Shadowing Practice: Breast Pathology Cases 3 and 4 - Learn English Speaking with Video

This is breast pathology cases 3 and 4.

This is a biopsy that was done for calcifications and from low magnification you can see we have multiple duct profiles that are being filled in by epithelial cells.

So let's take a closer look.

Closer inspection of this single duct shows that it's filled in by a population of atypical cells that are forming this cribriform architectural pattern.

Notice that these punched out spaces are relatively round and uniform and there is polarization of cells around the punched out spaces.

Here is a closer view of these cribriform structures.

Again, most of them are nice and round and uniform.

And lining these cribriform structures, you have a population of atypical cells with pleomorphic nuclei, hyperchromasia, pseudoinclusions, which is not a typical finding here.

But in general, lack of big prominent nucleoli.

There may be a few nucleoli in here, but for the most part, I would say it's relatively low to intermediate in its nuclear grade.

Let's step out one magnification and refer back to our previous case where we looked at a case of atypical

ductal hyperplasia and we said one of the key characteristics was basically partial duct involvement or involvement of a single duct profile.

Here we have, for the most part, most of these are complete duct involvement, meaning there's no residual normal ductal epithelium, no areas that look like usual ductal hyperplasia.

So we have a full duct profile here and we have several others that are fully involved as well.

So we have full duct involvement and multiple profiles that are involved.

So this meets criteria for ductal carcinoma in situ.

Then it comes down to really two things when you're dealing with ductal carcinoma in situ.

What is the nuclear grade and is there comedonecrosis?

There are various different subtypes of DCIS, and for the most part they're not important clinically.

What does matter is nuclear grade and presence or absence of comedonecrosis.

What you'll find with many cases of DCIS is you really have a spectrum of nuclear grade.

And in this particular case, I would say that most of the cells that we're seeing are relatively small and uniform.

We're not seeing a lot of nuclear membrane irregularities.

We're not seeing macronucleoli.

So I would call these low grade.

And then we have cells like this.

They're larger, they're a little more pleomorphic.

We have evacuated chromatin pattern and a lot of nuclear folds or nuclear membrane irregularities.

So in this particular case, I would call it ductal carcinoma in situ, low to intermediate nuclear grade.

And although I haven't shown the whole case, there was no comedonecrosis.

This is case four, which is also a biopsy done for calcifications.

And in this single focus, you can see that we have one, two, three, and maybe even four duct profiles involved by an intraductal proliferation.

Now it's clear from low power that for most people who are experienced what this is going to be, but let's walk through this systematically.

So we have an intraductal proliferation.

Is this invasive?

No.

Why?

It has rounded profiles, number one, and there's no desmoplasia.

Now there's a slight stromal reaction here, but it doesn't have an infiltrative pattern to it, and it's not pushing into the fat.

So we're dealing with an intraductal proliferation.

We had mentioned in our previous discussion that the general differential is between usual ductal hyperplasia, atypical ductal hyperplasia, and ductal carcinoma in situ.

So let's look closer at one of these duct profiles.

Here is a closer view showing several things.

First, there is a full duct involvement by this intraductal proliferation.

There is no residual normal duct epithelium and no areas that look like usual ductal hyperplasia, but let's explain why it's not usual ductal hyperplasia.

Remember that when we talked about usual ductal hyperplasia, we said that there was an intraductal proliferation that filled the lumen, and it was generally a disorderly arrangement as it moved into the lumen.

And in most cases of usual ductal hyperplasia, the cells get smaller as they move into the lumen.

Now you may say these cells look small, but this whole region here is all necrosis.

So let's ignore this for a moment and look at the viable cells.

So what do you see?

You see relative uniformity in the sense that they all look like a similar cell population, although there is pleomorphism.

Some are larger, some are smaller.

What do you see in terms of nuclear morphology?

Well, number one, the nuclei are enlarged.

The chromatin pattern is somewhat even although we do have some small nucleolite that are beginning to form.

There's abundant cytoplasm and there are conspicuous cell membranes.

There's even a mitotic figure here.

As they move into the lumen they become necrotic, so we have central necrosis.

