Neoplasia 3 Flashcards

1
Q

Describe the mechanisms to alter DNA, causes, & the source.

A
  1. Mechanisms
    -mutations = change in nucleotide seq
    -chromosomal alteration
    -epigenetic change = heritable change in gene expression resulting from something other than change in DNA seq
  2. Cause
    -spontaneous
    -ionizing radiation
    -chem carcinogens (non lethal genetic damage)
    -oncogenic virus
  3. Source
    -inherited in germ line
    -acquired somatic mutation
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2
Q

Describe germ line mutations.

A

-mutation passed on in the ova or sperm
-all cells of affected progeny
-involved in:
>pediatric cancer
>family predisposition
>ppl w more than 1 type of cancer
-humans inherit 60 new mutation that occur in ova or sperm
-<10% human cancer have inherited mutations

Know the breeds
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3
Q

Describe acquired somatic mutations.

A

-occur in individual cells & their progeny (not passed on in germ line)
-spontaneous mutation unavoidable in individual life time (10^10 mutations/gene in a life time)
-accumulate over time = association between old age & cancer
Bright side:
>DNA repair mech
>most mutation are lethal to cell not animal
>multiple mutation needed for cancer

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4
Q

Describe radiation.

A

*all forms are carcinogens - able to initiate & promote tumorigenesis w cont exposure
1. Ionizing
-x ray, gamma ray
-eject e- from mol
-DNA strand breaks
2. UV
-UVB
-form pyrimidine dimmer in DNA = overwhelms nucleotide excision repair
-cats ears (cutaneous squamous cell carcinoma) & cows eyes (ocular squamous cell carcinoma)

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5
Q

Describe chemical carcinogens.

A

-chem metabolically transformed to become active
-associated w other cancer predisposing mutations
-EX: bracken fern ingestion, aflatoxin (moldy food - hepatoma in rainbow trout), hepatic carcinoma, dioxins, nitrosamines, polycyclic aromatic hydrocarbons (cig smoke)
-mechanisms:
1. Genotoxic - directly damage DNA
2. Cytotoxic - inc cell prolif due to cell injury
3. Mitogenic - inc cell prolif w/o cell injury

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6
Q

Describe oncogenic viruses.

A

-lg # of epidemiologically related animals
-affect young animals
-DNA stage during viral rep
-interrupt host gene by:
1. Come w their own oncogenes
-ex. Papillomavirus E6/E7 proteins inactivate p53 & other tumor suppressor genes
2. Insertional mutagenesis
-ex: retrovirus - avian leukosis
3. Immunosuppression
-ex: Mareks

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7
Q

Describe other causes of carcinogenesis.

A
  1. Hormonal
    -hormonal stim of growth in target organ
    -OVH in dog dec risk of mammary carcinoma
  2. Chronic inflam/inf
    -mech not understood - inflam cytokines stim cell prolif ?
    -ex:
    A) Esophageal sarcoma in dog w s. Lupi inf
    B) Biliary carcinoma in cat & dog w liver fluke
    C) Gastric carcinoma & lymphoma in humans w helicobacter spp.
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8
Q

Describe the para neoplastic effects - mechanisms of host damage.

A
  1. Direct effects
    -organ/tissue destruction
  2. Paraneoplastic syndromes
    -occult neoplasm
    -treatment or lethal
    -symptoms due to spread or hormones
    -indirect & remote effect caused by tumor cell prod rather than primary tumor & its metastasis
    EX: cancer cachexia, cerebral atrophy secondary to oligodendroglioma
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9
Q

Describe tumor necrosis.

A
  1. Pathogenesis
    -secondary to inflam in tumor
    -trauma of tumor
    -tumor outgrows its blood supply
  2. Secondary inflam resp & cytokines (TNFa) impact host health
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10
Q

Describe cancer cachexia.

A

-animals w cancer show weight loss & debilitation
-loss of body fat & lean body mass, weakness, anorexia, anemia
-loss of fat + muscle + metabolic rate doesnt dec (vs starvation) *
-pathogenesis:
1. TNF, IL1, IL6, INFgamma, prostaglandins, PIF (Proteolysis inducing factor)
2. Anorexia, impaired digestion, nutrition demands of tumor, metabolic/endocrine changes
3. Cant fix w extra nutrition supplement

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11
Q

Describe endocrinopathies.

