Skin Cancer Flashcards
Why do basal cell carcinomas appear blue sometimes?
Its dervied from germinative keratinocytes from the basal layer
Where do squamous cell CA derive from?
These comes from the spinous layer from epidermal keratinocytes and thus are moer foten pink
Basal Cell carcinoma- ulcerated nodule with a pearly border and a lot of telangiectasias
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
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
What are the nonmelanoma skin cancers?
Basal cell and squamous cell carcinomas- very common
What are the main risk factors for BCC?
- UV exposure (chronic but intermittent)
- Fair complexion
- H/o sunburns (especially blistering)
- Family history
- Immunosuppression (but not as common as SCC)
Basal Cell Carcinomas can be very subtle and start as small papules before growing
How are basal cell carcinomas described?
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)
Subtypes of Basal Cell CA?
Nodular, Superficial, Pigmented, Cystic, Infiltrative, etc.
Look a likely different than nodular BCC because they just sit on the skin but still see telangiectasias
Pigmented BCC (pigment made by melanocytes but this is not a tumor of melanocytes)- more common in people with darker skin
T or F. BCC are more common in older patients
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
What is Basal Cell Nevus Syndrome (Gorlin Syndrome)?
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
How does PTCH work?
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)
Is metastasis in BCC common?
No, 0.5% BUT can be very locally aggressive and destructive (need to be removed)
What is Vismodegib approved for?
- Metastatic BCC
- recurrent disease
- Gorlin Syndrome patients
Step Note
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
What is this?
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
How do SCCs develop?
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
T or F. Sun induced SCC is not likely to metastasize
T. More common METs if on the lips or ears
Where do SCCs like to go to?
through lymph to lungs
How do SCCs progress?
- 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)
Normal skin with basket weave orthokeratosis
Can parakeratotis
Parakeratosis
Clinically: flat, scaly, and usually multiple on sun exposed areas of the body
Actinic keratosis
Invasive SCC
Invasive SCC (dont be fooled by the telangiectasias)
What are some genetic causes of SCCs?
no specific SCC oncogene or tumor suppressor has been ID’d but p53 mutations common
What are the main risks of developing SCC?
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
What is a common cause of SCC in women?
POST-RADIATION (just in general) but particularly in breast cancer
The risk of metastasis in CUTANEOUS SCC is related to what?
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
What are some situations with increased risk of METS in a SCC?
- actinic-induced on lip
- Marjolin’s ulcers (10-30%)
- Vulvar, penile HPV induced (30%)
Leukoplakia
METS to lymph and lungs
SCCs can be locally destructive as well
How are SCC treated?
Depends ond degree of progression
Actinic keratosis: topical therapy, cryotherapy
SCC in situ: topical some, excision
Invasive SCC: excision needed