And notice that the necrosis pushes on the epithelium and compresses it.

In other words it causes architectural change to the surrounding epithelium.

This is referred to as comedonecrosis.

So we have here ductal carcinoma in situ based on full duct involvement, based on multiple duct profiles, and also because we have a higher nuclear grade.

Let's look closer at some of these nuclei.

Here is a high magnification view of these cells.

So first of all, they are ductal epithelial in origin.

And you can tell that because you can make out the cell membranes and the cohesive nature of the epithelial cells.

When you're dealing with lobular neoplasia, either LCIS, which is lobular carcinoma in situ, or atypical lobular hyperplasia, one of its key characteristics is the lack of cellular cohesion, so it becomes more discohesive.

Here we have a cohesive process where you can make out cell membranes, abundant cytoplasm, And again, we have pleomorphic nuclei, some binucleation.

You can make out some notching and nuclear membrane irregularities.

The diagnosis for case 3 is ductal carcinoma in situ, low to intermediate grade.

The diagnosis for case 4 is ductal carcinoma in situ, high grade.

And you would also mention the presence of comedonecrosis.

Ductal carcinoma in situ is a neoplastic proliferation of ductal epithelial cells that is confined to the ductal or lobular system,

basically referring to the fact that it does not extend beyond the basement membranes and it retains an intact myoepithelial cell layer.

So if you were to use myoepithelial stains such as smooth muscle myosin, calponin, and you would see that these lesions would have an intact myopithelial cell layer.

These most commonly present as mammographic calcifications, and they have many different growth patterns that are described, many different subtypes that are described,

but as I had mentioned, the most important factors are nuclear grade, be it low grade, intermediate grade, or high grade,

and the presence or absence of comedonecrosis, which is a central type of necrosis that has architectural changes to the surrounding epithelium.

So it has a sort of compressive effect on the surrounding epithelium.

So we're going to go through a couple examples of DCIS and you need to name the type of DCIS.

This type would be cribriform because of its prominent cribriform architecture.

The next type would be solid.

Here it lacks the cribriform architecture although you can see a little bit over here, The solid type is essentially where you get a uniform proliferation of atypical cells within the lumen that lack any sort of cribriform architecture.

Here's an example of DCIS.

It's filling in the lumen, but even from low magnification, you can make out these fibrovascular cores.

It has a rounded border, so it's non-infiltrative.

There's no desmoplasia.

So this is DCIS of the papillary type.

What about this one?

Notice here we have atypical or malignant appearing epithelial cells filling in partially into the lumen, making these papillary-like structures, but they lack fibrovascular cores.

This is micropapillary DCIS.

What about this pattern?

Here we have central necrosis that's expanding and compressing the surrounding epithelium.

So this would be comedotype DCIS.

So with ductal carcinoma in situ, what to document?

You need to document nuclear grade, low, intermediate, or high.

And it's not uncommon to see a spectrum, so you can report low to intermediate or intermediate to high.

And then you need to document the presence and type of necrosis.

The most important type is that pattern that we saw, which is central with expansile features, which is called comedonecrosis.

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But you can also see punctate central necrosis that has no impact on the surrounding epithelium.

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And then you can report architectural patterns, although they are of less clinical significance.

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Here's an example of low-grade DCIS.

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You can see the relative uniformity of the cells that are filling in the lumen.

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They're not all that different than the ADH type nuclei that we had seen in the previous case except that it's full duct involvement and it's multiple ducts involved.

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Notice that the nuclei are round, they're monotonous, and the nucleoli are inconspicuous.

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Now it's hard to tell from this power, but in general you're not going to see prominent macronucleoli.

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You may find mitotic activity, but generally it's not going to be as frequent as you'll see in the higher grades of DCIS.

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Here's another example of ductal carcinoma in situ of the micropapillary type, low nuclear grade.

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Here's an example of high grade DCIS.

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This would be of the comedotype, so we have central necrosis that has an expansile appearance to it.

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We have markedly atypical nuclei, prominent nuclei, mitotic activity.

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This is high-grade DCIS.

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Here's another example of high-grade DCIS.

