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BMS 460 > Neoplasia, Carcinogenesis > Flashcards

Neoplasia, Carcinogenesis Flashcards

1
Q

how can neoplasias be classified?

A
  • clinical: refers to overall consequences to the host
  • histological: benign vs. malignant, can predict clinical behavior
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2
Q

characteristics of benign neoplasia

A
  • expansile growth
  • but, contained in capsule
  • homogeneous cut surface
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3
Q

characteristics of malignant neoplasia

A
  • invasive growth
  • necrosis
  • lymphatic invasion
  • nonhomogeneous surface
  • hemorrhage
  • vessel invasion
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4
Q

benign/malignant epithelial tumor

A

benign: oma
malignant: carcinoma

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5
Q

benign/malignant glandular tumor

A

benign: adenoma
malignant: adenocarcinoma

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6
Q

benign/malignant mesenchymal tumor

A
  • first of all, this is connective tissue, bone, or muscle origin
    benign: oma
    malignant: sarcoma
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7
Q

histological classification exceptions

A
  • hematopoietic/lymphoid
  • neural
  • germ cell
  • so, these ones have variable/inconsistent names
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8
Q

are all tumors that end in oma benign?

A
  • no!!
  • lymphoma, glioma, seminoma are malignant
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9
Q

blastoma

A

malignant tumors composed of embryonic/primordia cells

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10
Q

teratoma and teratocarcinoma

A
  • tumors from germ cells, mostly in the testis and ovary, that contain embryonic cells that differentiate into embryonic germ layers - so can have teeth/hair/etc
  • teratoma: benign
  • teratocarcinoma: malignant
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11
Q

what is the hallmark of malignant cells?

A
  • anaplasia!
  • benign cells closely resemble their tissue type of origin (well differentiated)
  • malignant cells do not (poorly differentiated)
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12
Q

anaplasia

A
  • lack of differentiated/specific features
  • presence of new features that are not inherent to tissue of origin
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13
Q

pleomorphism

A

variation in cell size and shape

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14
Q

describe anaplastic tumor cells in PAP smear

A
  • pleomorphism
  • large, heterochromatic nuclei
  • abnormal mitotic figures
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15
Q

tumor staging

A
  • done to predict clinical behavior
  • based on clinical exam, x-ray, biopsy, or surgical exploration
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16
Q

international TNM system

A
  • an international staging system!!
  • stands for tumor, node, metastasis
  • T1, N1, M0: tumor less than 1 inch, spread to 1 lymph node, no metastasis to distant sites
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17
Q

tumor grading

A
  • done to guide therapy
  • based on histological exam
  • main way to determine benign or malignant nature
  • grade I: well differentiated
  • grade II: moderately well differentiated
  • grade III: undifferentiated (so malignant)
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18
Q

does staging or grading have more prognostic value?

A

staging! i think this is because it indicates how far the disease has spread, not just what the cells look like?

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19
Q

list 6 hallmarks of cancer

A
  • cancer cells need to acquire traits that enable them to become tumorigenic and ultimately malignant
    1. sustained proliferative signaling
    2. evading growth suppressors
    3. activating invasion and metastasis
    4. enabling replicative immortality
    5. inducing angiogensis
    6. resisting cell death
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20
Q

elaborate on evading growth suppressors

A
  • genome instability generates genetic diversity that expedites the acquisition of these hallmarks
  • also underlying these hallmarks is inflammation
  • genetic diversity ultimately allows cancer cells to be unaffected by growth suppressors from host?
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21
Q

elaborate on inducing angiogenesis

A

blood vessels are produced to bring nutrients to cancerous cells

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22
Q

elaborate on resisting cell death

A
  • cancer cells do not undergo apoptosis after a certain amount of cell divisions like normal cells do
  • this means they are immortal
  • their rate of division may also be unregulated
  • the fact that they have nutrients allows this!
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23
Q

what are tumor suppressor genes (TSG’s)?

A

provide varied normal inhibitory mechanisms in cell proliferation or apoptosis in defective cells

24
Q

what is the most common TSG involved in cancer?

A
  • p53
  • more than 50% of all human cancers lack functional p53, meaning that both copies of it are damaged
25
Q

tumor related to Rb-1

A

retinoblastoma (eye)

26
Q

tumor related to tp53

A

numerous cancers like breast and colon

27
Q

tumor related to NF-1

A

neurofibromatosis 1 (peripheral nerves)

28
Q

tumor related to WT-1

A

Wilms’ tumor (kidney)

29
Q

tumor related to APC

A

familial adenomatous polyposis coli (large intestine)

30
Q

tumor related to BRCA1 and BRCA2

A

breast carcinoma and ovarian carcinoma

31
Q

describe reaction to ionizing radiation, carcinogens, and mutations in cells with normal p53

A

DNA gets damaged –> p53 gets activated and binds DNA –> transcriptional upregulation of p21 (CDK inhibitor), DNA repair genes, and apoptosis genes –> if repair is successful, cells go back to normal, and apoptosis if unsuccessful

32
Q

describe reaction to ionizing radiation, carcinogens, and mutations in cells with abnormal/damaged p53

A

DNA gets damaged –> p53 not activated –> no cell cycle arrest or DNA repair –> mutant cells –> expansion and additional mutations –> malignant tumor

33
Q

define oncogene

A
  • a mutant form of a gene that is associated with a disease
  • can transform a cell into a tumor cell in certain circumstances, so has the potential to cause cancer
34
Q

define proto-oncogene

A
  • normal form of a gene
  • regulates cellular growth-activating pathways
  • overactivity predisposes to cancer development
35
Q

describe 5 things that can happen with proto-oncogenes

A
  • point mutation: makes oncogenic protein
  • amplification: makes too much of a normal protein
  • nothing: normal protein made
  • chromosome rearrangement: overproduced or oncogenic fusion protein
  • viral gene insertion: makes oncogenic protein
36
Q

what is cancer primarily a disorder of?

