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Case Number : Case 875 - 25th October Posted By: Guest

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74 years old male. 3cm keratotic nodule right hand.

Case posted by Dr. Richard Carr.


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Dr. Mona Abdel-Halim

Posted

Squamous cell carcinoma in situ (Bowen's Disease), with involvement of adnexal (follicular) epithelium.

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Sasi Attili

Posted

Bowenoid in-situ SCC suspicious of early invasion.(island to the left of the hair follicle where the tumour is extending down..in picture on top right). However need to see a close up of it to be sure.

I would like to take this opportunity to express my thoughts (following on from a discussion I had with Dr. Carr recently) regarding invasive Bowens disease which is supposed to be a high risk SCC.

I was looking for scientific evidence of this notion (that this is a high risk SCC) and Richard pointed out the paper by Cassarino DS, Derienzo DP, Barr RJ. Cutaneous squamous cell carcinoma: a comprehensive clinicopathologic classification. Part one. J Cutan Pathol. 2006 Mar;33(3):191-206.

In the paper, the authors themselves say:

'However, up to 5% of Bowen’s disease may become invasive, and up to 13–20% of those patients develop metastases, although these numbers are based on small studies and may reflect referral bias.7,116,117,120.'

The statement at the end of the para 'Although large outcome studies have not been performed, given the relatively high rates of metastasis reported with invasive Bowen’s disease, it should be considered a potentially high-risk variant of SCC.', is a fail-safe rather than evidence based approach.

The refs are all ancient and are small studies indeed. So I don't think the notion that 'Bowen's disease (BD) with early invasion, is a high risk SCC' is a proven fact. However, if there is adjacent/ contiguous BD in a patient with a barn door SCC, that might be a different case, and carry a worse prognosis as it may suggest field change.

In fact most clinicians I know (including me) would consider BD with early papillary dermal invasion (not just the pushing margins, but proper single cells or small nests invading into the papillary dermis) to be of good prognosis once excised/ treated. [i]Maybe Breslow has a role to play here[/i]. But I don't think BD itself is a proven independent RF for SCC prognosis in these cases. I think there are a number of similar other unsubstantiated notions prevailing in SCC (incl KA) that need addressing....

Would certainly like to know what others think.......

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I would call this an early well differentiated squamous cell carcinoma with extensive in situ component (BD) in routine practice but am interested to know what others think.

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Mark A. Hurt MD

Posted

Bowen's disease with syringofibroadenomatous changes. I think this is a superficial lesion that surgery will serve to eradicate. Some of the findings are likely because of oblique sectioning.

To Sasi's point regarding "invasion," I don't like the word, as it is a military term that doesn't seem applicable here. As Ackerman indicated in a number of articles and opinion pieces, squamous cells in a squamous carcinoma do not leave the epidermal compartment and move to a different compartment (as do melanocytes in melanoma); rather, they extend from superficial to deep like a phalanx (another oft-used military term) through the dermis. Of course they often extend through the dermis in jagged patterns, which is commonly referred to as "invasion."

I think a critical issue in squamous carcinoma centers on what criteria have meaning for the appropriate treatment. In general, these are margin involvement, spacial location (whether superficial or deep -- through the dermis into fat), vascular or lymphatic embolization, and nerve involvement. There are probably others, but these seem to be the most important for treatment considerations. Epidemiologists will have to address the prognostic issues. Pathologists need to define the diagnostic criterion issues. Even better, both groups need to work together.

I don't think a "Breslow measurement" in squamous carcinoma is desirable or even applicable. Even the mechanics of doing it are much more difficult to consider than Breslow's method for melanoma, and the Breslow method is not without [u][i]its [/i][/u]problems. if it is ever done, it should not be called a Breslow measurement but should be named after whomever proves its merit.

Below are Ackermanian references on carcinoma in situ. His point of view in 2009 (published posthumously) is not what it was in 1979, which does not surprise me.

[size=3][font=arial,helvetica,sans-serif]1: Ackerman AB, Mones J. Squamous-cell carcinoma in situ is a fiction! J Cutan
Pathol. 2009 Jan;36(1):74-5; author reply 76. doi:
10.1111/j.1600-0560.2008.00984.x. PubMed PMID: 19125737.

2: Kessler GM, Ackerman AB. Nomenclature for very superficial squamous cell
carcinoma of the skin and of the cervix: a critique in historical perspective. Am
J Dermatopathol. 2006 Dec;28(6):537-45. PubMed PMID: 17122500.

