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Case Number : Case 2647 - 28 August 2020 Posted By: Dr. Richard Carr

Please read the clinical history and view the images by clicking on them before you proffer your diagnosis.
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M80. Horn. ?AK ?SCC

Edited by Admin_Dermpath


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Richard Logan

Posted

Cutaneous horn arising from acantholytic Bowen's disease.

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Eman El-Nabarawy

Posted

Follicular SCC, small in situ lesion.

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Acantholytic and mucin producing squamous cell .atypical lesion, KA-like and infiltrative...it should be a SCC, follicular variant, as Eman said. 

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Krishnakumar subramanian

Posted

Carr, R. A., Taibjee, S. M., Turnbull, N., & Attili, S. (2014). Follicular squamous cell carcinoma is an under-recognised common skin tumour. Diagnostic Histopathology, 20(7), 289–296. doi:10.1016/j.mpdhp.2014.05.003 

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Krishnakumar subramanian

Posted

i read this article and it is too good

Thanks a lot for posting this case sir

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Dr. Richard Carr

Posted

Kind words indeed. Sadly when we submitted our series of 103 cases to the Am. J. Dermatopathology the reviewer did not agree with our hypophesis and rejected our paper (one that took me over 5 years to complete after collecting the data meticulously and many re-writes to make it close to perfect). I suppose it took a few generations to learn the world was not flat too! Hopefully the next journal reviewers will view it in a different light. Some immunostains & EVG on the above example to follow.

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Richard Logan

Posted

Richard, can you help me here?  What is it that tips this lesion over from "Bowen's disease" into a lesion which presumably has metastatic potential?  Is it the morphology of the expansile lobules at the base of the lesion, or a combination of several features which I clearly haven't appreciated?

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Dr. Richard Carr

Posted

Okay this I called "follicular" squamous cell carcinoma, the bulk of the lesion has entirely circumscript and rounded pushing only borders and I am sure would have minimal potential for metastasis. Having said that there are deep pushing downgrowths and we can see in the third image (2nd down on the left) the pushing borders focally give way to budding pattern that in my (subjective) opinion favours an invasive lesion and the EVG highlights the budding borders and there is a tiny focus of collagen entrapment (arrow). In MDM discussion of such a case I would suggest a low risk for metastasis but perhaps not the zero rate that I'd expect with a lesion with completely circumscribed borders only. Regarding the "follicular" designation I think most SCC arise from the hair follicle and in particular many "horns" are follicular actinic or follicular bowenoid actinic kertoses. In those cases you see the compact parakeratosis emanating from the pits as opposed to the crests. I presume follicular keratin is by it's nature more compact and horn forming after all I presume animal horns are modified hair follicles. Note the horn in this case on the low power comprising the highly compact parakeratin emanating from the pits of the lesion. The other diagnostic criteria are circumscrpt connections with the epidermis at the sites of follicular infundibular (images 1 & 2), often lobulated profile with subtle nuclear palisading (image 4). Abrupt tricholemmal keratinisation in the base with rather distinictive squamous morules and often central glassy keratincytes resembling KA. A common clue is the presence of central acantholytic mucin pools (beautifully seen in this case) attracted to the infundibular component of the lesion (similar to follicular mucinosis of mycosis fungoides). The latter finding was previously undescribed in the literature and is a helpul clue that a lesion has infundiublar differentiation and may be seen in other tumours including seborrhoeic keratosis/inverted follicular keratosis and tricholemmoma. The upper parts of the lesion often resemble closely inverted follicular keratosis and this differential may be highly challenging although you will see a mutant or aberrant profile for p16 / p53 in >90% of folliclar SCC.  There should be a lack of horizontal bowenoid dysplasia but one may see actinic keratosis or even bowenoid dysplasia in continuity with an otherwise typical follicular SCC and I've seen examples with different p16/p53 patterns between some of the collisions. I have to say since I've realised most SCC fulfill many of the criteria above and it's actually quite difficult to apprectiate a purely epidermal SCC arising from non-bowenoid actinic keratosis most SCC follicular features as described above or have hybrid follicular features with actinic keratosis also present (maybe actinic keratosis is a marker of SCC rather than the origin in most cases). In the case above we see the finding of a completely null p16 (a features I'm coming to recognise as highly undesirable in a KA-like lesion) that is present in >50% of all types of cutaneous SCC (superficial adnexal carcinoma and AFX/AFX-type cutaneous sarcomas) and appears to have been completely over-looked in the literature (to my amazement as it rather stares you in the face) although it is now becoming widely used in MELTUMPs. Note the reactive / wild type mosaic or checker-board pattern in the epidermis, follicle and sebaceous unit). I will leave it to you to guess what pattern is seen in KA (although my Lisbon and recent RCPath lectures available to those interested - e-mail richard.carr@swft.nhs.uk - I think some of you already have access to my "St John's" folder of talks and papers). In this case the p53 is aberrantly highly expressed perhaps wild type in compensation for p16 mutant pattern but you can see staining tails off centrally. Ki67 in this case is abnormal. In reactive lesions and KA the staining is limited to the peripheral 1 to 3 cells but in this example the staining extends well into the mid-zones (make sure to ignore inflammatory cells which may permeate all layers but are usually folded or haloed).

