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Neoplasia > Quiz Lecture 1-4 > Flashcards

Quiz Lecture 1-4 Flashcards

1
Q

Benign tumors are associated with serious diseases such as what?

A

Sturge-Weber angiomatosis; hemangioma along trigeminal nerve.

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2
Q

What is the most common type of skin cancer

A

Basal cell carcinoma

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3
Q

What is the #1 cause of death from skin cancer?

A

Melanoma

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4
Q

What is the main tissue of a tumor and why it its important?

A

The main tissue of a tumor is parenchyma, which are clonal neoplastic cells. They are important because they determine tumor behavior and pathologic consequences.

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5
Q

What is reactive stroma?

A

Connective tissue, blood vessels, macrophages, and lymphocytes

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6
Q

What is an adenoma?
Adenocarcinoma?
Sarcoma?

A

Adenoma is a benign glandular tumor.
Adenocarcinoma is a malignant tumor of epithelial origin.
Sarcoma is a malignant mesenchymal tumor.

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7
Q

What is squamous papilloma?

What is SCC?

A

Squamous papilloma: benign epithelial origin.

SCC: malignant epithelial origin

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8
Q

What is reactive stroma?

A

Connective tissue, blood vessels, macrophages, and lymphocytes.

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9
Q

What determines the growth of a tumor?

A

Blood supply and stroma. The blood supply leads to proliferation of tumor cells. The stroma provides structural framework (stony hard or fleshy)

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10
Q

Malignancies of epithelial origin are called ___________.

Malignancies of mesenchymal origin are called __________.

A

Malignancies of epithelial origin: carcinoma.

Malignancies of mesenchymal origin: sarcoma.

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11
Q

What is a cyst adenoma?

A

Benign tumor with hollow spaces/cysts inside.

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12
Q

What is a mixed tumor?

A

A mixed tumor is due to divergently differentiating. Bone, cartilage, and other tissues may be present.

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13
Q

What is a teratoma?

A

A tumor tissue with multiple germ layers.

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14
Q

What is a hamartoma?

A

Disorganized mass of cells indigenous to the site.

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15
Q

What is a choristoma?

A

A choristoma is normal tissue in an abnormal site.

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16
Q

What is a hemangioma?

A

A benign blood vessel tumor that blanches upon pressure.

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17
Q

What is pleomorphic adenoma?

A

A benign mixed tumor of the salivary gland.

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18
Q

What is metaplasia?

A

A replacement of one adult cell type with another. This occurs to replace it with a cell better suited for the environment it exists in. i.e. squamous metaplasia of salivary ducts is when cuboidal cells become squamous to protect the acini. This also can occur with gastric acid reflux.

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19
Q

Dysplasia is an _____________.

A

abnormal maturation e.g. epithelial dysplasia, a precancerous lesion in the oral mucosa

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20
Q

What are the names for fibrous tissue benign and malignant tumors?

A

Benign is fibroma. Malignant is fibrosarcoma.

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21
Q

Which vasculature tumors are benign and malignant?

A

Benign: hemangioma, lymphangioma
Malignant: angiosarcoma, Kaposi’s sarcoma

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22
Q

Which nerve tumors are benign and malignant?

A

Benign: neuroma, neurilemma, and neurofibroma
Malignant: neurogenic sarcoma

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23
Q

Which salivary gland tumors are benign and malignant?

A

Benign: pleomorphic adenoma, monomorphic adenoma. Malignant: mucoepidermoid carcinoma and acidic cell carcinoma

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24
Q

What must occur for a pre-cancerous lesions to be considered cancerous?

A

It must invade into the underlying connective tissue.

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25
Q

What are 3 ways metastatic cancer can occur?

A

Direct seeding
Lymphatics (usually carcinomas)
Blood vessels (usually sarcomas)

26
Q

Are promoters tumorigenic?

A

No, Promoters induce tumors in initiated cells but are themselves NOT tumorigenic.

27
Q

What are the steps in carcinogenesis?

A

Initiation: a rapid irreversible genotoxic event(s) leading to permanently altered cells that are at increased risk for neoplastic transformation
- Dysplasia (mild in basal 3rd, moderate in middle 3rd, severe in upper third) —> carcinoma in situ (full thickness) —> carcinoma
* note: carcinoma in situ is NOT carcinoma *
Promotion
Progression

28
Q

What growth factor is over expressed in 90% of SCC?