3: Ackerman AB. Carcinoma in situ. Hum Pathol. 1979 Mar;10(2):127-8. PubMed PMID:
217817.[/font][/size]

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Guest Jim Davie MD

Posted

Agree with SCC in-situ. I agree with Mark that tangential sections of in situ carcinoma may account for the "superficially invasive" component. The multifocal/clonal nature the proliferation, and high-grade atypia help exclude the other low-power differential diagnosis considerations of hypertrophic lichenoid actinic keratosis or hypertrophic lichenoid keratosis.

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Sasi Attili

Posted

Thanks Dr. Hurt. I have just read Ackerman's papers you have referenced. This does not still answer my question as to why we should/ shouldn't accept the common notion that invasive BD is a high risk SCC. I suppose you are hinting at the fact that this point is moot because both are SCC (a view the Ackerman purported). If this is the case, I am afraid I have to disagree, as the nomenclature/ diagnosis has therapeutic and prognostic implications (as per existing literature anyway). If this is called BD, this is a low-risk tumour with excellent prognosis once treated. If we call this invasion, then this is classed as a 'high- risk' tumour as per existing notion/ literature and management would be different.

I don't want this discussion to overshadow the interesting spot today but since you have mentioned his papers, in the absence of an alternative forum I shall reply to these interesting points raised.

I do not quite agree that prognostication is the duty of epidemiologists (As Ackerman also hints in his papers) and pathologists have no responsibility. As a clinician I can say the same thing and say that it is my duty as a clinician to just treat the patient and I do not need to prognosticate as i am not an epidemiologist! That would be silly for me to then refer the patient to an epidemiologist, or worse, leave the patient with an open ended diagnosis of cancer!

Certain tumour parameters determine prognosis. Prognosis determines the treatment modality. Its all interlinked. For ex. Low-risk in-situ SCC's and some superficial BCC's ([url="https://dermpathpro.com/blog/12/entry-119-superficial-bcc-why-it-is-important-to-measure-depth/"]my recent blog post on this[/url]) can be treated by non-surgical means; SCC's with neurovascular invasion/ high risk, might need adjuvant radiotherapy etc, and hence risk-stratification is important and this is the role of both the clinician and pathologist (hence we have MDT's in the UK- hopefully its the same in the US).

Regarding the concept of the phalanx , Ackerman says (I hope it is not one particular phalanx he is talking about!) :):

'That is not the case, however, for so-called squamous cell carcinoma
in situ in which, in vivo, neoplastic keratocytes
do not move as discrete aggregations from the
epidermis into the dermis, but when they do extend
ever so slowly deeper and deeper into the dermis,
they do that in the form of a phalanx, thereby
making it impossible for a histopathologist, no
matter how skilled, to determine where the presumed
in situ’ malignancy ends and the supposed
invasive’ malignancy begins.'

But, the same can be said about melanocytes, and often it is difficult to differentiate in situ from 'invasive' disease. So I am not sure I necessarily agree with him on this, unless I can't really understand what he is trying to explain. From what I understand, he is trying to draw a distinction between invasion of cells into the dermis and cells pushing into the dermis (not pushing borders), when in fact both are the same pathological processes wherein a tumour cells lose their usual homeostatic relation with their native surrounding cells and develop the ability to survive in tissue's that are not native, thus migrating up or down! This is the same whether the tumour cell is a melanocyte or keratinocyte. I cannot see the distinction. Both have the same (albeit difference in grade) prognostic implications. I have utmost respect for Dr. Ackerman, but on this occasion, I am afraid he has lost me!

His arguments re in-situ SCC still being an SCC are well known and understood. However prognostically and clinically there are huge implications for the patient and the distinction has to be made. Perhaps topical/ non-surgical modalities weren't popular in his time. However, times have changed and so should we :)

P.S: I don't mind the new terminology for Breslow being named after me :D

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Dr. Richard Carr

Posted

I called this adnexotropic bowenoid actinic keratosis (although "warty" carcinomas can also occur at this site). I did not mention the mild syringofibroadenomatous hyperplasia (I like not to confuse the clinicians any more than absolutely necessary) but thanks Mark for noticing it. There were four other blocks of this large lesion and I saw no convincing dermal invasion. I don't use the term carcinoma in situ as it promotes a knife mentality and as Sasi says there are other therapeutic options. I do mention the depth of adnexotropic downgrowths from the granular layer as I think this might prompt a surgical approach to some cases where this feature is extreme (i.e. thicker than 1mm). Happy for this to be known in future as "Carr's pragmatic mearsurement". I agree with Sasi that we need a better system of stratifying invasive Bowenoid SCC for prognostication. The current WHO approach obviously has many flaws and the RCPath dataset does not mention follicular SCC subtype yet (it appears that this is the dominant SCC subtype on the head and neck in my practice).

