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Patho 2023 > Neoplasia (Final Exam) > Flashcards

Neoplasia (Final Exam) Flashcards

1
Q

What are the characteristics of malignant tumors?

A
  1. Large
  2. Poorly demarcated
  3. Rapidly growing with 4. hemorrhage and necrosis
  4. Locally invasive
  5. Metastatic
  6. Poorly differentiated
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2
Q

what are the characteristics of benign tumors

A
  1. Small
  2. Well demarcated
  3. Slow growing
  4. Non-invasive
  5. Nonmetastatic
  6. Well differentiated
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3
Q

how do you name a benign tumor?

A
  1. Adding suffix -oma to parenchymal tissue type
    –> Ex: adenoma, osteoma, hemangioma, leiomyoma, neuroma, glioma
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3
Q

what is a carcinoma and examples of them

A
  1. Malignant tumor of epithelial tissue origin
    –> Ex: adenocarcinoma
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4
Q

what is a sarcoma and examples of them?

A
  1. Malignant tumor of connective, muscle, endothelial tissues
    –> Ex: osteosarcoma, leiomyosarcoma, hemangiosarcoma
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5
Q

what is leukemia

A

malignant tumor of blood cells

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6
Q

what is a blastoma and examples of them

A
  1. Malignant tumor of neural tissues
    –> Ex: neuroblastoma, glioblastoma
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7
Q

what is grading a cancer mean?

A
  1. Determined by examination of tumor cell morphology
  2. Largely quantitative in nature
  3. Based on differ state and number of mitoses of tumor
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8
Q

what are the grades of cancers

A

Grade X, Grade I, Grade II, grade III, Grade IV

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9
Q

what is a grade X

A

Cannot be assessed (undetermined)

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10
Q

what is a Grade I

A

Well differentiated (low grade)

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11
Q

what is a grade II

A

Moderately differentiated (intermediate)

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12
Q

what is a grade III

A

Poorly differentiated (high grade)

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13
Q

what is a grade IV

A

Undifferentiated (high grade)

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14
Q

what does staging of cancers mean

A
  1. Based on size of primary lesion (T), extent of spread to lymph nodes (N), and presence or absence of metastases (M)
  2. Largely quantitative in nature
  3. The TNM system (tumor, node,metastasis)
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15
Q

what are the stages of tumors in TNM system?

A

T0, T1, T2,T3, T4

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16
Q

what are the stages of nodes in the TNM system

A

N0, N1, N2, N3

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17
Q

what are the stages of metastasis in the TNM system

A

M0, M1

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18
Q

what are oncogenes

A

Genes that encode proteins that promote cancer

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19
Q

what is some more information about oncogenes

A
  1. Translocation that makes protein with new function
    –> BCR-ABL
  2. Mutation that makes more active version of protein
    –> K-Ras
  3. Gene duplication and overexpression of normal protein involved in cell growth
  4. Dominant altercations and often single allele
  5. Normal version is proto-oncogene
  6. BCR-ABL results as chromosomal translocation
    –> Produces hyperactive kinase that drives proliferation in leukemia
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20
Q

what are tumor suppressor genes

A

Genes that encode proteins that inhibit cancer

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21
Q

what is some more information about tumor suppressor genes

A
  1. Most recessive and need homozygous deletion/mutation on both alleles
    –> RBI
    –> TP53 (gene of p53)
  2. Heterozygous mutations can be inherited and families can show inc. susceptibility
  3. Non-carriers require mutation on both alleles to develop cancer
  4. Carriers already have a recessive mutation on one; one more mutation on the other allele can cause cancer
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22
Q

what does a loss of differentiation mean in cancer cells?