A

EGFR

29
Q

What is EGFR?

A

EGFR is a RTK with ligands EGF, TGF-alpha and amphiregulin. It induces PI3K/AKT, MAPK, and STAT signaling pathways. —> Proliferation, invasion, metastases, and angiogenesis

30
Q

What are the protein products of tumor suppressor genes?

A
  • Inhibitors of cell proliferation
  • Cell adhesion molecules
  • Membrane binding proteins
  • Transcription factors
  • Inhibitors of angiogenesis
  • Inducers of differentiation
31
Q

How does differentiation impact growth?

A

More differentiated, slow growth.

32
Q

What is an example of a tumor suppressor gene?

A

Retinoblastoma

33
Q

What are the genes that regulate apoptosis and DNA repair?

A
  • p53 —> promotes apoptosis
  • Bcl2 —> promotes survival
  • BRCA1 —> promotes DNA repair (homologous recombination)
  • Ku80 —> promotes NHEJ ** Ku80 in HPV negative oral cancer is a predictor of treatment failure and mortality following radiation **
34
Q 
Squamous Papilloma
Verruca vulgaris 
Condyloma acuminatum
Verruciform xanthoma
Focal epithelial hyperplasia
... These are on the DD for what type of lesions?
A

Benign and premalignant oral epithelial lesions

35
Q

Squamous Papilloma

- Which HPV #?

A
  • HPV origin: 6 and 11
  • 81% normal adults have HPV in buccal epithelial cells
  • Usually pedunculated
  • Where? Tongue, lip and soft palate
  • Appearance? Finger-like or cauliflower
  • Color varies with keratinization
  • Histologically: papillary proliferation of epithelial connective tissue stalk
  • What is treatment? Excision
36
Q

Verruca vulgaris (common wart)

A
  • HPV origin: 2,4,6,40
  • Contagious - autoinocculation
  • Clinical features: children, common on skin (hands), oral: vermillion, labial mucosa, anterior tongue
  • Presents as? Papule, nodule —> papillary or pebbly
  • Pedunculated or sessile
  • Usually white <5mm. Multiple lesions are common.
37
Q

What is the histology of verruca vulgaris?

A

Papillary proliferation of epithelium, axially inclined rete ridges, prominent granular layer parakeratin layering, koilocytes (HPV altered cells).

38
Q

How is verruca vulgaris treated?

A

Skin: liquid N2, cryotherapy, excision
Oral: laser, cryotherapy, electrosurgery

39
Q

Condyloma acuminatum (venereal wart)

A
  • Where? Genitilia, perianal region, mouth, larynx
  • HPV origin 2,6,11,53,54,16,18. 1-3month incubation
  • 20% of all STDs
  • Occurs at site of sexual contact, trauma - auto inoculation brings to other sites
  • Teenagers and young adults - kids w/ this should bring up suspicion for child abuse
  • Oral location: labial mucosa, soft palate, lingual frenum
  • Multiple, clustered, sessile, pink, non-tender
    • Condyloma acuminatum HPV 16 and 18 —> Risk of SCC in anogenital region **
40
Q

What is the treatment for Condyloma acuminatum?

A

Excision, laser. It must be removed because it is contagious.

41
Q

What is the histology of condyloma acuminatum?

A
  • Blunted papillary proliferation
  • Acanthotic, keratitis
  • koilocytes
42
Q

Focal Epithelial Hyperplasia = Heck’s Disease

A
  • Native America, Eskimos (Inuits)
  • HPV origin: 13,32
  • Children
  • Oral location: labial, buccal and lingual mucosa
  • Multiple, papules, plaques <1cm
  • Same color as adjacent mucosa or pale
  • Discrete —> cobblestone, fissured appearance
  • Spontaneous regression
  • Similar lesion in AIDS pt
43
Q

What is the histopathology of Heck’s disease?

A
  • Abrupt acanthosis
  • Extends upward
  • Koilocytes
  • Mitosoid cells - nucleus resembles mitotic figure
44
Q

What is the treatment of Focal Epithelial Hyperplasia?

A

Spontaneous regression

45
Q

Leukoplakia is a diagnosis of exclusion!

What has to be ruled out before diagnosing leukoplakia?

A 
Morsicatio buccarum
Frictional keratosis
Tobacco pouch keratosis
Nicotinic stomatitis
Leukoedema
Candidiasis
Lichen planus
46
Q

What are some etiological facts of leukoplakia?

