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In this section we have spot diagnoses posted on a daily basis since June 2010, now over 1700! You can review the archived cases and read the suggested diagnoses by users and the final comment by Dr Uma Sundram, the Editor-in-Chief and main spot diagnosis host. Case are uploaded each week day by 10 a.m. UK time with the correct diagnosis will generally be posted at 8 p.m. UK time. Why not view the most recent spot diagnosis and proffer a diagnosis?

Case Number : Case 2702 - 13 November 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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F95. Upper lip. Rapidly grown nodule now stopped. 19 weeks. ?KA


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Abrupt keratinization, with some tricky likeness to polar tumor of the scalp...?Malignant Pylar Tumor. 

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Krishnakumar subramanian

Posted

 ? well differentiated Squamous cell carcinoma

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Victor Delgado

Posted

Well differentiated SCC vs. Trichilemmal Carcinoma

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p16 null expression, SCC-like; ki67 too high in a stopped growth; p53 difficult to interpret for me; EVG could point a quick cellular growth( too quick in a well differentiated tumor), KA-like..waiting for the Richard’s comments.

 

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Dr. Richard Carr

Posted

Yes it's a follicular (mainly tricholammal pattern) SCC but does appear to connect focally to the surface upper left. Agree not well differentiated give the pattern.

p16 mutant (mainly null) in ~80% of folliclular SCC and is a game changer. p53 is wild type here slight up-regulation with peripheral accentuation. Ki67 mirrors a wild type p53 (peripheral in well differentiated SCC and KA proliferative stage). Agree there is entrapment on EVG which confirms and invasive tumour but is variable in both KA and SCC. However I'd say it is much more common to see a completely circumscript FSCC c/w KA (<10% have completely circumscript borders except for regressing lesions). Our work has pretty much definitively confirmed KA are now distingihsed from SCC by mutant patterns for p16 and p53 in 90% of the latter but wild type in all typical KA. Most prolfierative KA are highly challenging for diagnosis. I'm finding my favoured KA diagnosis is supported by wild type markers in around 90%. That leave a few with a proliferative KA-like lesions with a mutant pattern and I've even seen one case that I would have favoured KA on review (that had metastasised) and it was p16 null. So if I favour KA on CLIN-H&E/EVG criteria but see a mutant pattern for p16 or p53 I now label it "uncertain" for malignancy till we get more evidence. Obviously if there are clear-cut features for malignacy and the IHC is not clear cut mutant (not common) you have to except the markers are only 90% sensitive (but that it impressive for only two markers). No typical KA with some proliferative foci was mutant so that means that a mutant pattern is specific for SCC up till now. Basically KA that metastasised were mis-diagnosed folliclar SCC (good mimics). I think bone fide malignant transformation is also very uncommon in KA (<5% as we have not collected regressed KA in our audit). We also found only 5% of SCC arose in the setting of bowenoid actinic keratosis that lacked some follicular type features so MOST SCC hair bearing skin are either pure follicular pattern or hybrid surface / follicular pattern. Recognising follicular SCC led to better diagnostic criteria for KA which led to the first study of known diagnostic markers that has showed a very clear-cut differentiation between KA and SCC. If you want to complete attend my Zoom talks this friday you would have to take the KA challenge - e-mail me at richard.carr@swft.nhs.uk

Regards to all - it's been a very long road to get this far!

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