A

-consequence of neoplasm in endocrine organs (over/under produce hormone)
-non endocrine neoplasm make hormone active substance not normally found in tissue of tumor origin (ectopic hormone prod)
-EX: hypercalcemia of malignancy *
>prod of parathyroid hormone related protein by neoplasm
>90% of cases in dogs due to apocrine gland adenocarcinoma of anal sac
>lymphoma, multiple myeloma also common in dogs

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12
Q

Describe the 2 main mechanisms that cancer can lead to hypercalcemia.

A
  1. Local action on bone
    -multiple myeloma or carcinoma that metastasize to bone
  2. Tumor that secrete humoral factors
    -stim bone reabsorption (PTHrP)
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13
Q

Describe hypertrophic osteopathy.

A

-dog & cat
-lameness
-X-rays show periosteal new bone growth
-space occupying thoracic lesions
-pathogenesis not known - abnormalities of growth hormone ?

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14
Q

Describe cytologic diagnosis.

A

-aspirate of mass
-faster, cheaper, less invasive than histology
-determine type of neoplasm & differentiate benign VS malignant
-histopath to confirm
-round cell tumor:
>mesenchymal neoplasm
>plasma cell tumor, histiocytoma, mast cell tumor, lymphoma, TVT

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15
Q

Describe margin assessment.

A

-surgical margin w surgical ink
>bc cant tell where the lab cut VS where the surgeon cut otherwise
>tissues slip apart from sample during transport/handling
>help orientate which margin is which (lateral VS deep)
-pathologist report if margins are clean or dirty based on absence/presence of tumor cells respectively
>can provide distance between tumor cells & sx margin
-complete excision imp prognostic factor
>clean margins dont mean complete excision

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16
Q

Describe histopathologic diagnosis.

A

-biopsy sample from tumor & stained w H&E
>incisional = diagnosis affect surgical/Rx plan
>excisional = diagnosis NOT affect surgical/Rx plan
-examine morphology to determine cell of origin/differentiation
-special histochemical stains for diagnosis of some tumors
>mast cell tumor = granules stain toluidine blue
>Fontana Massons = melanin in amelanotic melanomas
-criteria of malignancy:
1. Degree of differentiation
2. Invasion
3. Mitotic rate
4. Features of anaplasia - pleomorphism, anisokaryosis/anisocytosis, nuclear hyperchromasia, high N:C ratio, prominent nucleoli

17
Q

Describe histopathologic grading.

A

-assigned by pathologist to designate how abnormal the neoplastic cells are
-prognostic factor/indicator to predict biologic behavior of neoplasm & inform treatment
>vet: tumor type, grade, stage, complete excision = treatment plan
-grading depend on tumor type & use:
1. Degree of differentiation
2. MC
3. Amount of necrosis
4. Invasiveness
*dont confuse w staging (spread)

18
Q

Describe clonality assays.

A

-used in lymphoma diagnosis
>atypical lymphoid hyperplasia VS early lymphoma
>clonality add more weight to lymphoma
>PCR for T or B lymphocyte Ag receptor rearrangement (PARR) if cells have same rearrangement = clinical prolif

19
Q

Describe sentinel LN & sentinel LN biopsy (SLNB).

A

-first LN that cancer cells are most likely to spread from a primary tumor (can be more than 1 sentinel LN)
-SLNB:
>sentinel LN ID, removed, & examined to determine if cancer cells are present - used in ppl already diagnosed w cancer
>neg SLNB = cancer not spread yet to nearby LN or organs
>pos SLNB = cancer in sentinel LN & may have spread to other nearby LN (regional LN) & other organs
—helps doctors determine stage of cancer & treatment

20
Q

Describe what happens during a SLNB.

A

-sentinel LN located by surgeon inj radioactive substance (blue) near tumor & use device to detect LN that have the dye
-incision to remove LN once ID
-sentinel LN checked for cancer by pathologist & remove additional LN if pos

21
Q

Describe clinical staging.

A

-plan & prognosis (affect patient & respond to treatment)
-extent of tumor growth & spread
-varies by tumor:
>size of primary tumor
>depth of invasion
>involvement of regional LN
>extent of distant metastasis
-cytology, histology, diagnostic imaging
*TNM (tumor, LN, metastasis) system