Shadowing Practice: Breast Pathology Cases 5 through 7 - Learn English Speaking with Video

This is breast pathology cases 5, 6, and 7.

Cases 5, 6, and 7 are related so we will go through these together.

This is case number 5.

This is an older slide and somewhat faded but you can still make out the pathology.

So let's see what we have here.

We have a terminal duct lobular unit here and a part of one here.

here, but let's focus on this particular terminal duct lobular unit.

First of all, is this terminal duct lobular unit normal or abnormal?

Well it's abnormal.

Why is it abnormal?

It's abnormal because it has expansion of these acini, these acinar structures, which would normally just have a single layer of epithelium and a lumen, and instead what we have is filling in of the acini within a terminal duct lobular unit.

Overall, I would say the degree of expansion is somewhat mild, although obviously that can be subjective.

But let's look at the cytology of the cells.

You can see that they're relatively uniform, so the nuclear size and shape throughout most of these expanded acini look relatively uniform.

They have ovoid nuclei, relatively abundant cytoplasm.

You can make out these clear cells on the periphery of the acini.

These are the myoepithelial cells.

And notice in particular that you see a lot of white space in between the individual epithelial cells.

That is a feature that points towards discohesion or dis-heasion, however you want to say it.

So there is a lack of adhesion between many of these cells.

Upon closer inspection we can make out some of the nuclear details.

You can see that they have somewhat granular chromatin.

We do have conspicuous nucleoli.

They've got relatively abundant cytoplasm.

Again, unlike the previous cases that we saw, you can't really make out the cell membranes and the adhesion between the epithelial cells.

Also notice a clue here.

There is a vacuole within the cytoplasm of some of these epithelial cells.

Here's another magnified view you can see this little mucin vacuole within the epithelial cell that is compressing the nucleus.

Here is an immunohistochemical stain that was performed on this particular focus.

There are some folds so ignore those.

This is E-cadherin.

So you can see that most of these cells that are filling in the lumen within these expanded acini are negative for E-cadherin.

It's not uncommon to have scattered staining but for the most part they're negative.

So the diagnosis for this case is atypical lobular hyperplasia, and it's somewhat subjective.

Some may call this lobular carcinoma in situ.

We'll talk more about criteria in a bit.

This is the next case.

This is case number six.

And this case will actually show you how subjective this can be.

So what we have here, although less discrete than we saw in the previous biopsy, we have a terminal duct lobular unit that has expanded asini.

Upon closer inspection, similar to what we saw in the previous case, you can actually make out some vacuoles at this lower magnification.

And you can make out the relative lack of cohesion among the cells so you can see some spaces in between the epithelial cells.

Higher power magnification shows somewhat uniformity among the nuclei, but we do have a typical We have hyperchromasia, we have some pseudo-inclusions, we have some programmed cell death.

At this power you can make out more clearly the vacuoles within some of these epithelial cells causing compression of the nucleus.

You can also make out a distinct layer of cells that looks different than the the cells that are filling in the lumen.

These are likely myoepithelial cells.

Here is another E-cadherin stain, so this is negative.

And the diagnosis for this biopsy was lobular carcinoma in situ.

Now to my eye, the difference between the two cases is not that great.

I think either one could have been called atypical lobular hyperplasia or lobular carcinoma in situ.

This is case 7, and in this case you once again make out a terminal duct lobular unit, although this is less clearly defined to my eye compared to the previous cases.

But it's still an expansion of asinine that are relatively close to one another that you might consider to be a part of a single terminal duct lobular unit.

These are much more expanded than our previous cases, and there's variability to the extent of expansion.

On higher magnification you can see there is a greater degree of nuclear pleomorphism than we saw in our previous case.

Some of the nuclei are much larger than the others, so we have at least a several fold variation in nuclear size.

We also have prominent nucleoli throughout most of these cells.

They've got relatively abundant cytoplasm.

You can make out vacuoles, similar to our two previous cases within the cytoplasm, and evidence of discohesion among the cells.

Here is a higher power view, making out here the vacuoles within the cytoplasm.

Another view here showing the coarseness of the chromatin, the prominent nucleoli, and the variability in nuclear size and shape.

Again, see how the cells are pulling apart.

So there is a problem with cellular cohesion within this type of lesion.

And here is a focus of comedonecrosis.

E-cadherin was performed in this case, showing complete negative staining within the lesion.

So the diagnosis for this case, case 7, is pleomorphic lobular carcinoma in situ.

Lobular carcinoma in situ is a proliferation of small and generally loosely cohesive neoplastic epithelial cells within the terminal duct lobular units.

The difference between lobular carcinoma in situ and atypical lobular hyperplasia is basically the extent or the degree of involvement of the terminal duct lobular units.

Generally, LCIS and ALH are considered as generalized risk markers, and that's bilateral risk, and they are not generally considered to be direct invasive breast cancer precursors.

This is an example of lobular carcinoma in situ.

Essentially what you have is enlarged terminal duct lobular units that have expanded acini.

The page criteria for lobular carcinoma in situ is that at least 50% of the acini within these terminal duct lobular units is expanded by the atypical cells.

If it's less than 50% using the Page criteria, then you're best to classify it as atypical lobular hyperplasia.

Here is a closer view showing the asini that's expanded by the loosely cohesive population of cells.