A

Tobacco
- 80% of pt are smokers
- Heavy smokers have more and larger lesions
Alcohol- NOT associated w/ leukoplakia
** mouth rinse with>25% may be associated with gray buccal mucosa plaques **
Candida albicans
- Candidal leukoplakia, candidal hyperplasia
- Granular plaque with red, white color
HPV 16,18
Sanguinaria extract (herbal)
- Keratosis of maxillary vestibule of alveolar mucosa with epithelial dysplasia but no evidence for transformation. May persist after product cessation.

47
Q

Leukoplakia facts..

A
  • Affects people >40 years
  • Prevalence increases with age - occurs in 8% of men >70 years
  • 70% of lesions occur in males
  • Lip vermillion, buccal mucosa, gingiva
  • “Danger zones”: tongue, vermillion, floor of mouth - 90% dysplasia SCC
  • Homogenous, granular, nodular, verrous or speckled
48
Q

What are the morphological features of Epithelial Dysplasia?

A
  • “Drop” shaped rite ridges
  • Loss of orientation and polarization
  • Basilar hyperplasia
  • Keratin pearl formation
  • Loss of cell adhesion
49
Q

What are the cytologic features of epithelial dysplasia?

A
  • Dyskeratotic cells
  • Nuclear pleomorphism
  • Nuclear hyperchromatism
  • Increased & Abnormal mitoses
  • Increase nuclear/cytoplasmic ratio
  • Large, prominent nucleoli
50
Q

Erythroplakia..

A

91% of asymptomatic SCC have erythroplakic component! Low incidence. Clinical features”: homogenous or speckled

51
Q

What else can be on the DD for erythroplakia?

A

Mucositis, candidiasis, psoriasis, vascular lesions, and erosive lichen planus

52
Q

What is the least common type of immune cell?

A

Basophils

53
Q

How do we recognize pathogens?

A

PAMPS

54
Q

What are the 4 vascular changes of inflammation

A

Vasodilation
Increased permeability
Leukocytes margination
Exchange of fluid between blood vessels and ECM

55
Q

What is transduate, exudate, and edema?

A

Transduate: protein-poor infiltrate
Exudate: protein-rich infiltrate
Edema: net outflow of water and ions into EC,

**translate is protein poor cuz I have to transfer money. when I exit school I will be rich! **

56
Q

Mechanisms of Vascular Leakiness

A
  • Endothelial cell contraction: reversible. Most common. Short lived. Induced by histamine, bradykinin, leukotrienes, etc.
  • Direct injury: arterioles, capillaries, and venules. Toxins, burns, chemicals. Fast. May be long-lived.
  • Leukocyte-dependent injury: mostly venules, pulmonary capillaries, sites where leucocytes can adhere to endothelium and release ROS/proteolytic enzymes. Late response.
  • Increased transcytosis: venules. Intracellular channels are formed by fusion of uncoated vesicles. Induced by VEGF
57
Q

Acute inflammation - Cellular events

A
  1. Endothelial Activation - Upregulation of selecting and selection ligands.
  2. Leukocyte rolling - Selectin-mediated loose binding
  3. Firm adhesion - ICAM-1/ VCAM-1 mediated tight binding
  4. Transmigration - CD31 (PECAM-1) mediated
58
Q

Cytotoxic T lymphocytes need 3 signals! What are they?

A

Signal 1 Activation TCR, MHCII
Signal 2 Survival CD28 co-stimulatory molecule
Signal 3 Differentiation into specific type of T cell depending on the environment

After these 3 conditions are met –> T cell activation

59
Q

PD-1 expressed by T cells can engage ligand like PD-L1 from cancer cells or macrophages
PD-L1 inhibits acute and chronic pain by suppressing nociceptive neuron activity via PD-1

A

True

60
Q

CONCLUSIONS
-Immunotherapy offers promise to about 15-20% of patients with R/M HNSCC
-Mutations in cancer can be seen by the immune system, and many mutations usually lead to strong immune response.
-Some tumors with low mutation burden can also be seen by the immune system. Immunotherapy is not confined to high mutation burden cancers
-Cancer can develop adaptive resistance mechanism to immune effector cells.
-Immunotherapy usually needs to be combined with strategies to prime the immune system.
[For anti-PD1 NEED to prep and make the tumor Hot - have more T cell infiltration]

A

true

Neoplasia (3 decks)

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