Skin Cancer

Question 1

Why do basal cell carcinomas appear blue sometimes?

Answer 1

Its dervied from germinative keratinocytes from the basal layer

Question 2

Where do squamous cell CA derive from?

Answer 2

These comes from the spinous layer from epidermal keratinocytes and thus are moer foten pink

Question 3

Answer 3

Basal Cell carcinoma- ulcerated nodule with a pearly border and a lot of telangiectasias

Question 4

Answer 4

PTCH- tumor suppressor gene (mutations common in a basal cell carcinoma)

Classic histology: middle- blue, nodules in the dermis that have clefting and a palisyde of nuclei around edge

Question 5

Answer 5

Location on the ear

SCC tend not to metastasize (but it can; risk factors: immunocompromised, being HPV mediated)

the ears and lips are probably the places most common for squamous cell carcinoma because skin is thin and vascular

Question 6

What are the nonmelanoma skin cancers?

Answer 6

Basal cell and squamous cell carcinomas- very common

Question 7

What are the main risk factors for BCC?

Answer 7

• UV exposure (chronic but intermittent)
• Fair complexion
• H/o sunburns (especially blistering)
• Family history
• Immunosuppression (but not as common as SCC)

Question 8

Basal Cell Carcinomas can be very subtle and start as small papules before growing

Answer 8

Question 9

Question 10

How are basal cell carcinomas described?

Answer 10

These are basophilic hyperchromatic cells that form nodules, often extending from the surface epidermis with peripheral cells forming a “picket-fence” palisade and showing retraction/clefting from the dermis

Note that there are different patterns (this describes nodular)

Question 11

Subtypes of Basal Cell CA?

Answer 11

Nodular, Superficial, Pigmented, Cystic, Infiltrative, etc.

Question 12

Look a likely different than nodular BCC because they just sit on the skin but still see telangiectasias

Question 13

Pigmented BCC (pigment made by melanocytes but this is not a tumor of melanocytes)- more common in people with darker skin

Answer 13

Question 14

T or F. BCC are more common in older patients

Answer 14

T. Only about 20% of BCC present before the age 50, and it rarely before 25. Note that the presence of one makes it more likely that youll have more

Question 15

What is Basal Cell Nevus Syndrome (Gorlin Syndrome)?

Answer 15

AD disease caused by mutation of PTCH1 (tumor suppressor gene) characterized by BBCs in 20s, jaw cysts, MSK defects, and puts one at an icnreased risk of medulloblastoma or fibrosarcoma

Question 16

How does PTCH work?

Answer 16

part of SHH pathway that prevents SHH binding from SMO (which upregulates basal cell proliferation)

Drug: Vismodegib is aggressive BCC (causes many GI problems so not used lightly)

Question 17

Is metastasis in BCC common?

Answer 17

No, 0.5% BUT can be very locally aggressive and destructive (need to be removed)

Question 18

What is Vismodegib approved for?

Answer 18

• Metastatic BCC
• recurrent disease
• Gorlin Syndrome patients

Question 19

Step Note

Answer 19

BCC are more common on the upper face and

SCC are more common on the lower face and especially the lips (may or may not be true)- due to chronic sun exposure

Question 20

What is this?

Answer 20

SSC- more variable in its presentation that BCC but consistently makes more keratin and it derived from the upper layers of the epidermis and the extra-production of keraitn tends to make them more commonly crusted at the top

Question 21

How do SCCs develop?

Answer 21

Sunlight is very important in the initation- UV light causes DNA dimerization and sometimes they cannot be contained and give rise to abnormal clones (commonly with a p53 mutation) and as they proliferate can get new mutations (non-specific)

SCC of the epidermis is called in-situ and when it break through the basemnet membrane is called invasive

Question 22

T or F. Sun induced SCC is not likely to metastasize

Answer 22

T. More common METs if on the lips or ears

Question 23

Where do SCCs like to go to?

Answer 23

through lymph to lungs

Question 24

How do SCCs progress?

Answer 24

• minimal atypica (Actinic keratosis)
• Full thickness epidermal atypia confined above the basement membrane (SCC in situ) (aka Bowen’s disease or Erythroplasia of Queyrat- if develops on glans penis (HPV induced))
• Invasive SCC (well, moderately, or poorly differentiated)

Question 25

Normal skin with basket weave orthokeratosis

Answer 25

Can parakeratotis

Question 26

Parakeratosis

Clinically: flat, scaly, and usually multiple on sun exposed areas of the body

Answer 26

Question 27

Actinic keratosis

Answer 27

Question 28

Answer 28

Question 29

Answer 29

Question 30

Invasive SCC

Answer 30

Invasive SCC (dont be fooled by the telangiectasias)

Question 31

What are some genetic causes of SCCs?

Answer 31

no specific SCC oncogene or tumor suppressor has been ID’d but p53 mutations common

Question 32

What are the main risks of developing SCC?

Answer 32

Chronic UV exposure

HPV (types 16, 18, 31, and 35)

Immunosuppression

Arsenic exposure

Chronic inflammation (e..g osteomyelitis with draining sinus dract)

Burn scars

Leukoplakia

Question 33

What is a common cause of SCC in women?

Answer 33

POST-RADIATION (just in general) but particularly in breast cancer

Question 34

The risk of metastasis in CUTANEOUS SCC is related to what?

Answer 34

size of tumor, depth of invasion into dermis, anatomic site, and host immune status:

-larger than 2cm in diameter or deeper than 4mm in depth and higher risk on lips and ears

Question 35

What are some situations with increased risk of METS in a SCC?

Answer 35

• actinic-induced on lip
• Marjolin’s ulcers (10-30%)
• Vulvar, penile HPV induced (30%)

Leukoplakia

METS to lymph and lungs

Question 36

SCCs can be locally destructive as well

Answer 36

Question 37

Answer 37

Question 38

Answer 38

Question 39

How are SCC treated?

Answer 39

Depends ond degree of progression

Actinic keratosis: topical therapy, cryotherapy

SCC in situ: topical some, excision

Invasive SCC: excision needed