Pathogenesis of BCC SCC Flashcards Preview

DERM (18) Skin Growths > Pathogenesis of BCC SCC > Flashcards

Flashcards in Pathogenesis of BCC SCC Deck (32)
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1
Q

What is the main regulator of G1?

A

p53

2
Q

What are the 4 phases of cell cycle

A

G1, S, G2, M G–>growth S–> synthesize DNA M–> mitosis (prophase, metaphase, ananphase, teleophase)

3
Q

What is the resting phase?

A

G0

4
Q

What are the main proteins that promote cell division

A

Cyclin

5
Q

What type of protein is RB?

A

Tumor suppressor

6
Q

Which major protein stimulates G1–> S

A

E2-F

7
Q

What gene encodes p16

A

CDKN2A

8
Q

Do protooncogenes tend to act as dominant or recessive mutations?

A

Dominant. done through mutation of one allele or amplification (transformation, it gets moved to after the promotor region of a different gene.

9
Q

3 mechanisms of apoptosis

A

I. death promoting signals : TNF

II. Lack of growth factors: EGF (EGFR receptors work this way, no signal going through so cell death)

III. DNA damage: UV-induced DNA damage

all pathways increase caspases

10
Q

What is the major anti-apoptotic protein

A

BCL2

11
Q

What is the major pro-apoptotic protine

A

BAX

12
Q

Describe the SHH signaling

A

Smoothened is a cell surface protein, once it is activated it initiates downstream signaling. Patched is next to it and it is normally inhibiting smoothened. SH binds to patched and makes it remove its inhibition of smoothened. Smoothened then activates GLI which is a factor which increases transcription of GLI, PTCH (gene), BCL2

13
Q

Where does vismodegib or sonidegib act?

A

Inhibits activated smoothened. Resistance to this medication occurs with mutations of smoothened

14
Q

Why do vismodegib/sonidegib cause alopecia?

A

The transition between hair cycles is controlled by SHH signaling

15
Q

What type of UV radiation leads to BCC

A

Intermittentn or intense UV exposure (# of sunburns when younger)

16
Q

BCC is a tumor of what skin unit?

A

Pilosebaceous unit –> hence seborrheic distribution

17
Q

Is there a precancerous lesion to BCC

A

No, there are no precursor lesions

18
Q

Why do BCC’s rarely metastasize

A

They are highly dependent on stromal tissues

19
Q

What chromosome is PTCH located on?

A

9 (9 is inverse of P)

20
Q

What chromosome is p53 located on?

A

Chr 17

21
Q

What is the primary risk factor for SCC?

A

Cumulative lifetime UV radiation

22
Q

What are the 3 major areas that are higher risk of SCC metastasis?

A

Lips, genitals, ears (mucous membrane)

23
Q

Clinical risk factors for SCC metastasis?

A

Tumor >2cm, poorly differentiated, invasion of subcutaneous fat, perineural invasion, immunosuppression

24
Q

Verrucous SCC is induced by what HPV types?

A

HPV-6, 11

25
Q

What genes are usually mutated in SCC?

A

p53 m/c TSG mutation/ dysregulated

26
Q

What is the increase in risk of skin cancer for those with xeroderma pigmentosum?

A

100x increased risk of skin cancer

27
Q

What is the mutation in xeroderma pigmentosum?

A

Defect in nucelotide excision repair (NER) gene

28
Q

What is the mutation for li-Fraumeni syndrome?

A

AD, germline mutation with p53 Not much skin cancers

29
Q

What is the mutation in basal cell nevus syndrome?

A

AD, gemrline PTCH gene mutaiton.

30
Q

What occurs in basal cell nevus syndrome?

A

Odontogenic keratocysts, palmoplantar pits, calcification of falx cerebri, MEDULLOBLASTOMAS, meningiomas, cardiac and ovarian fibromas

31
Q

What test should you consider with new dx of Gorlins?

A

MRI for medulloblastomas, also EKG for cardiac fibroma

32
Q

What is the mechanism of keratinocyte carcinoma related to BRAF inhibitor treatment?

A

RAS mutations/activation of the MAPK pathway