal vs. Abnormal p53 Gene

A

-Role of P53 (TP53) in maintaining the integrity of the genome. Damage to DNA in cells with functional P53 stalls the cell cycle so that DNA can be repaired. If repair fails, then the cell undergoes apoptosis to prevent the proliferation of DNA-damaged cells. If the P53 is not functional, genetically unstable cells may be allowed to survive and proliferate.

Normal cell will have small amount of p53

  • In case of DNA damage (ex. Hypoxia) this will activate p53 which binds to DNA and stops proliferation to give chance for the cell to repair
  • Some cases it is successful
  • The same gene also monitors state of cell, and if it cannot heal then the same gene will actually activate apoptosis pathway
  • However, when cells contain a mutation of p53 this is no longer possible which means the cell will be able to proliferate regardless of the damage
25
Q

BRCA1 / BACR2 Genes

A
  • Tumor suppressor genes
  • Associated with breast cancer
  • Family history and inherited defect in BRCA1 increases risk of breast cancer
26
Q

Synergy btw Oncogenes may be necessary to initiate malignant growth

A
  • Ras in mutated state is responsible for anchorage-independent
  • All cells taken and attempted to be cultured will need to adhere to this culture to pick up nutrients to proliferate
  • However, these mutated cells will actually start proliferation despite the fact they do not anchor (independently)
  • However, when they take the offspring in a lab animal, they were not able to initiate tumor growth
  • Myc  immortality
    When inoculated in recipient = no tumor growth
  • Together = produce tumor
    Separately they are not enough
27
Q

what is the multi-step nature of carcinogens

A

1) initiation
2) promotion
3) progression

28
Q

Initiation of carcinogens

A

Initiating Events:
- Genetic mutations; inappropriately activate proto-oncogenes and inactivate tumour suppressor genes

Proliferation:
- required for cancer development

Complete carcinogens:
- capable of initiating cell damage and promoting cellular proliferation

Partial carcinogens:

  • stimulate growth
  • incapable of causing genetic mutations sufficient to singly initiate cancer
  • Cell looks normal > proliferate to form adenoma > proliferate more; abnormal cells > invasive carcinoma
29
Q

promotion of carcinogens

A
  • cell proliferates
  • regulated by growth factors

*cancer cells produce telomerase = immortality of cancer cells
- Normally telomeres “cap” chromosomes & stabilize their structure
- With repeated DNA replication telomeres get shorter
- When telomeres are too short, chromosomes become unstable & fragment, followed by cell death
- Advanced Cancer cells activate “telomerase”
Stabilizes & protects telomeres

30
Q

Progression of carcinogens

A
  • Mutant, proliferating cells begin to exhibit malignant behavior
  • Cells whose phenotype gives them a growth advantage proliferate more readily
  • Evolved tumor cells differ significantly from the normal tissue
  • Progress to malignant characteristics: Laminin receptors, Lytic enzymes, Anchorage independent, Bizarre karyotype
31
Q

Define Metastasis

A

Process by which cancer cells escape their tissue of origin and initiate new colonies of cancer in distant sites

  • Specialized enzymes and receptors enable them to escape their tissue of origin and metastasize
  • Specialized enzymes and receptors allow them to replicate at new site
32
Q

Patterns of spread

A
  • Cancer cells generally spread via circulatory or lymphatic systems

Tumor markers help identify parent tissue of cancer origin

  • Rely on some retention of parent tumor characteristics
  • Some released into circulation
  • Others identified through biopsy
  • Enzymes/proteins typically used as tumor markers
  • Help track tumor activity
  • Increased blood levels: progression and proliferation
33
Q

Angiogenesis

A
  • Process by which cancer tumor forms new blood vessels in order to grow
  • Usually does not develop until late stages of development
  • Triggers are not generally understood
  • Inhibition of angiogenesis is important therapeutic goal
34
Q

Grading & Staging Tumors is useful for?

A

To predict clinical behavior of malignant tumor and guide therapeutic management

35
Q

Grading tumours:

A
  • Histologic characterization of tumor cells
  • Degree of anaplasia
    3 or 4 classes of increasing degrees of malignancy
  • Greater degree of anaplasia=greater degree of malignant potential
36
Q

Staging Tumours and TNM System

A
  • Location and patterns of spread within the host
  • Tumor size
  • Extent of local growth
  • Lymph node and organ involvement
  • Distant metastasis

TNM
-T-tumor
N-nodes involved
M-metastasis

37
Q

Effects of Cancer on Body

A
  • Depends on location of tumor and extent of metastasis
  • Early stages may be asymptomatic
  • Tumor increases in size and spreads; more symptoms become apparent
38
Q

Cancer and pain

A

Common and feared complication

May be due to metastasis, tissue destruction / inflammation

May be caused by cancer treatment

39
Q

Cachexia

A
  • Overall weight loss and generalized weakness

Loss of appetite (anorexia)
Increased metabolic rate
Nausea/vomiting

Immune system suppressed by cancer cell secretions

Some cancers can elude immune system detection

40
Q

Bone marrow suppression

A

Contributes to anemia, leukopenia, and thrombocytopenia

Due to invasion and destruction of bone marrow cells, poor nutrition, and chemotherapy

Anemia: Deficiency in circulating red blood cells

41
Q

Leukopenia

A

Deficiency in circulating white blood cells

Primary cause:
- Malignant invasion of bone marrow

Contributing factors
- Malnutrition
Chemotherapy

Opportunistic organisms can only infect immunocompromised host

Infections difficult to manage
Try to prevent

May cause changes in chemotherapy treatment
- May be suspended until WBC count recovers

42
Q

Thrombocytopenia

A

Deficiency in circulating platelets

  • Important mediators in blood clotting
  • Predispose to life-threatening hemorrhage, esp., if count is below 20,000
43
Q

Other effects…

A

Hair loss and sloughing of mucosal membranes

  • Complications of chemotherapy and radiation therapy
  • Damaged mucosa primary source of cancer pain and anorexia
  • May provide a portal for infection

Paraneoplastic syndromes: tumor production of hormones or cytokines

  • Hypercalcemia
  • Cushing syndrome secondary to ACTH secretion
  • Hyponatremia and water overload secondary to excess ADH secretion

BI416 (5 decks)

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