Derm: Squamous Cell Carcinoma: Free MSRA Podcast

⚕️ FREE MSRA PODCAST – Squamous Cell Carcinoma (SCC)
🎧 A high-yield breakdown of this common but potentially serious skin cancer – essential for MSRA prep and clinical practice.

🧠 Key Learning Points

📌 Definition
• SCC is a malignant tumour of squamous cells in the epidermis.
• It is the second most common non-melanoma skin cancer and has metastatic potential.

📌 Causes & Risk Factors
• Chronic UV radiation exposure ☀️
• Fair skin, older age, male gender
• Immunosuppression (e.g. transplant patients, HIV)
• Chronic inflammation (old burns, scars, ulcers)
• Exposure to arsenic or past radiotherapy
• Premalignant lesions (actinic keratosis, Bowen’s disease)
• Genetic conditions (xeroderma pigmentosum, albinism)
💡 Mnemonic: "SUN BURN" – Sun, Ulcers, Neoplasia in situ (Bowen's), Burns, UV, Radiotherapy, Nevus (genetic)

📌 Pathophysiology
• UV-induced DNA mutations → dysregulated squamous cell growth
• Tumour invades dermis, then lymphatics or blood → local/distant spread
• Risk factors amplify mutation accumulation

📌 Symptoms
• Firm, red nodule or scaly ulcer that won’t heal
• Can bleed easily, ulcerate or crust over
• Typically found on sun-exposed areas: face, ears, lips, scalp, hands
• May arise from actinic keratosis or Bowen’s disease

📌 Differential Diagnosis
• Keratoacanthoma
• Basal cell carcinoma (pearly appearance)
• Amelanotic melanoma
• Actinic keratosis
• Pyogenic granuloma
• Warts or chronic verrucae (esp. periungual)

📌 Diagnosis
• Clinical suspicion + histological confirmation via biopsy
• Excisional or punch biopsy preferred
• Imaging (CT/MRI) if deep invasion suspected
• Always refer suspected cases via 2-week wait pathway

📌 Management
• Surgical excision with clear margins (4–6mm depending on size)
• Mohs surgery for high-risk or cosmetically sensitive areas
• Cryotherapy or curettage for superficial lesions
• Radiotherapy if surgery contraindicated
• Topical 5-FU or Imiquimod for SCC in situ (Bowen’s disease)
• MDT involvement for advanced or recurrent disease

📌 Complications
• Local invasion (e.g. lip, eye, cartilage, bone)
• Perineural spread (causing pain or numbness)
• Lymphatic or haematogenous metastasis (lungs, liver, brain)
• Cosmetic disfigurement, post-surgical scarring

📌 Prognosis
• Excellent with early diagnosis and complete excision
• Poorer outcomes if: lesion >20mm, depth >2–4mm, poor differentiation, perineural invasion, immunosuppressed, lip/ear site
• Most recurrences within first 2 years – regular follow-up vital

📎 More MSRA Resources for Squamous Cell Carcinoma
📝 Revision Notes: https://www.passthemsra.com/topic/squamous-cell-carcinoma-revision-notes/
🧠 Flashcards: https://www.passthemsra.com/topic/squamous-cell-carcinoma-flashcards/
💬 Accordion Q&A Notes: https://www.passthemsra.com/topic/squamous-cell-carcinoma-accordion-qa-notes/
🚀 Rapid Quiz: https://www.passthemsra.com/topic/squamous-cell-carcinoma-rapid-quiz/
🎓 Full Course: https://www.passthemsra.com/courses/dermatology-for-the-msra/

#MSRA #MSRARevision #MSRATextbook #MSRAQuiz #MSRAQuestionBank #MSRAFlashcards #MSRAQ&ANotes #MSRAAccordions #MultiSpecialtyRecruitmentAssessment #MSRAOnlineRevision #MSRARevisionWebsite #SquamousCellCarcinoma