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Dr. Mona Abdel-Halim

Posted

But isn't it by definition that in actinic keratosis dysplastic cells do not involve the adnexal structures but only descend on the outer surface of acrosyringial structures and hair follicles. I will consider the extensive involvement of the follicular epithelium as a point in favour of Bowen's (SCC in situ), would love to know Dr Carr's opinion in this point...

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Sasi Attili

Posted

Dr. Mona. Bowenoid Actinic Keratosis is used synonymously with BD. It is used for full thickness dysplasia (Bowen's disease) in the context of a sun-exposed site (in contrast to non-sun exposed legs where classical BD is supposed to occur). So essentially this is Bowen's disease, but in a sun-exposed setting. Richard will correct me if I am wrong.....

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Mark A. Hurt MD

Posted

I added a few comments below [color=#ff0000]in red[/color]:

MAH

[quote name='Sasi Attili' timestamp='1382712682']
Thanks Dr. Hurt. I have just read Ackerman's papers you have referenced. This does not still answer my question as to why we should/ shouldn't accept the common notion that invasive BD is a high risk SCC. I suppose you are hinting at the fact that this point is moot because both are SCC (a view the Ackerman purported). If this is the case, I am afraid I have to disagree, as the nomenclature/ diagnosis has therapeutic and prognostic implications (as per existing literature anyway). If this is called BD, this is a low-risk tumour with excellent prognosis once treated. If we call this invasion, then this is classed as a 'high- risk' tumour as per existing notion/ literature and management would be different.

[color="#ff0000"]from MAH: No, I don't think the point is moot, but I'm not so sure what the patterns mean. Based on diagnostic criteria, I can speculate that most "invasive" Bowen's disease-like deep carcinomas are probably less aggressive than their "ragged" counterparts (which, in my experience, exhibit more nerve involvement). [/color]

I don't want this discussion to overshadow the interesting spot today but since you have mentioned his papers, in the absence of an alternative forum I shall reply to these interesting points raised.

I do not quite agree that prognostication is the duty of epidemiologists (As Ackerman also hints in his papers) and pathologists have no responsibility. As a clinician I can say the same thing and say that it is my duty as a clinician to just treat the patient and I do not need to prognosticate as i am not an epidemiologist! That would be silly for me to then refer the patient to an epidemiologist, or worse, leave the patient with an open ended diagnosis of cancer!

[color=#ff0000]from [/color][color="#ff0000"]MAH: I don't subscribe to the principle of duty; I adhere to the principle of "chosen obligation." Pathologists have chosen the obligation of evaluating the histopathological features of lesions and establishing a diagnosis. Prognosis is contained within a diagnosis, to be sure, but when a pathologist evaluates tissue changes under a microscope, he or she does not identify a prognosis; rather, they identify the morphologic changes -- concrete in nature -- that lead to the establishment of a diagnosis. The full meaning of the diagnosis is tempered in the fires of outcomes, but the diagnosis is an interaction of the mind of the pathologist with the morphologic changes in the tissue -- in this context. As a clinician, you have added another dimension to the equation, one that many if not most pathologists do not have direct access.[/color]

Certain tumour parameters determine prognosis. Prognosis determines the treatment modality. Its all interlinked. For ex. Low-risk in-situ SCC's and some superficial BCC's ([url="https://dermpathpro.com/blog/12/entry-119-superficial-bcc-why-it-is-important-to-measure-depth/"]my recent blog post on this[/url]) can be treated by non-surgical means; SCC's with neurovascular invasion/ high risk, might need adjuvant radiotherapy etc, and hence risk-stratification is important and this is the role of both the clinician and pathologist (hence we have MDT's in the UK- hopefully its the same in the US).

