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This is breast pathology, case 2.
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This is breast pathology, case 2.
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This is a biopsy that was done for calcifications.
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And we found this focus here, which stood out from low power due to its complex architecture and presence of hyperchromasia.
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So let's take a closer look.
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So upon closer inspection, what do we notice?
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First of all, there's some residual normal ductal epithelium here on the periphery, but what's happening is it's filling in the lumen with epithelial cells, and that is what puts it into that proliferative category.
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Now that could be either ductal hyperplasia of the usual type called usual ductal hyperplasia, or it may be atypical, or it may be ductal carcinoma in situ.
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So that's what we need to figure out.
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So let's take a closer look at this lesion.
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First of all, we're dealing with a proliferative lesion.
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We're not dealing with an invasive carcinoma, so you can actually see on the periphery, number one, it has a rounded appearance to it.
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It doesn't look infiltrative.
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There's no stromal reaction.
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And if you were to look closer, you'll actually see myoepithelial cells, or if you were to do immunohistochemistry for myoepithelial cells, you would see they were intact.
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So we're dealing with an intraductal proliferative lesion.
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And so the question is, is it typical, which we call usual ductal hyperplasia?
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Is it atypical, which we would call atypical ductal hyperplasia?
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Or is it an in situ carcinoma, which we would call ductal carcinoma in situ?
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So let's consider those possibilities.
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So first let's consider the architecture.
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Number one, it's making these rounded structures.
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As it fills in the lumen, it's forming these rounded, cleared out areas that we call cribriform architecture.
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However, it still has what would be considered an intact, uninvolved areas of the duct.
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In other words, this single lining here which is not quite filling into the lumen.
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And we'll notice that more as we look down further on this particular duct profile.
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This is the lower edge of that same ductal proliferation, and notice that the intraluminal process starts to go away.
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So we're dealing with partial duct involvement, and that's going to be helpful for our differential.
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Now let's look at the cytology.
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Notice several things.
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First, we have relatively uniform nuclear morphology, meaning that each of the nuclei look somewhat similar to the others.
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So that monotony is actually more in keeping with an atypical process.
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The other thing is the organization of the nuclei are somewhat regular as they form around these rounded cribriform structures.
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So the uniform nuclear morphology plus the regularity of the distribution is considered atypical.
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But is it enough for ductal carcinoma in situ?
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To answer that question, first let's look at the nuclear morphology and ask ourselves whether or not we consider these to be low-grade nuclei or high-grade nuclei.
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High grade nuclei would have a greater degree of nuclear pleomorphism, meaning greater variability, yet they would still have hyperchromasia to put them into that atypical category.
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And also the high grade nuclei tend to have prominent macronucleoli.
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So we are dealing with low nuclear grade.
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Now let's consider again the extent of involvement of this duct profile.
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So again here I'm showing you the area of this duct profile that is uninvolved, meaning that these cells are not filling in the lumen, they're not forming complex architecture, so we have partial duct involvement.
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The best diagnosis for this case is atypical ductal hyperplasia.
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So atypical ductal hyperplasia fits within the broader category of intraductal proliferative lesions.
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And so this intraductal proliferative lesion category would include, number one, usual ductal hyperplasia, number two, atypical ductal hyperplasia, and number three, ductal carcinoma in situ.
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Distinguishing among these three choices depends on architecture and cytology and also the extent of involvement.
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Under this discussion, we will now consider usual ductal hyperplasia and atypical ductal hyperplasia.
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So for usual ductal hyperplasia, the extent can vary from mild to florid, and it's really the florid usual ductal hyperplasia that's more clinically important.
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And florid usual ductal hyperplasia does have an increased risk for developing breast cancer.
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It fits within that proliferative breast disease category.
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So here's a focus of ductal hyperplasia.
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We said that what defines this intraductal proliferative lesion is filling in the lumen with epithelial cells.
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But notice that this intraluminal proliferation is composed of cells with bland nuclei.
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It's rather disordered in its architecture, and it lacks that cribriform pattern that we saw in our case.
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So here's another example of usual ductal hyperplasia.
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There is a proliferation of ductal epithelial cells filling the lumen that have a disorderly appearance as they move into the center.
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And they are forming these slit-like spaces rather than the rounded, punched-out cribriform spaces that we saw in our case.
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Here is a closer view of usual ductal hyperplasia.
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Notice that there is a disorderly arrangement of the nuclei as they fill in the lumen.
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There's nuclear overlap, there's poorly defined cell borders, and there's no regular orientation around any of these spaces.
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Also the spaces are slit-like and not round and uniform.
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Here is another example of usual ductal hyperplasia showing swirling of nuclei within the center of the ductal proliferation.
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Atypical ductal hyperplasia is defined as a ductal epithelial proliferation that is composed of atypical ductal epithelial cells that have nuclear features that are similar to that seen in low-grade DCIS.
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What distinguishes atypical ductal hyperplasia from ductal carcinoma in situ is that there is only partial duct involvement, meaning that the duct profile that's involved usually has some mixed usual ductal hyperplasia or residual normal epithelium.
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But, by definition, the changes of atypical ductal hyperplasia will border on low-grade DCIS.
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So it really comes down to the extent of the atypical proliferation.
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So let's look at some criteria.
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Partial duct involvement by an atypical ductal proliferation is the defining feature of atypical ductal hyperplasia.
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If there's full duct involvement, how much is enough to call ductal carcinoma in situ?
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Well, it depends on which criteria you use.
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The page criteria says that involvement of a single duct profile should be classified as atypical ductal hyperplasia.