I think recognising follicular SCC is not entirely academic because our submitted paper of 103 cases indicates that roughly 50% of lesions (that extend often deeply into the dermis) have completely circumscript borders without elastic entrapment and can be regarded as in situ for practical purposes (none led to metastasis - although larger studies are required and proving a negative is of course impossible) and a similar cautious approach using EVG, would apply to thickish bowenoid actinic keratosis or superficial adnexal carcinoma as seen in the last few fridays and discussed at length. Do not trust a bowenoid lesion with pushing borders but elastic & collagen entrapment and indeed the above case I include as untrustworthy. But if I'm correct and >50% of SCC currently reported are un-recognised follicular lesions (in Clark's level 4 at least) and 50% of those are in situ for practical purposes then 1000's of patients are currently being followed up in hospital clinics for lesions that carry minimal risk. In our hospital patients (who are not being followed-up for other reasons) with circumscript folliclar SCC are discharged.

But...the recognition of the follicular aspect of most SCC has led to better diagnostic criteria to define KA-like and crateriform follicular SCC and in the last 18 months I've experienced a substantial break-through in the use of immunostains to support a diagnosis of SCC or, when wild type, not refute a preferred clinico-pathological diagnosis of KA. I think we are approaching close to a new paradigm in the assessment of KA-like lesions: Clinical-Morphological-and now Immuno- and soon to follow hopefully -Molecular) as an exact parallel to our approach in challenging naevi/melanocytomas, MELTUMPs and naevus-like melanoma. I should not be surprised that KA-like SPL to share many of the molecular characteristics described in melanocytic lesions. KA for example seem to be favouring intermittently sun-damaged skin of the limbs and trunk occurring at a somewhat younger age (~75y and less biased towards men - akin to SSMM (i.e. intermediate sun-damage) while SCC favour the severely sun-damaged skin of the head & neck (high CSD cancers akin to lentigo maligna melanoma) in the elderly (~80y) and more heavily biased towards men.  

As yet you should use the IHC cautiously in the diagnosis of KA and KA-like lesions as there are many potential pitfalls but I hope our work will be helpful to you when published fully in due course. I feel I'm getting a better understanding having experience of around 500 cases now. KA is always a challenging diagnosis and requires the utmost care.

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"Having said that there are deep pushing downgrowths and we can see in the third image (2nd down on the left) the pushing borders focally give way to budding pattern that in my (subjective) opinion favours an invasive lesion and the EVG highlights the budding borders and there is a tiny focus of collagen entrapment (arrow)". Fully agree.

But, most oof all, thanks, Richard, for your teaching points. 

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Richard Logan

Posted

Thank you Richard for such a comprehensive discussion.

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