A
  • Anaplasia
  • Resemblance to undifferentiated or embryonic cells
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23
Q

what does genetic instability mean in cancer cells

A
  1. Aneuploidy - loss of gain of chromosomes
  2. Point mutations
  3. Microsatellite instability - short, repetitive sequences of DNA
  4. Intrachromosomal instability - insertions, deletions, amd amplification of genes
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24
Q

what do growth factor independence mean in cancer cells

A

Proliferation even in absence of growth factors

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25
Q

what does loss of cell density dependent inhibition mean in cancer cells

A
  1. Lack of contact inhibition
  2. Necessary for invasion
  3. Rampant growth without regard for adjacent tissue
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26
Q

what does anchorage independence mean in cancer cells

A
  1. Critical for metastasis
  2. Cancer cells frequently remain viable and multiply without normal attachments to other cells and the extracellular matrix
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27
Q

what does faulty cell to cell communication mean

A

Formation of intercellular connections and responsiveness to membrane derived signals are frequently interfered in cancer cells

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28
Q

what does unlimited life span mean

A

Cancer cells divide unlimited number of times

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29
Q

what does antigen expression mean in cancer cells

A
  1. Cancer cells express many cell surface molecules or antigens that are immunologically identified as foreign (tumor antigens)
  2. Ex: fetal protections that are nor expressed by comparable cells in adult
  3. Tumor antigens may be clinically useful as cancer biomarkers
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30
Q

what does abnormal production of proteins, hormones, etc. mean

A
  1. Cancer cells secrete degradative enzymes that enable invasion and metastatic spread
  2. Cancer cells may synthesize hormones that promote their own growth (ex: estrogen production by breast cancer)
  3. cancer cells may produce and secret procoagulant substances that affect clotting mechanisms
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31
Q

what does cytoskeletal changes mean in cancer cells

A
  1. Changes in intermediate filament, actin filaments, and microtubules
  2. Abnormal cell morphology
  3. Facilitate invasion and metastasis
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32
Q

explain the 2 hit hypothesis for tumor suppressor genes

A
  1. Assumption that retinoblastoma requires two mutations
  2. Accurately predicts the number of cases of the cancer over time in hereditary and non hereditary retinoblastoma
    –> Originally mathematically based on incidence of retinoblastoma by alfred knudsen in 1971
33
Q

what are the risk factors that increase the cancer risk

A

age, environmental factors, genetics, inflammation, and viruses

34
Q

explain age and its characteristics

A

1, Frequently require multiple mutations and often take 20 years or more to develop
2. 2 common causes
–> Accumulation of somatic mutations
–> Decline in immune function

35
Q

explain environmental factors

A
  1. Time required for cancer development decreases with increased mutation rate
    –>Smokers develop lung cancer much faster than non-smokers
36
Q

what are examples of environmental factors

A
  1. Carcinogens
    –> Can induce genetic changes of tumors
    –> Most react with DNA to lead to mutations or DNA damage
    –> Ex:
    —— Mustard gas
    —— N-nitrosos cmpds. In cured meat
    —— Chemotherapy
    —— Benzo9a0pyrene from coal tar or cig smoke
  2. UV radiation
  3. Ionizing radiation
    –> Ex: x-ray, decay of radioactive isotopes
37
Q

explain genetics

A
  1. Inherited mutations in tumor suppressor genes
  2. Many are DNA repair genes
38
Q

what is the function and cancer of the gene mutation BRCA 1/2

A
  • double strand break repair
  • ovarian and breast cancer
39
Q

what is the function and cancer of the gene mutation XP (xeroderma pigmentosum)

A
  • nucleotide excision repair
  • skin cancer
40
Q

what is the function and cancer of the gene mutation ATM (ataxia telangiectasia)

A
  • double strand break repair
  • lymphoma and leukemia
41
Q

what is the function and cancer of the gene mutation BLM (Blooms’ Syndrome)

