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Spring 23: DVM 640 BOD > Neoplasia Module > Flashcards

Neoplasia Module Flashcards

1
Q

Anaplasia

A

the loss of the mature or specialized features of a cell or tissue (as in malignant tumors)

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2
Q

Describe factors involved in maintaining appropriate cell mass in tissue

A

Maintenance of tissue structure/function requires a coordinated balance between tissue growth and tissue loss

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3
Q

teratoma

A

a congenital (present prior to birth) tumor formed by different types of tissue

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4
Q

Agenesis

A

Failure to develop all, or part, of an organ during embryonic growth, resulting in its absence (i.e. anopthalmia)

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5
Q

Aplasia

A

an organ, tissue or body part didn’t develop normally

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6
Q

hypoplasia

A

lack of cell growth

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7
Q

atresia

A

an orifice or passage in the body is closed or absent

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8
Q

atrophy

A

decrease in size or wasting away of a body part or tissue

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9
Q

hamartoma

A

A benign (not cancer) growth made up of an abnormal mixture of cells and tissues normally found in the area of the body where the growth occurs

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10
Q

Choristoma/Ectopic tissue

A

Abnormal amounts of tissue not native to a location (hamartoma)

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11
Q

hypertrophy

A

the enlargement of an organ or tissue from the increase in size of its cells.
“the hypertrophy of the muscle fibers”

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12
Q

hyperplasia

A

Increased cell number. Causes: Increased functional demand, endocrine stimulation, increased nutrition, chronic irritation, chemical and physical agents (drugs, toxins, radiation)

*can be progressive changes leading to neoplasia

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13
Q

metaplasia

A

transformation from one differentiated cell type to another, stem cell reprogramming. Causes: typically from highly specialized cells to less specialized cells. Epithelial (squamous, glandular [mucous]). Mesenchymal (chondroid, osseous, myxoid).

*can be progressive changes leading to neoplasia

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14
Q

dysplasia

A

abnormal pattern of tissue growth. Causes: developmental or acquired (degenerative i.e. hip dysplasia, or proliferative i.e. abnormal size, shape, or organization of adult cells)

*can be progressive changes leading to neoplasia

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15
Q

neoplasia

A

“new growth”. tumor = swelling, neoplasm (malignant, benign)

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16
Q

List the basic characteristics of cancer cells and elements of altered cell physiology

A
  • self-sufficient growth: insensitivity to anti-grow signals, unlimited ability to divide
  • evasion of apoptosis: progression of cycle through abnormal DNA, fixation of defect in progeny cells
  • sustained angiogenesis: tumor-induced microvasculature supports increased tissue mass
  • tissue invasion and metastasis: loss of inhibition by normal tissue barriers (matrix enzyme to destroy normal barriers), cell surface molecules to attach to new tumor bed
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17
Q

multistep nature of carcinogenesis

A

initiation, promotion, progression

reversability? n,y,n
DNA mutation? y,n,y
morphologic change? n,y,y

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18
Q

Four genomic themes relevant to most cancers

A
  1. Nonlethal genetic damage (to the individual cell) is at the heart of carcinogenesis
  2. A tumor is formed by clonal expansion of a single mutated precursor cell
  3. Four classes of normal regulatory genes are the principal targets of cancer-causing mutations:
    Proto-oncogenes (growth promoters)
    Tumor suppressor genes (growth inhibitors)
    Apoptosis-related genes (programmed cell death)
    DNA repair genes
  4. Carcinogenesis results from the accumulation of complementary mutations in a stepwise fashion over time.
19
Q

proto-oncogenes

A

Normal cellular genes involved in cell growth and/or division

proto-oncogene can become an oncogene

20
Q

tumor suppressors

A

P53, PTEN, RB

21
Q

oncogenes

A

a mutated proto-oncogene

22
Q

What is the function of telomeres?

A

Telomeres- specialized DNA-protein complexes which cap ends of linear chromosomes
Maintain genetic stability - Protect DNA ends from being recognized as damaged DNA leading to recombination, fusion, etc
magic caps at end of chromosomes to keep them from degrading

23
Q

Describe characteristics of tumor cells

A

uncontrolled cell proliferation
loss of apoptosis
tissue invasion and metastasis
angiogensis

24
Q

What is the convention for naming tumors of epithelial vs connective tissue origin?