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This is one that is known as the clinging type, where you have essentially a single layer of malignant-appearing cells.

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In this particular case, we have some central necrosis.

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Here's an example of intermediate grade DCIS.

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We have mild to moderate nuclear pleomorphism, and the nucleoli are variably conspicuous.

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Question, which of the following statements regarding low grade DCIS is false?

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So let's just go through each one and say true or false.

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Low-grade DCIS typically shows strong and diffuse expression of ER and PR.

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True.

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Low-grade DCIS typically has a low proliferative rate by KI-67.

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True.

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Low-grade DCIS typically lacks expression of cytokeratin 5-6.

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True.

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So you can exclude this one.

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They do not typically have HER2 overexpression.

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Now you should not, there's two things I would note here.

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On all cases of DCIS, you're going to order estrogen and progesterone receptor.

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There's no need to order a KI-67 and there's no reason to order HER2.

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But you will find if you do have cases of invasive ductal carcinoma in which HER2 is ordered that it's not uncommon for it to be overexpressed in cases of high-grade DCIS, but generally it's going to be negative in cases of low-grade DCIS.

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Question, what immunohistochemical stain is the most clinically relevant for DCIS?

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Answer, estrogen receptor.

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So tamoxifen significantly reduces the risk of local recurrence in patients with ER-positive DCIS.

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So ER is important.

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Question.

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Which of the following features is associated with local recurrence following breast conserving treatment for DCIS?

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You may pick more than one.

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Answer.

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All of these features.

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So high nuclear grade, presence of comedor necrosis, a young patient age, less than 45 years, a large lesional size, and a positive margin are all associated with increased risk of local recurrence.

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The most important among these is positive margin.

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With respect to recurrence, around half of cases are DCIS and the other half are invasive carcinoma.

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You make the diagnosis of low-grade DCIS on a needle core biopsy.

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To what degree is this patient's risk elevated for developing invasive carcinoma?

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Eight to tenfold.

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What breast site is at risk?

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Is it ipsilateral, contralateral, or bilateral?

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Ipsilateral.

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So to summarize, low-grade DCIS, 8 to 10-fold increased risk of developing invasive carcinoma, with the greatest risk being the ipsilateral breast.

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So to summarize, we had said in the previous case that atypical ductal hyperplasia is associated with a 3-5 fold increased risk of developing invasive carcinoma.

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With low-grade DCIS, it's elevated beyond that, it's 8-10 fold.

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We mentioned that with atypical ductal hyperplasia, the risk was bilateral.

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With low-grade DCIS, it puts greater risk on the side of the DCIS.

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The treatment for atypical ductal hyperplasia is watching the patient, number one, and the and potentially tamoxifen to help reduce the risk.

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For patients with low-grade DCIS on a needle core biopsy, the DCIS has to be surgically eradicated.

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So there needs to be a resection with a negative margin.

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And generally speaking, for a pathologist, a negative margin means it's not at ink.

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But for DCIS, it needs to be beyond 2 millimeters.

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So this completes cases 3 and 4.

Wat is de Shadowing-techniek?

Shadowing is een wetenschappelijk onderbouwde taalleermethode die oorspronkelijk is ontwikkeld voor professionele tolkentraining en gepopulariseerd door polyglot Dr. Alexander Arguelles. De methode is eenvoudig maar krachtig: je luistert naar native Engelse audio en herhaalt het onmiddellijk hardop — als een schaduw die de spreker volgt met slechts 1–2 seconden vertraging. In tegenstelling tot passief luisteren of grammaticadrills, dwingt shadowing je hersenen en mondspieren om echte spraakpatronen tegelijkertijd te verwerken en te reproduceren. Onderzoek toont aan dat het de uitspraaknauwkeurigheid, intonatie, ritme, verbonden spraak, luisterbegrip en spreekvaardigheid aanzienlijk verbetert — waardoor het een van de meest effectieve methoden is voor IELTS Speaking-voorbereiding en echte Engelse communicatie.

Shadowing Practice: Breast Pathology Cases 3 and 4 - Learn English Speaking with Video

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