A
  • DNA helicase
  • various
42
Q

describe inflammation

A
  1. Chronic inflammation results in persistent regenerative cell proliferation or hyperplasia and DNA damage by reactive oxygen and nitrogen species produced by immune cells
  2. Long unhealed skin wounds characterized by persistent damage can lead to skin cancer
  3. Cirrhosis of the liver can lead to hepatocellular carcinoma
  4. Chronic gastritis due to long lasting H.pylori infection can lead to gastric cancer
  5. Chronic ulcerative colitis can lead to colorectal cancer
  6. Villous adenomas (hyperplastic polyps) of the colon can lead to colorectal cancer
43
Q

explain the mechanisms of viruses

A

1.Integration into the genome (retroviruses) can cause modulation of oncogenes or tumor suppressor genes
2. Chronic inflammation caused by HBV and HCV increases the risk of liver cancer
3. Coral proteins may alter cellular pathways
–> Inactivation of tumor suppressors (ex. E6 in HPV)
–> Disruption of normal cell cycle control

44
Q

what are the 2 types of oncogenic viruses

A

DNA and RNA

45
Q

describe DNA Viruses

A
  1. EBV (Epstein Barr Virus)
  2. KSHV (kaposi’s Sarcoma- Associated Herpesvirus)
  3. HPV (Human Papillomaviruses)
  4. MCPV (Merkel Cell Polyomavirus)
  5. HBV (Hep B Virus)
46
Q

describe RNA viruses

A
  1. HCV (Hep C Virus)
  2. HTLV1 (Human T-Cell Lymphotropic Virus Type 1)
47
Q

what are the 6 hallmarks of cancer

A
  1. evading apoptosis
  2. sustained angiogenesis
  3. self-sufficiency in growth signals
  4. insensitivity to anti-growth signals
  5. tissue invasion and metastasis
  6. limitless replicative potential
48
Q

what does G0/G1 in the cell cycle do

A

cell is quiescent or accumulating building blocks required for division

49
Q

what does S in the cell cycle do

A

cell replicates DNA

50
Q

what does G2 in the cell cycle do

A

cell assembling machinery for chromosomal segregation and cytokinesis

51
Q

what is M in the cell cycle

A

mitosis

52
Q

what is the cell cycle and what is it driven by

A
  1. Determines when cell moves from one phase to next
  2. Driven by cyclins paired with (CDKs)
  3. R point (restriction) is critical time point when cells decide to enter or not into cycle
53
Q

what do checkpoints mean in the cell cycle

A

Block the passage into next cycle when cells not ready

54
Q

what does hallmark 1 (self-sufficiency in growth signals) do

A
  1. Activation of kinase signal transduction that respond to mitogenic signals (GFs)
    GF receptors are RTKs
  2. Activation of RTK
    –> Gain of function
    —— EGFR in lung cancer
    –> Amplification
    —— HER2 in breast cancer
55
Q

what does Hallmark 2 (resistance to growth inhibitory signals) do

A
  1. May arise through loff of expression of growth inhibitory proteins (tumor suppressors)
    –> TGF-b, p53
    –> p16(INK4a)
    –> E2F (transcription factor in G1/S)
56
Q

what does Hallmark 3 (evading apoptosis) do

A
  1. Disruption of apoptotic pathways preventing cell death upon DNA damage or cell cycle checkpoint activation
  2. Tumor suppressors
    –> P53 - transcription factor
    –> P21 - CDK inhibitor
    –> BAX - pro-apoptotic regulator
57
Q

what does Hallmark 4 (limitless replicative potential) do

A
  1. Normal cells can divide only 40-60x (Hayflick limit)
  2. Telomere shortening leads to chromosomal abnormalities and cell death
    –> Loss of genes near end of chromosome
  3. Tumor cells overexpress telomerase, leading to immortalization
58
Q

what does Hallmark 5 (sustained angiogenesis) do

A
  1. Tumor cells can trigger angiogenesis (neovascularization)
  2. Solid tumors can’t grow beyond 1-2 mm without blood supply
    –> Deficient in oxygen/nutrient
    –> Unable to get rid of metabolic waste (lactic acid/CO2)
  3. Tumor cells produce VEGF to promote angiogenesis
    – HIFa
    —> Transcription factor for hypoxia genes (VEGF)
    – VHL - von hippel lindau
    —> Tumor suppressor E3 ligase for HIFa
59
Q