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So with that system, you need more than one duct profile that's fully involved in order to call it low-grade ductal carcinoma in situ.
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Tavisoli and Norris criteria says it should be size-based.
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If it's 2 millimeters or less in greatest dimension, classify it as atypical ductal hyperplasia.
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If it's greater than 2 millimeters, classify it as low-grade ductal carcinoma in situ.
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I would say in general when you're dealing with borderline lesions on a needle core biopsy, it's probably best to be more conservative and go with atypical ductal hyperplasia.
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The idea is that a diagnosis of atypical ductal hyperplasia on a needle core biopsy will prompt a surgical resection, generally a lumpectomy.
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This is an example of atypical ductal hyperplasia.
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Notice first there's partial duct involvement.
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In this case, it's a little more difficult to tell, but on these edges you can still see somewhat residual, normal, single layer epithelium within the duct.
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And then here towards the left, it's more uniformly filled in with rounded cribriform punched out spaces and uniformity of both nuclear morphology and also distribution.
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So this is partial duct involvement, low-grade nuclei, so it would be classified as atypical ductal hyperplasia.
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Another example, here on the right, demonstrating only partial duct involvement, and on the left, filling into the lumen by these atypical cells, including rounded cribriformed spaces, uniformity of nuclear morphology, and distribution.
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So this is atypical ductal hyperplasia.
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Another example, this one shows more clearly the partial duct involvement.
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So this area is uninvolved.
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This area is filled in.
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Some are somewhat compressed, but for the most part they're round and rigid in appearance.
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And it's that uniformity of these cells that fill in the lumen that define atypical ductal hyperplasia.
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With atypical ductal hyperplasia, the nuclei are generally round, somewhat small and uniform, and they're even in their distribution.
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They're said to be polarized around these punched out spaces.
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That just basically means that they're well organized.
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They're not overlapped and haphazard like we saw within the florid usual ductal hyperplasia.
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Question.
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You are evaluating a needle core biopsy from the breast of a 40-year-old female.
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find this focus.
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So let's look at the focus.
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So we're dealing with an intraductal proliferative lesion, so it's filling in the lumen.
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What we have are compressed, irregular spaces.
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The cells on the inside vary in their nuclear morphology.
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Some are more rounded, some are more elongate like those, and they're disorderly in their arrangement around these punched out spaces.
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You decide to do a cytokeratin 5-6, and it shows what we call a mosaic pattern of staining.
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This basically refers to a mixed positive and negative population with respect to the cells that are filling in the duct lumen.
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If you ordered an estrogen receptor stain, you would also see this mosaic pattern.
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Some are negative, some are strongly positive, some are more intermediate to weak in their staining intensity.
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So this mixed population of cells is more in keeping with what diagnosis?
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The answer is usual ductal hyperplasia.
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So the defining features are the disorderly arrangement, the lack of uniform punched out spaces, the mosaic pattern of cytokeratin 5, 6 expression.
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Remember the cells that fill in the lumen of both atypical ductal hyperplasia and ductal carcinoma in situ are going to be negative for cytokeratin 5, 6.
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And also the heterogeneity of the ER expression point towards usual ductal hyperplasia.
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ADH and low-grade DCIS are generally uniform and also generally strongly positive for estrogen receptor.
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Here's an example of cetokeratin 5-6 staining in a case of atypical ductal hyperplasia.
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See these uniform cells that are filling in the lumen, forming these punched out spaces are negative.
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Now, it's not uncommon you'll see scattered positive cells, but for the most part you have a uniform population of cells that are negative for cytokeratin 5-6.
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Question, is usual ductal hyperplasia associated with an increased risk of developing breast cancer?
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Yes, and we're really referring here to florid usual ductal hyperplasia.
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Typically the mild cases of ductal hyperplasia are not even mentioned, it's generally the florid cases that we put into a diagnostic line.
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So florid usual ductal hyperplasia does have an increased risk of developing breast cancer, but the question is to what degree?
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And it's around one and a half to two-fold increase in risk.
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So is this risk for the ipsilateral, contralateral, or bilateral breasts?
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It's going to be bilateral, so it's general risk.
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So fluorid usual ductal hyperplasia implies a general risk of developing breast cancer to both breasts, and it's around a one and a half to two-fold increase in risk.
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Atypical ductal hyperplasia is associated with an increased risk of developing breast cancer.
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How much is the risk increased?
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The answer is three to five-fold.
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there's a three to five-fold increase in risk of developing breast cancer in patients with atypical ductal hyperplasia.
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Which breast is at risk?
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Is it ipsilateral, contralateral, or bilateral?
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It's bilateral.
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Again, atypical ductal hyperplasia, three to five-fold increase in risk, and it's a general marker of risk that involves both breasts.
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To make the diagnosis of atypical ductal hyperplasia on a needle core biopsy, what percentage of cases will have a worse lesion, meaning DCIS or invasive carcinoma, on the lumpectomy specimen?
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The answer is 15%.
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Patients with atypical ductal hyperplasia on a biopsy are generally going to be treated with a lumpectomy, and it's around 15% of cases that will have carcinoma, either ductal carcinoma in situ or invasive carcinoma on the lumpectomy specimen.
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If all you find on the lumpectomy is atypical ductal hyperplasia, then they are managed by close follow-up.
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Tamoxifen and aromatase inhibitors may be used to help reduce risk.
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So the idea is that if you have ADH on a biopsy, there may be something worse on the resection specimen or the lumpectomy specimen.
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If all you have is ADH after resection or after the lumpectomy is done, then you're just dealing with a general marker of risk as we had mentioned before.
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So that's the end of case two.

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