A

genes and gene expression!

37
Q

ways that chromosomes can be abnormal in cancer cells

A
  • numerically abnormal
  • structurally abnormal
38
Q

describe numerical chromosomal abnormalities in cancer cells

A
  • benign cells usually have a normal number of chromosomes
  • malignant cells are often aneuploid
39
Q

describe structural chromosomal abnormalities in cancer cells

A
  • deletions, translocations, or newly formed fragments arise from disorderly mitoses in malignant tumors
40
Q

what is a common translocation in a specific cancer that we talked about?

A
  • Burkitt’s lymphoma
  • the c-myc gene, which is on chromosome 8, gets translocated onto chromosome 14
  • now, it is next to the Ig gene, which is highly expressed in B cells (lymphocytes) because they make so many antibodies
  • this causes the c-myc gene, which normally has a role in regulated cell growth/division, to be overactivated
  • this results in overproliferation of B cells - causing tumors that are lymphomas because the gene that is causing them is active in lymphocytes
41
Q

what are some other examples of cancers caused by oncogenes activated by translocation?

A

ALL- acute lymphoblastic leukemia
AML - acute myeloid leukemia
MLL - myeloid-lymphoid or mixed lineage leukemia

42
Q

what are some exogenous factors that have been identified as carcinogens?

A
  • physical agents
  • chemicals
  • viruses
  • they have been identified as carcinogens because of their mutagenic potential!!
43
Q

what might carcinogens cause?

A
  • point mutations or singel base substitutions
  • proto-oncogene can become an oncogene upon introduction of an oncogene into a host cell by retrovirus
44
Q

potential causes of skin cancer?

A
  • sunlight
  • UV radiation
45
Q

potential causes of lung cancer

A
  • inhalation carcinogens
  • ex: 3.4-benzyprene
46
Q

potential causes of thyroid cancer?

A
  • x-rays
  • radioactive isotypes
  • these can also cause skin cancer
47
Q

potential causes of lymphoma?

A
  • viruses
  • ex: HTLV-1 virus
  • affects thymus, lymph nodes
48
Q

potential causes of intestinal cancer?

A
  • metabolic carcinogens like nitrates and nitrites
  • get converted to nitrosamines to cause intestinal cancer
49
Q

potential causes of liver cancer?

A
  • metabolic liver carcinogens
  • ex: aflatoxin
50
Q

potential causes of bladder cancer?

A
  • metabolic excretory carcinogens
  • ex: azo dyes
  • affects bladder because carcinogen gets excreted
51
Q

how does the study of the etiology of human cancer begin?

A
  • with clinical observations
  • these are amplified by data from epidemiologic studies that initially identify carcinogens
  • after identification, experimental studies are done on animals
  • overall goal is identification and isolation of cancer genes!!
52
Q

describe the steps of chemical carcinogenesis

A
  1. convert potentially harmful substance (procarcinogen) into a carcinogen
  2. initiation: the carcinogen induces irreversible change in DNA (mutation)
  3. promotion: initiated cells can be stimulated to proliferate, either through continuous exposure to carcinogen or another non-carcinogenic growth factor
  4. conversion: promoters are applied until the cell can proliferate on its own and convert to a new cell type
  5. progression: converted cells acquire new genetic features, expand, and progress to form clones. they do not regress even after removal of carcinogen or promotor
  6. clonal expansion: clones rapidly grow to give rise to identical clones
  7. proliferation of divergent clones: made possible by mutations in tumor cell genome since tumor cells are genetically unstable - tumor cell heterogeneity!!
  8. selection: most favorable/strong clone is selected, outgrows the others
53
Q

result of overactivity of mutated proto-oncogenes and underactvity of TSGs?

A
  • enhanced cell proliferation
  • inhibition of appropriate cell death
  • note: synergy between oncogenes may be necessary to have malignant growth!!
54
Q

three main pathways of metastasis

A
  1. through lymphatics
  2. via blood (hematogenous)
  3. by seeding surface of body cavities
55
Q

describe the process of cancer cells passing through the basement membrane

A
  • tumor cells produce receptor proteins, like fibronectin and laminin receptors (for these two basal lamina glycoproteins)
  • then, they produce enzymes like type IV collagenase, which allow them to break down the type IV collagen in the basement membrane. they also produce plasminogen activator, so plasmin can’t be made from plasminogen to break down blood clots
  • next, they make autocrine factors, basically telling themselves to become motile so they can get through the broken basement membrane

BMS 460 (28 decks)

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