Episode Transcript

(00:00):
Welcome to the Deep dive. Today we're taking a closer look
at squamous cell carcinoma SEC. We've got some really focused
revision notes here. You know, the kind aimed at high
yield learning thinking. Maybe MSRA prep.
Yeah, exactly. So the plan is to break down the
key info, what it is, why it happens, what it looks like, the

(00:20):
absolute essentials. Right, our mission then simplify
SEC. Make it memorable.
Highlight those exam friendly bits and practical points too.
Let's. Do it.
We'll just go through the main areas, connect the dots so you
get the big picture. Perfect.
So let's start right at the beginning.
What is squamous cell carcinoma exactly?
OK, so Simply put, it's a type of skin cancer.

(00:42):
It starts in the squamous cells.Those are the ones on the
surface. Yeah, the flat sort of scale,
like cells making up the outer layer of your skin, the
epidermis, and it's. Common, but not the most common.
That's a key point, definitely. It's the second most common skin
cancer overall, specifically thesecond most common non Melanoma
skin cancer. And location wise, yeah, mostly

(01:02):
sun exposed areas, head, neck, arms, hands.
But, and this is important, it can also show up in places like
chronic wounds, old scars, areasof long term inflammation.
OK, didn't know that. Yeah, it comes from those
keratinizing cells in the epidermis.
And yes, it is malignant. It can spread, but you know,
often it's more locally invasive.
And the good news is it's often highly curable, especially if

(01:25):
you catch it early. OK, so second most common.
Watch out for odd locations likescars, but generally curable
early on. Yeah, that leads us to wow, how
common is it, the epidemiology? Right.
Well, skin cancers in general are super common, particularly
non Melanoma types in the UKSCC makes up about maybe 23% of

(01:46):
those non Melanoma skin cancers.So significant.
And are we seeing more of it? Unfortunately, yes, the
incidence is rising. Mostly diagnosed in people over
50, but you do see it in youngerpeople too.
And geography matters, I guess. Sun exposure.
Hugely, it's way more common in fair skinned people and the
rates are really high in places with lots of sun like Australia,
especially among Caucasian populations.

(02:08):
OK Oh and it's generally more common in men.
Probably linked historically anyway.
Maybe more outdoor work or recreation so higher UV exposure
over a lifetime. That makes sense.
OK, now really big question. Why does it happen?
Aetiology and risk factors. If you remember one thing, it's
UV radiation. Ultraviolet light from the sun.

(02:29):
From the sun, Yeah. Or tanning beds.
That's the number one cause globally, right?
Basically, the UV damages the DNA in the skin cells over time.
If that damage isn't repaired properly, mutations build up.
And that leads to cancer. Exactly leads to uncontrolled
cell growth, which is the tumour.
Is it only UV though? Are there other?
Things UV is the big one but definitely not the only factor.

(02:50):
There are others to know things like exposure to certain
chemicals, arsenic for example, those chronic wounds or burn
scars we mentioned a weakened immune system is a big one
right? And having had radiation therapy
in the past to an area. So key risk factors to list off
fair skin, history of bad sunburns, using tanning beds,
older age, being male. Any other really crucial ones?

(03:11):
Maybe less obvious ones for exams.
Yeah, good point. Immunosuppression.
Think organ transplant, patientson anti rejection meds, people
with HIV, AIDS, certain autoimmune conditions.
Their risk is much higher and the SEC's can be more
aggressive. OK, immunosuppression is key.
Definitely also chronic inflammation like an old scars
or chronic ulcers, some rare genetic conditions like

(03:33):
Xeroderma pigmentosum where DNA repair is faulty or albinism.
Even certain types of HPV, the human papilloma virus, are
linked to SEC's in specific sites, often not sun exposed
ones. And what about those things that
aren't quite cancer yet, but could become it?
Yes, the pre malignant conditions very important.
Actinic keratosis, often called a KS or solar keratosis and