what does Hallmark 6 (tissue invasion and metastasis) do

A
  1. Adhesion and invasion of basement membrane
  2. Passage through extracellular matrix
  3. Invasion of vascular basement membranes and vascular ingress (intravasation)
  4. Travel via the vasculature
  5. Adhesion to basement membrane at destination
  6. Invasion of vascular basement membrane and vascular exit (extravasation)
  7. Metastatic deposit
  8. Angiogenesis and growth
60
Q

what are the three steps in multistep carcinogenesis

A
  1. initiation
  2. promotion
  3. progression
61
Q

what is the initiation step

A
  1. Exposure of cells to appropriate doses of carcinogenic agent
  2. Irreversible change in genome
  3. Amount of total exposure matters
62
Q

what is the progression step

A
  • Acquisition of malignant characteristics
    –> Invasiveness, metastatic competence
63
Q

what is the promotion step

A
  1. Unregulated and accelerated growth of mutated cells
  2. Triggered by growth factors and chemicals
  3. May occur after long latency periods
64
Q

what are the manifestations of cancers

A
  1. wasting syndrome
  2. fatigue and sleep disorder
  3. anemia
  4. pain
65
Q

describe wasting syndrome

A
  1. Cancer anorexia-cachexia syndrome)
  2. Reduced food intake (anorexia) and wasting of body fat and muscle tissue (cachexia)
  3. Oral or parenteral nutritional supplement does nor reverse cachexia
  4. Significant cause of morbidity and mortality
66
Q

describe fatigue and sleep disorder

A
  1. Tiredness, weakness, and lack of energy not relieved by sleep or rest
  2. Poor sleep quality, insufficient sleep, nightmare awakening, and restless sleep
67
Q

describe anemia

A
  1. Blood loss, hemolysis, impaired red blood cell production
  2. Drugs used in treatment may also decrease red blood cell production
68
Q

describe pain

A
  1. Common in late-stage cancers
  2. Most dreaded aspects of cancer
  3. Pain management is necessary even for patients with incurable cancers
69
Q

what are the methods for targeting cancer therapy

A
  1. FISH
  2. IHC
  3. DNA sequencing
70
Q

what are the targeting cancer therapies

A
  1. BCR-ABL translocation
  2. Estrogen receptor (ER)
  3. HER2 Overexpression
  4. EFGR mutations
  5. Ras mutations
71
Q

describe BCR-ABL translocation

A
  1. BCR-ABL inhibitors
    EX: Gleevec/imanitib
72
Q

describe Estrogen receptors

A
  1. BCR-ABL inhibitors
    EX: Gleevec/imanitib
73
Q

describe HER2

A

anti-HER2 antibodies
EX: Herceptin/trastuzumab

74
Q

describe EGFR mutations

A

EGFR inhibitors

75
Q

describe Ras mutations

A

targeted inhibitors

76
Q

describe cancer biomarkers

A
  1. Proteins are highly expressed in cancer tissue and also used as biomarkers in blood
  2. Not so useful for diagnosis due to high false positive rate
  3. Useful in monitoring treatment response and recurrence
77
Q

what are examples of biomarkers

A
  1. PSA
    –> Prostate specific antigen
    –> Prostate cancer
  2. AFP
    –> A-fetoprotein
    –> Primary liver cancer and germ cell cancer of testis
  3. CA 125
    –> Cancer antigen 125
    –> Ovarian cancer
78
Q

why are biomarkers Not so useful for diagnosis due to high false positive rate

A
  1. Levels can be elevated by other causes
  2. Can be used in combo with other diagnostics
79
Q

what are biomarkers Useful in monitoring treatment response and recurrence

A
  1. Decrease after surgery/treatments confirms effectiveness
  2. Increase later may suggest tumor recurrence

Patho 2023 (37 decks)

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