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401 Exam 3 > Cancer/Neoplasia > Flashcards

Cancer/Neoplasia Flashcards

1
Q

Define benign neoplasia

A

a benign tumor is a growth of cells that does not invade into adjacent tissue and has no propensity to spread to distant sites

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2
Q

Define malignant neoplasia

A

aka cancer. The malignant tumor invades into adjacent tissue and may spread to distant sites (metastasis).

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3
Q

Two keys hallmark of cancer (malignancy)

A
  • To invade
  • To metastasize
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4
Q

Why metaplasia is concerning for a pre-malignant condition?

A

Metaplasia is a change in differentiation of cells. Think of a cat that starts smoking. Mucosal surface will change differentiation towards a squamose epithelium.

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5
Q

Aniscytosis?

A

variation (aniso) in cell (cyto) size and shape

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6
Q

Anisokaryosis?

A

variation (aniso) in nuclear (karyo) size and shape

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7
Q

Monomorphism?

A

In a homogenous population, all cells appear the same - more indicative of cancer.

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8
Q

Pleomorphism?

A

Homogenous population (one cell type) that appear very different. Think of bobbies shape!

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9
Q

How a homogenous, pleomorphic population can resemble a
heterogeneous population on a biopsy?

A

Multiple cell populations (heterogenous) mean physiology, inflammation; while one cell population is a concern for neoplasia. The degree of pleomorphism can help us determine how likely a specific cell population is to be malignant or how malignant it might be.

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10
Q

Anaplasia?

A

Loss of differentiation, often to a point where it is hard to recognize what an individual cell is/what type of cell it is.

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11
Q

Why anaplasia is a concern?

A

More anaplastic, more likely it is malignant. The more similar cell resembles a normal tissue, the more likely it is benign.

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12
Q

Initiation - reversible or irreversible?

A

ALWAYS irreversible. Genetic irreversible.

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13
Q

What is initiation? Example?

A

Cell proliferation and mutagenesis. “Locking” of an acquired mutation into the genome of a cell.

Sunburn will give us initiated cells.

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14
Q

Promotion - reversible or irreversible?

A

Nongenetic reversible

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15
Q

Example of promotion that can be reversible?

A

Spay! to discontinue estrus cycle. Mammary gland epithelial cell amplifies its EGFR gene - every time dog enters estrous, more EGF secreted leading to outgrowth. Since this process depends on physiologic stimulus, it can be reversible.

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16
Q

Progression - reversible or irreversible?

A

genetically irreversible; and also nongenetially reversible.

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17
Q

Example of progression?

A
  • If more cell division because of EGF secretion, the likelihood of mutation during cell division will be irreversible.
  • If tumor progress to inflammation, progression can be reversible by given anti-inflammatory.
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18
Q

Adenoma vs. carcinoma in situ vs. carcinoma

A
  • Adenoma: cells are abnormal looking but very similar to “normal” cells, not invading.
  • Carcinoma in situ: pleomorphism present, but not invading to neighboring layers.
  • Carcinoma: invading, pleomorphism.
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19
Q

Hamartoma

A

proliferation of benign cells but restricted to a location on the body (birthmark).

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20
Q

Choriostoma

A

Proliferation of benign cells located in a position where it’s not usually found

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21
Q

Teratoma

A

a germ cell tumor. Ew!!

22
Q

Features of epithelial tumors

A

Large, polygonal cells, defined borders. Arranged in sheets, tubules, acini, glands.
- Benign may pedunculated (outy)
- Malignant: scirrhous response (scar forming), ulceration, umbilication.

23
Q

Features of round cell tumor

A

individualized cells
Cells are round to polygonal. Cells are often infiltrate into adjacent tissue.
Think of Pepper’s lymphoma.

24
Q

Features of mesenchymal tumors

A
  • Spindle-shaped cells: fibroblasts, muscle, adipose tissue, bone, cartilage.
  • Often accompanied by stroma or matrix (smooth appareance)
  • HIGH nuclear:cytoplasm ratio
25
Q

How mesenchymal tumors are identified: e.g. how do you know something is
a fibrosarcoma versus an osteosarcoma?

A

If you can identify what kind of stroma the cell is secreting, you can identify what the cell is. Hence, you can identify what the tumor is.

26
Q

Describe 3 general histologic hallmarks of benign vs. malignant tumors

A
  • Benign: 1) local growth, 2) growth via expansion and pedunculate, 3) well circumscribed and encapsulated.
  • Malignant: 1) metastasis, 2) growth through invasion/infiltration, 3) poorly circumscribed, unencapsulated, increased angiogenesis.
27
Q

Identify two common gross features of carcinomas

A
  • Loss of glandular arrangement (solid areas, unencapsulated invasion into adjacent stroma and blood vessels).
  • Increase cellular pleomorphism and atypia.
28
Q

How is cancer-associated vasculature different than normal?

A
  • Abnormal structure: leakage, fragility
  • Abnormal signal: paracrine (change in neighbor cells, blood vessel grow toward) and autocrine (change in cells - grow out to reach blood vessels).
  • Continued growth of vasculature.
28
Q

Diagram how a metastatic carcinoma cell would enter and grow within a lymph node

A

Entered via afferent (draining) lymphatics [cortex], exit through efferent lymphatics [hilus]. Tumor looks at subcapsular sinus where they aggregates.

28
Q

Diagram the specific steps involved in metastatic (vascular) spread of malignant
neoplasia to the lung

A
  • Loosening of intercellular junction
  • Attachment (by integrins) to laminin
  • Degradation through basement membrane (secrete collagenase)
  • Migration
29
Q

Explain why the lung is such a common site for metastatic disease

A

Because there are lots of of capillaries (small blood vessels) in the lungs lobe make cancer cells easy to invade. Thin wall of capillaries makes it easy to migrate out.