(03:57):
Bowen's disease. What are they?
A KS are usually small rough scaly patches on sun exposed
skin. Often people have lots of them.
Boa's diseases technically SEC in situ, meaning it's confined
to the epidermis. It usually looks like a single
larger persistent red Staley patch.
So finding and treating those can prevent actual SEC.
Exactly. They represent that abnormal

(04:17):
growth stage before it becomes invasive.
So yeah, UV is the main story. But definitely remember
immunosuppression, chronic inflammation, and those
precancerous lesions like AK's and Bowens.
OK, got it. So UV damages, DNA, risk
factors, make you more susceptible.
How does that actually turn intoa tumour at the cellular level?
The Pathophysiology. Right, keeping it

(04:40):
straightforward, it starts with those genetic mutations in the
squamous cells, mostly UV driven.
These mutations mess up the normal controls on cell growth
and division. So they just start multiplying.
Pretty much, yeah. Uncontrolled proliferation.
They divide when they shouldn't,don't die when they should.
This builds up into a mass, the tumour initially just in the
epidermis. And then it invades.

(05:00):
That's the next step. If it progresses, it can
breakthrough the sort of floor of the epidermis, the basement
membrane, and get into the deeper layer, the dermis that's
invasion. From there, it could potentially
get into lymphatic vessels or blood vessels, and that's how it
can spread to nearby lymph nodesor much less commonly for skin
SEC to distant parts of the body.

(05:20):
But it all starts with that initial uncontrolled growth from
DNA damage, right? Makes sense.
So moving to what we actually see, what does SEC look like?
You mentioned it can vary a lot.It really can be a bit of
chameleon sometimes, which is why you need to be suspicious,
but typical signs include a lesion that just won't go away.
It might be scaly or crusted over.

(05:41):
And bleeding is a bad sign. Yeah, big red flag is if it
bleeds easily, maybe with minor trauma, or if it ulcerates,
breaks open and forms a sore that doesn't heal properly.
Can you describe the different ways it might look?
Sure, sometimes it's a firm reddish lump or nodule, other
times it's flatter, more like a persistent red patch, maybe
slightly raised. It can also look quite rough and

(06:04):
raised, almost like a wart. Often not initially, but it can
become tender or painful as it grows or if it gets infected.
And remember the location thinkssun exposed sites face, ears,
lips, back of hands, scalp and boldman.
The classic description is oftenan indurated lesion, meaning it
feels firm or hard to the patch that's crusted or ulcerated.

(06:26):
OK, let's try a quick mental picture.
Say an older guy, maybe worked outdoors a lot, has this spot on
the top of his ear, looks scabby, hasn't healed for ages,
feels kind of hard. Is that classic SEC territory?
Absolutely. That's a perfect mini vignette.
Persistent, non healing, firm orindurated lesions, sun exposed
site like the ear SEC should be very high on your list of

(06:47):
possibilities there. Definitely warrants
investigation. Right.
And Speaking of possibilities, what else could look like SEC?
What are the main differential diagnosis we need to think
about? This sounds crucial.
It is because things can look similar.
Top of the list maybe is Keratoacanthoma or Kaa.
Why is that tricky? Because it often looks exactly
like an SEC, grows rapidly, often Dome shaped with a central

(07:08):
crusty bit. Even under the microscope it can
be hard to tell apart sometimes.K as can sometimes resolve on
their own, but you can't rely onthat, so you generally treat
them like an SEC until proven otherwise.
OK KA definite look alike. What else?
Well, basal cell carcinoma or BCC, that's the most common skin
cancer usually looks different, more pearly, maybe with little

(07:29):
blood vessels. But some types like nodular or
superficial BCC's could potentially be confused.
Malignant Melanoma definitely need to consider that,
especially the immelanotic type.The ones without colour.
Exactly, they can just be a pinkor red lump or patch.
So they could mimic an SCC or even a pyogenic granuloma.