And by that, what we refer to are these spaces that you can see in between the cells, unlike what we saw with ductal carcinoma in situ where you could see the cell membranes and there was cohesion between the cells.

Here it's more of a discohesive pattern.

The cells are atypical.

They're generally uniform, small round nuclei with hyperchromasia.

Here's another example.

Again, this is a terminal duct lobular unit.

These are acini, and greater than 50% of these acini are expanded by these atypical cells, qualifying this as lobular carcinoma in situ.

Lobular carcinoma in situ can be composed of two different cell types, so-called type A and type B cells.

This is an example here of type B cells, and they essentially consist of slightly more atypical epithelioid cells than you usually see with LCIS.

And they can be confused because of their atypical features and conspicuous nucleoli with pleomorphic LCIS.

But as we saw in the previous case, pleomorphic LCIS has a much greater degree of nuclear polyomorphism, with generally a two to three fold variation in nuclear size.

So although these look atypical with nucleoli, they lack that two to three fold variation.

These are type B cells.

This example shows the smaller central type A cells in comparison to the larger type B cells on the periphery.

Another consistent feature seen in both atypical lobular hyperplasia and lobular carcinoma in situ are these small cytoplasmic vacuoles within the cytoplasm of the atypical epithelial cells.

Pleomorphic lobular carcinoma in situ basically represents the high-grade form of lobular carcinoma in situ.

It is actually not very common, and when you see it, you're more likely to confuse it with ductal carcinoma in situ.

It retains this discohesive nature that you see within these lobular lesions, and what What makes it unique is the high-grade nuclei and the two- to three-fold nuclear variability.

Again, you'll also see prominent nuclei.

This is an example of pleomorphic lobular carcinoma in situ with comedonecrosis, calcifications, high-grade cells.

They easily can be confused with ductal carcinoma in situ, and in this case also a high mitotic rate.

Question, which of the following results is the most likely for classic lobular carcinoma in situ.

Is it going to be ER negative, PR positive, HER2 positive, ER positive, PR positive, HER2 negative, triple negative, or positive for all three?

Classic lobular carcinoma in situ is going to co-express ER and PR and will be negative for HER2.

The exception to the rule is pleomorphic lobular carcinoma in situ, which can be negative for ER and PR and can be positive for HER2.

Question, what protein generally shows absence of expression in atypical lobular hyperplasia and lobular carcinoma in situ?

100

Answer, E-cadherin.

101

Next question, what is the chromosomal location of the E-cadherin gene?

102

chromosome 6q22.1 and losses at 16q are a feature of LCIS.

103

16q loss may also be seen with flat epithelial atypia, atypical ductal hyperplasia, and DCIS.

104

Here's an example of E-cadherin immunohistochemistry here on the left, negative in LCIS, and then positive in the normal underlying ductal structures.

105

Question, you make a diagnosis of LCIS on a needle core biopsy.

106

What is the patient's risk of developing invasive carcinoma?

107

Answer, 8 to 10 fold increase in risk, which is similar to what we saw with low grade DCIS.

108

The next question is, which breast is at risk?

109

Is it the ipsilateral, contralateral, or bilateral breasts?

110

The answer is bilateral.

111

Some studies found that the ipsilateral breast may have slightly more risk in the first 5-10 years after diagnosis, but generally for the board examinations when you're dealing with LCIS lesions, the risk is considered to be bilateral.

112

Question.

113

The majority of invasive breast cancers that develop in women with LCIS are of what type?

114

Watch out for trick questions like this because the answer is invasive ductal carcinoma.

115

Classic LCIS is not generally considered to be a precursor to invasive carcinoma, but is rather a marker of risk, and again that risk is for the bilateral breasts.

116

These patients can develop invasive ductal carcinoma or invasive lobular carcinoma, but invasive ductal carcinoma is the most common.

117

The most appropriate management of these patients with classical LCIS is close observation with or without ER modulators such as tamoxifen.

118

Question true or false, assessment of margins is important for the management of patients with LCIS?

119

The answer, false.

120

See the previous comments.

121

Again, this is a marker of risk and not a direct precursor of invasive carcinoma.

122

True or false, pleomorphic LCIS may behave more like DCIS?

123

are true, these lesions should be excised with negative margins in a manner similar to DCIS.

124

And the same is also suggested for cases of LCIS with comedonecrosis.

125

So essentially you treat these as if they're DCIS.

126

You found this on a breast biopsy.

127

Your immunohistochemistry lab is on strike, so what is the diagnosis?

128

Here's a closer view.

129

So you have expansion of a terminal duct lobular unit as well as the acini and greater than 50% of the acini within the terminal duct lobular unit.

130

On close examination, you do have some of these cribriform-like structures.

131

Notice what's missing.

132

You're missing that discohesive pattern and you're also missing those cytoplasmic vacuoles.

133

So the diagnosis is DCIS involving terminal duct lobular units.

134

Polarization of these cells at the periphery is a feature of DCIS, so that was one clue.

135

And microasini, or these cribriform-like structures, is also another feature of DCIS.

136

And again, in terms of pertinent negatives, the lack of discohesive properties and the lack of setoplasmic vacuoles all point towards ductal carcinoma in situ.

137

So this completes cases 5 through 7.

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 5 through 7 - Learn English Speaking with Video

About This Lesson

Key Vocabulary & Phrases

Practice Tips

Wat is de Shadowing-techniek?