A

malignant epithelial is carcinoma

malignant mesenchymal is sarcoma

benign is “-oma”

25
Q

arrest

A

telomeres are shortened with each cell replication and shortening to a critical length triggers cell growth arrest

26
Q

tumor cell origin theory

A

The classic theory proposes that cancer develops as a result of a defect in a protooncogene or tumor-suppressor gene. This leads to a lack of normally functioning tumor-inhibitory proteins, with simultaneous activation of oncogenes that stimulate cells to proliferate.

27
Q

stem cell theory

A

The stem cell theory of cancer proposes that among the many different types of cells within a cancer, there exists a subpopulation of cells called cancer stem cells that multiply indefinitely, are resistant to chemotherapy, and are thought to be responsible for relapse after therapy.

28
Q

stem cells

A

special human cells that are able to develop into many different cell types

29
Q

tumor latency

A

the amount of time that elapses between the initial exposure to a carcinogen (cancer-causing substance) and the diagnosis of cancer.

30
Q

neoangiogenesis

A

growing tumors stimulate neoangiogenesis

New vessels sprout from existing ones. Deliver nutrients and oxygen to tumor. New endothelium secretes growth factors (like PDGF) that stimulate growth of adjacent tumor cells.

31
Q

Mechanisms of Angiogenesis

A
  1. The adventitial cells and pericytes retract
  2. Basal membrane of the pre-existing vessels is degraded by proteases (MMP produced by the activated endothelial cells)
  3. Endothelial cells migrate from pre-existing vessels towards the angiogenic stimuli and proliferate
  4. Migration of endothelial cells is based on cell-extracellular interaction that is mediated by vascular cell-adhesion molecules (integrin αvβ3)
  5. Endothelial cells, after migrating, are structured into tubes to form capillary-like structures
  6. Structures mature into functional capillaries
  7. blood flow is initiated
32
Q

Two basic components of tumors

A
  1. neoplastic cells that constitute the tumor parenchyma (Classification of tumor and biologic behavior mostly determined by parenchyma)
  2. Reactive stroma made up of connective tissue, blood vessels and variable numbers of cells of the adaptive and innate immune systems (growth pattern and spread mostly determined by this factor)
33
Q

What is tumor grading and what are the strengths and weaknesses?

A

Determined by histological features.
Based on degree of differentiation of tumor cells (May include number of mitoses, May include specific architecture features). Usually breaks tumor subsets down into low grade or high grade (sometimes more categories)

Pros: Prognostically significant, Alter treatment decisions, Efficient, Cost effective, Low tech

Cons: Drift to middle grades, Subjective, Tumor heterogeneity, Sample size, Time consuming

34
Q

tumor staging

A

greater clinical value than grading

Determined by surgical exploration or imaging
Based on: Size of primary tumor, Extent of spread to regional lymph nodes, Presence or absence of blood-borne metastases, Criteria vary between tumors

35
Q

What is the difference between tumor grading and tumor staging?

A
36
Q

What features of neoplastic cell functions are estimated by grading schemes?

A

mitoses and architecture features

37
Q

list neoplastic diseases of animals caused by viruses, list the virus responsible for each and list the tumor type caused

A

papilloma, herpes, hepadna, pox, adenovirus, polyoma viruses

38
Q

steps in tumor invasion

A

Loosening of intercellular junctions (irreversible)
Degradation of basement membrane
Attachment of cell to extracellular matrix components
Migration of tumor cells

39
Q

herpes viruses

A
  • Lymphomas monkeys
  • Marek’s disease (lymphoma) fowl
  • Renal (Lucke) carcinoma in frog
  • Epstein-Barr Virus in humans
    - Burkitt’s lymphoma
    - Nasopharyngeal carcinoma
40
Q

tumors that herpes viruses cause

A
  • Lymphomas monkeys
  • Marek’s disease (lymphoma) fowl
  • Renal (Lucke) carcinoma in frog
  • Epstein-Barr Virus in humans
    - Burkitt’s lymphoma
    - Nasopharyngeal carcinoma
41
Q

aflatoxins

A

a family of toxins produced by certain fungi that are found on agricultural crops such as maize (corn), peanuts, cottonseed, and tree nuts.

42
Q

types of promoters

A

hormones, dietary fat, chemicals

43
Q

tumors that hepadna viruses cause

A

Hepatitis viruses:
Human hepatitis B
Woodchuck hepatitis virus

44
Q

tumors that pox viruses cause

A

Fibromas and myxomas in squirrels:
Usually limited to cutaneous masses
Rare natural systemic involvement
Systemic involvement common experimentally

Spring 23: DVM 640 BOD (4 decks)

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