(07:49):
Then there's the precancerous actinic keratosis we mentioned.
Sometimes it's hard to tell if one has crossed the line into
invasive SEC just by looking. Any benign things that can cause
confusion? Yeah, sometimes an irritated
seboroic keratosis, those commonwarty looking growths older
people get, can look inflamed. Pyogenic granuloma, that's a
benign vascular thing that growsquickly and bleeds easily, can

(08:11):
look alarming. OK.
And one specific one mentioned is around the nails periungual
SEC. It can look like a stubborn wart
or verruca that just won't clearup.
So the bottom line is, if a lesion looks suspicious,
especially in a high risk personor site, keep that list of
differentials in mind. Don't just assume.
Right. Suspicion is key.

(08:32):
So you suspect it. How do you confirm it?
What are the investigations? OK, so clinical judgement gets
you started, but confirmation always comes down to Histology.
Looking at the tissue biopsy exactly, the key investigation
is a skin biopsy. It might be a small punch biopsy
or an incisional biopsy if it's large, taking a representative
slice. Or ideally, if the lesion is

(08:52):
small enough and you're pretty confident, an excisional biopsy
where you try to remove the whole thing first time.
And the results of that biopsy dictate what happens next.
Absolutely. The Histology report tells you
if it is SCC, how deep it goes, how abnormal the cells look, the
differentiation based on that, and the size and location.
You might need further surgery to get clear margins.

(09:15):
Clear margins. Yeah, removing a safety border
of normal looking skin around the tumour site.
The standard margins mentioned are often 4 millimetres for
tumours less than 20 millimetresacross and maybe 6 millimetre
for larger ones. That's a high yield detail.
OK, 4 millimetre or 6 millimetremargins, What about imaging?
Imaging like CT or MRI isn't routine for most small SCCS, but

(09:37):
you'd use it if you were worriedthe cancer had gone deep, maybe
into bone or cartilage or spreadalong nerves.
Especially important for head and mech SCCS.
And if lymph nodes nearby feel enlarged, they'd need
investigating too. Maybe with ultrasound and
biopsy? The referral pathway.
Crucial point, any suspected SEC, especially if it has
concerning features or there's diagnostic uncertainty, needs an

(09:58):
urgent cancer pathway referral, usually the two week wait
pathway in the UK. Prompt assessment makes a huge
difference. Oh and the notes also mentioned
TNM staging. Just remember T is for tumour
size and invasion, N is for regional lymph node involvement,
and M is for metastasis, meaningspread to distant sites.
It's the standard way to classify how advanced the cancer

(10:19):
is. OK, so biopsy confirms staging,
assesses spread, urgent referralis key.
Got it. Once it's confirmed, how do we
treat IT management options? Right.
For most typical localised SCC's, surgical excision is the
main treatment, the gold standard.
Cut it out with those clear margins.
That's usually curative. But there are other ways.

(10:40):
Yes, definitely depends on the situation, the tumour
characteristics, patient factors.
Options include things like cryotherapy, freezing it off.
Like rewards. Similar idea yeah, but usually
for very superficial or small lesions or maybe pre cancers.
Curetage and cautery is another option, scraping it away and
sealing the base with heat again.
For smaller shallower ones, radiation therapy is important

(11:01):
too. It can be used as the main
treatment if surgery isn't suitable, or maybe afterwards if
there's a high risk of recurrence or if it has spread
to lymph nodes. What about creams?
Topical treatments creams like 5Florisil, 5 FU or Emiki Mod are
mainly used for the precancerousat clinic keratosis or for SEC
and situ Bowen's disease, not usually for invasive SEC itself.

