Neoplasia I - Nichols Flashcards

1
Q

Define desmoplasia.

A

formation of abundant fibrous stroma by some carcinomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is carcinoma in situ?

A

tissue with all the cytologic (individual cel) features of malignancy without visible invasion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What differences would you see between anaplastic and dysplastic cells under a microscope? What about malignant cells?

A

anaplasia - lack of visible differentiation of cells. Larger in size, larger nuclei and smaller cytoplasms, varying size and shape, angulated shape, hyperchromatism, clumped chromatin, mistoses and nuclei.

Dysplasia - disordered growth and varying size. Will look more varied than anaplasia and have different cell types.
Malignant - invasive, usually extending through basement membranes. Lack of differentiation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the 5 most common causes of cancer in the US in order?

A
  1. smoking
  2. obesity
  3. alcohol
  4. diet
  5. HPV
  6. UV light
  7. asbestos and other carcinogens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the 4 most common causes of cancer death in the US in order?

A
  1. Lung
    2-3. Breast (women) and Prostate (men)
  2. Colon
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the 9 most common types of cancer caused by smoking?

A
  1. over 90% in lungs
  2. mouth
  3. pharynx
  4. larynx
  5. esophagus
  6. stomach
  7. pancreas
  8. kidneys
  9. bladder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the 6 hallmarks of cancer?

A
  1. self-sufficiency in growth signals
  2. insensitivity to suppression signals
  3. evasion of apoptosis
  4. sustained angiogenesis
  5. limitless replicative potential
  6. ability to invade tissue and metastisize
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the RB tumor suppressor gene?

A

Involved in retinoblastoma. Normally prevents cell proliferation by binding to E2F transcription factor when it is hypophosphorylated. When Rb is phosphorylated by cyclinD-CDK4 and cyclinE-CDK2 complexes it releases E2F and E2F is activated, stimulating cell proliferation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the APC tumor suppressor gene?

A

tumor suppressor gene that controls intestinal stem cell proliferation by WNT signaling. Breaks down beta-catenin so it does not bind to transcription factor TCF, which activates many genes that promote cell proliferation. Mutations in APC are present in 100% of familial colon cancers.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the p53 tumor suppressor gene?

A

tumor suppressor gene. prevents propagation of genetically damaged DNA, arresting the cell cycle to enable DNA repair and initiating apoptosis when repair is impossible. Half life of only 20 minutes and is degenerated by ubiquitin. Is destroyed by MDM2.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the NF-1 tumor suppressor gene?

A

suppressor genes in neurofibromatosis. activates a GTPase, creating GDP that binds to cell membrane RAS protein, inactivating the RAS so it does not transduce growth factors for proliferation. Mutations will cause uncontrolled growth factor production.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the Von Hippel Lindau tumor suppressor gene?

A

(VHL). tumor suppresssor. Causes ubiquitination and degradation of HIF-1 (hypoxia inducible transcription factor-1) that would cause increased PDGF and VEGF if left around. Mutations in it cause kidney cancer, pheochromacytoma (adrenal medullary tumor), retinal angioma and other tumors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the features of the HER2 oncogene?

A

is an EGFR receptor that is commonly overexpressed in breast cancers.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the features of the K-RAS oncogene?

A

oncogene that codes for a GTPase in the cytoplasm on the inner side of the cell membrane bound to the EGFR. It carries out signal transduction from cytoplasm to nucleus when EGFR binds growth factors, causing the cell to proliferate. When EGFR binds, it stimulates K-RAS to make more GTPase to convert the GTP to GDP. High GTP levels cause unrestricted proliferation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is a teratoma?

A

a mixed germ cell tumor. Has componenets of more than one germ cell layer, usually all three (ectoderm, mesoderm and endoderm). Can be benign or malignant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is a hamartoma?

A

mass of mature but disorganized tissue indigenous to its site and a is a developmental anomaly.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is a choristoma?

A

ectopic rest or mass of normal tissue present outside its normal site. A developmental anomaly.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is Li-Fraumeni syndrome?

A

defect in p53 gene.

19
Q

What is xeroderma pigmentosum?

A

defect in nucleotide excision repair causes inability to repair damage from UV rays in sunlight. The affected will develop multiple basal cell carcinomas and other skin cancers with even minimal exposure

20
Q

What is ataxia-telangiectasia?

A

Defect in ATM gene, which repairs double stranded DNA breaks. Results in ataxia and telangiectasia (small dilated blood vessels)

21
Q

What do BRCA mutations cause?

A

predisposition to breast cancer

22
Q

Can neoplasms ever revert back to becoming non-autonomous after it has started replicating independent of growth controls?

A

No. Neoplasms can halt for a while, but they never truly stop being autonomous after making the change.

23
Q

What are the gross differences between benign and malignant tumors?

A

Benign have cohesive local growth, and commonly surrounded by fibrous capsule.

Malignant are progressively invasive with their local growths and commonly destroy surrounding tissue.

24
Q

What are sarcomas derived from?

A

mesenchyme - embryonic tissue that gives rise to connective tissues like bone, cartilage and vasculature

25
Q

What are the 3 patterns of metastatic spread? What types of cancers are common for each method?

A
  1. lymphatic (to lymph nodes) - carcinomas
  2. hematogenous (to lung or liver) - sarcomas
  3. seeding (of body cavities) - ovarian carcinoma
26
Q

What is a polyp?

A

a macroscopic projection above a mucosal or epidermal surface.

27
Q

What is a pedunculated polyp?

A

one on a stalk

28
Q

What is a sessile polyp?

A

flat, plateau-like polyp with no stalk

29
Q

What is adenoma?

A

benign epithelial neoplasm forming glands or derived from glands

30
Q

What is anaplasia?

A

lack of visible differentiation of malignant tumor cells, making them appear unspecialized. Larger than differentiated cells, higher nuclear:cytoplasm ratio, vary in size and shape, hyperchromatism.

31
Q

What is acquired dysplasia?

A

disordered growth that is typically premalignant. Can be reversible.

32
Q

What is MDM2?

A

a protein that destroys p53 and gives tumors resistance to it. Also causes resistance to chemo and radiation therapy.

33
Q

What is PTEN?

A

important in cancers of the endometrium and brain.

34
Q

What role does TGF-beta play in cancer?

A

it is a cell proliferation inhibitor. mutations in it are common in pancreatic carcinomas and many other tumors.

35
Q

What is WT-1?

A

plays a role in Wilms tumor

36
Q

What are cadherins?

A

important in carcinomas of esophagus, colon and other sites

37
Q

What is KLF6?

A

important in prostate cancers

38
Q

What effect does hypophosphorylation have on Rb gene?

A

when it is not very phosphorylated, it prevents cell proliferation by binding to transcription factor E2F.

When it is phosphorylated by cyclins, it releases E2F and cells proliferate

39
Q

What would a mutation in L-MYC likely cause?

A

some small cell lung cancer

40
Q

What would a mutation in C-MYC likely cause?

A

Brukitt lymphoma.

41
Q

What would amutation in K-RAS likely cause?

A

some colon, lung, pancreas tumors.

42
Q

What would a mutation in HER2 likely cause?

A

breast cancer

43
Q

What test is used to diagnose HER2 overexpression for breast cancer?

A

FISH.

44
Q

Will EGFR blocking therapy be effective for K-RAS mutations? For HER2 mutations?

A

EGFR blockers are not effective for K-RAS mutations because K-RAS is downstream from EGFR and if it is mutated, blocking something upstream from it won’t matter.

HER2, however, will be affected by EGFR blockers and it is a useful therapy. Drug is cetuximab.