30
Q

What is carcinomatosis?

A

this is a unique form of metastasis, a direct-implanting, or seeding of a surface by malignant cells. When it happens, it usually occurs in malignant epithelial tumors (hence the name). Cells arrive by exfoliation and implanting on adjacent surfaces, rather than by a vascular route.

31
Q

Diagram how UV-B radiation contributes to initiation, promotion, and progression

A
  • Initiation: UVB irradiation - T/T dimers
  • Promotion: continued inflammation - proliferative signals
  • Progression: genomic instability, disregulation
32
Q

Routes of metastasis

A
  • Blood (hematogenous) - sarcoma; Lymph (lymphatic) - carcinoma; direct (carcinomatosis)
33
Q

what are the checkpoints in replication, and name two tumor suppressor proteins controlling them

A
  • G1/S checkpoint
  • G2/M checkpoint
  • Two major TSGs act to inhibit G1/S: p53 and retinoblastoma (Rb). p53 can act through a secondary messenger, p21, to block the transition at either G1/S or G2/M. Rb acts to inhibit the transcription factor family E2F, necessary for completion of G1/S.
34
Q

Define an oncogene and tumor suppressor gene, and give an example of each.

A
  • Oncogene: any gene that promotes cell survival and proliferation. c-Kit, EGFR, Ras.
  • Tumor suppressor gene: any gene that functions to limit cell cycle progression. p53 and Rb.
35
Q

List 3 major functions for p53 as a tumor suppressor gene

A
  • Function at both checkpoints.
  • Upregulating expression of the gene p21. p21 is a CDK inhibitor (CDKi) and works to slow down the cell cycle.
  • Functions as a tumor suppressor gene (upregulate gene for DNA damage repair or apoptosis).
36
Q

Explain how mutations in Ras would promote cancer

A
  • Ras functions in signal transduction: signal from a receptor to initiate intracellular signaling events.
  • Mutated Ras is unable to inactivate - it stays in a conformation that continues to bind GTP, thus is always on, and constitutively producing downstream signaling, even without receptor activation.
37
Q

Diagram an example of Loss of Heterozygosity (LOH) in cancer

A

2-hit hypothesis: both alleles of a TSG must be lost before cancer develops. When one allele is lost, that cell now only has one functional allele left, and is thus homozygous (or has lost heterozygosity- LOH). So a cell that has LOH in a TSG may not be sufficient for cancer formation, but that cell is certainly predisposed, needing only one more hit.

38
Q

Do all TSGs require loss of both
alleles?

A

Some TSGs are so important that even a partial loss of function (such as LOH) are sufficient to cause cancer. So NO.

39
Q

Contrast genomic vs. epigenetic regulation of gene expression

A
  • Epigenetic: changes in how the cell expresses its genes, without changing the coding sequence of the gene. In other words, it changes the regulation of genes, not the gene itself.
  • Genomic alterations: these are physical changes to the genomic code in a cell.
40
Q

Cell senescence: define the term and list 3 reasons that cells enter this

A

(Think of nursing home)
- DNA damage response
- Telomere shortening
- Oncogene induced

41
Q

Explain how a BENIGN brain tumor can kill a patient

A
  • Tumors are proliferation of cells.
  • They exhibit compression against adjacent tissue causing atrophy of normal tissue or alter its function.
  • Meningiomas are benign but causes significant morbidity (seizures, altered mentation).
  • Meningiomas secrete VEGF stimulates blood vessel growth and increase vascular permeability, producing edema in adjacent brain.
42
Q

Define paraneoplastic syndrome- why are these important?

A
  • Systemic effects of neoplastic disease (neoplastic mediators), resulted in significant morbidity (animals appear so sick!).
  • Important to understand common syndromes to recognize tumor/cancer.
43
Q

Diagram out the basic mechanisms of cancer cachexia

A

Start @ hypothalamus
* Fat breakdown
* Decreased muscle production
* Muscle breakdown
* Insulin resistance
* Decreased pain threshold (increased pain)
* Anorexia
* Increased glycolysis
* Fever, systemic pain
As the actual metabolism is being reprogrammed by the cancer, feeding and supplemental nutrition have minimal, if any, impacts on these patients. It is like having “the flu” for every day while a cancer is causing this syndrome.

44
Q

What is meant by initiation, promotion, and progression of cancer?

A
  • Initiation: mutagens, DNA damage/mutation
  • Promotion: a positive selective pressure for initiated cells
  • Progression: genomic/epigenetic events increase malignancy
45
Q

Diagram the pathogenesis of solar-induced carcinoma

A
  • Start with exposed skin/mucus membrane.
  • Initiation: Pyrimidine dimer formation
  • Promotion: Inflammation, induce COX2 expression and cell proliferation.
  • Progression: Onset of genomic instability
46
Q

Describe the basic mechanisms of viral transformation in DNA and RNA viruses and give 2 examples of each

A
  • DNA virus: transform by production of viral protein. Papilloma, Herpes, Pox, Polyoma
  • RNA virus: transform by inserting into the host genome. Lymphoma in cats and cows.
47
Q

What are E6 and E7 viral proteins? Name a virus that makes them and describe how they drive cell proliferation

A

E proteins promote cell divisions.
- E6: inhibit p53 = remove TSG function, allow cell cycle to pass check point and proceed.
- E7: inhibit Rb = allow E2F to activate and pass G1/S, enter cell cycle.

48
Q

Give 1 example each of bacterial- and parasite-induced cancer.

A
  • Bacterial: helicobacter spp. and other spirochetes.
  • Parasite: Spirocera lupi (esophageal sarc in dogs)

401 Exam 3 (4 decks)

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