(11:23):
And for more difficult cases like on the face or if it comes
back. That's where Moe's surgery comes
in, Moe's micrographic surgery. It's a specialised technique
used for high risk SEC's ones incosmetically sensitive areas
like the nose or eyelids, or forrecurrent tumours.
How does that work? Basically they remove the tumour
layer by layer and check each layer under the microscope

(11:45):
immediately. They keep going just until all
the cancer is gone, which sparesas much healthy tissue as
possible. Very precise.
Wow. OK.
And for really advanced SEC thathas spread widely, systemic
treatments like chemotherapy or newer immunotherapy drugs like
semaplimab which was mentioned might be used.
So treatment sounds very personalised.
It really is and often, especially for complex cases, it

(12:06):
involves A multidisciplinary team and MDT, dermatologists,
surgeons, oncologists, pathologists, all discussing the
best approach. And importantly, after
treatment, regular follow up is essential to check for
recurrence or new skin cancers, plus reinforcing sun safety
advice. Right.
Makes sense. So with all these options,
what's the general outlook, the prognosis for SEC?

(12:27):
It varies a lot and those prognostic factors we touched on
earlier are key here for your standard early stage SEC on the
skin caught and removed properly, the prognosis is
generally excellent. Very high cure rates.
That's reassuring. When does it become more
worrying? It's when the tumour has those
high higher risk features. The notes lay these out nicely.
Think bigger size, over 20 millimetres is a marker.

(12:50):
Deeper invasion more than two millimetres deep, especially
over 4 millimetre. Poor differentiation meaning the
cancer cells look very abnormal under the microscope.
If it's invaded nerves, that's perineural invasion.
If the patient is immunosuppressed, certain
locations are higher risk too, like the ear or the lip or SCC
arising in an old scar or chronic wound.
So those things increase the risk of it coming back or

(13:12):
spreading. Exactly.
They increase the risk of local recurrence, spread to lymph
nodes, and less commonly but more seriously distant
metastasis. And if it does, spread far away.
That changes the picture significantly.
While distant spread from a typical skin SEC isn't that
common overall, maybe less than 5%.
If it does happen, the prognosisis much poorer.

(13:34):
The five year survival rate can drop quite dramatically, down to
maybe 2540%. Wow.
Yeah, and most recurrences or metastases tend to happen within
the first few years after treatment, particularly the
first two years, hence the need for follow up.
So catching it early and knowingthose risk factors for
recurrence is really critical, yeah.
What are the main things that can go wrong if SCC isn't

(13:55):
treated well or if it's aggressive?
The complications? Well, the complications really
follow from its potential to grow and spread locally.
It can destroy tissue. If it's near the eye, nose,
mouth. It can invade those structures
causing functional problems, issues with sight, breathing,
eating. Nerve invasion can cause pain or
numbness. Then there's spread to lymph
nodes that requires more treatment like surgery to remove

(14:18):
the nodes or radiation, and it definitely worsens the overall
prognosis. And then the most serious
complication is distant metastasis, spreading to organs
like the lungs, liver or brain, which we just discussed has a
poor outlook. And cosmetically, it can be an
issue too. Absolutely.
Depending on the size and location, the tumour itself can

(14:39):
be disfiguring and the treatment, especially surgery,
can leave scars or defects, particularly on the face or
hands. So again, it all comes back to
early detection and effective treatment to minimise all these
potential problems. That's quite a journey from
potentially just a little rough patch to something with
significant implications if it'snot managed properly.
It really is understanding the whole spectrum, the risks, the

(15:00):
appearance, the need for biopsy,the treatment options and what
predicts the outcome. That's really the core of
managing SEC effectively. And seeing how those factors,
size, depth, immune status can dramatically shift the prognosis
really drives home why understanding these details is
so important, especially for exams, but just for general
knowledge too. Exactly.
It's about building that mental framework so you can recognise

(15:23):
it, know the next steps and understand the potential
outcomes. For more free MSRA revision
resources, definitely check out free m-sra.com and for the full
Premium Revision Toolkit, head over to pass them sra.com.
And maybe just a final thought to leave you with, given that UV
exposure is the main driver for the vast majority of these
cancers and we know how to protect ourselves, sun avoidance

(15:45):
clothing, high SBF, sunscreen, it does make you wonder, doesn't
it? How do we better bridge that gap
between knowing the risks and actually changing long term
behaviour on a large scale to prevent conditions like SCC?
Something to think about.