[color="#ff0000"]from MAH: [u][i]All[/i][/u] knowledge is interlinked, as you indicate, but not all of the data is accessible at a given time. Furthermore, many of the linkages are not obvious and are abstract, gleaned only from meta-analysis of diagnostic criteria. The diagnostic criteria precede the meta-thinking, but both are necessary and both serve to temper each other for deeper for a deeper understanding of the clinicopathologic diagnosis.[/color]

Regarding the concept of the phalanx , Ackerman says (I hope it is not one particular phalanx he is talking about!) :):

'That is not the case, however, for so-called squamous cell carcinoma
in situ in which, in vivo, neoplastic keratocytes
do not move as discrete aggregations from the
epidermis into the dermis, but when they do extend
ever so slowly deeper and deeper into the dermis,
they do that in the form of a phalanx, thereby
making it impossible for a histopathologist, no
matter how skilled, to determine where the presumed
in situ’ malignancy ends and the supposed
invasive’ malignancy begins.'

But, the same can be said about melanocytes, and often it is difficult to differentiate in situ from 'invasive' disease. So I am not sure I necessarily agree with him on this, unless I can't really understand what he is trying to explain. From what I understand, he is trying to draw a distinction between invasion of cells into the dermis and cells pushing into the dermis (not pushing borders), when in fact both are the same pathological processes wherein a tumour cells lose their usual homeostatic relation with their native surrounding cells and develop the ability to survive in tissue's that are not native, thus migrating up or down! This is the same whether the tumour cell is a melanocyte or keratinocyte. I cannot see the distinction. Both have the same (albeit difference in grade) prognostic implications. I have utmost respect for Dr. Ackerman, but on this occasion, I am afraid he has lost me!

[color=#ff0000]from [/color][color="#ff0000"]MAH: My understanding of Bernie's point is that when a melanocyte moves into the dermis -- whatever one calls that phenomenon -- it moves from one compartment (the epidermis) into another compartment (the dermis). This is not true with keratocytes in squamous carcinomas. They begin as epithelial cells in the epithelium (the surface), and they move through the dermis; they do not change compartments.[/color]

His arguments re in-situ SCC still being an SCC are well known and understood. However prognostically and clinically there are huge implications for the patient and the distinction has to be made. Perhaps topical/ non-surgical modalities weren't popular in his time. However, times have changed and so should we :)

[color="#ff0000"]from MAH: No argument from me, if one can prove efficacy.[/color]

P.S: I don't mind the new terminology for Breslow being named after me :D

[color=#ff0000]from [/color][color="#ff0000"]MAH: Nor do I; just state your criteria and offer an objective way to do it. [/color] :)

[/quote]

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Sasi Attili

Posted

Thanks dr. Hurt. Re- Pathologists not having any clinical responsibility reminded me of this cartoon I saw recently :)
[img]https://lh3.googleusercontent.com/-TxQgD4kG85c/Um0e7kyBRpI/AAAAAAAAhPw/ADKC0lr4rQM/w855-h553-no/1235424_533230903431893_1564887619_n.jpg[/img]



I still do not understand Dr. Ackerman's theory regarding the Phalanx though! Why are epithelial cells not changing compartments, when moving from the epidermis to the dermis. Does he mean that they are taking the epidermis with them and the entire epidermis is moving into the dermis? Am I missing something very obvious? O.o

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Mark A. Hurt MD

Posted

Dear Sasi,

Unfortunately, I cannot speak for Dr. Ackerman, but my interpretation of his point of view is that the epidermis is its own compartment as the dermis is [u][i]its [/i][/u]own. Thus, there is no clear distinction of "invasion" in squamous cell carcinoma, as the epidermis does not leave itself (it stays connected to the surface) to enter the dermis -- as do melanocytes, when they move from the epidermal compartment into the dermal compartment.

If I can clarify this issue later on by understand his works in a deeper manner, I will attempt do so. I think it's a line of thought worth exploring.

Mark

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Dr. Richard Carr

Posted

Dear Mona,

Sasi is right. I use the term bowenoid epidermal dysplasia for full thickness dysplasia on non-sun exposed sites (or on exposed skin without prominent solar elastosis e.g. lower leg often) and Bowenoid actinic keratosis for cases like the one here on sun-exposed sites with accompanying moderate to severe solar elastosis. I don't remember seeing adnexotropic actinic keratosis so I think the adnexotropism must just reflect the grade of dysplasia (in bowenoid actinic keratosis or bowenoid epidermal dysplasia).

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