Shadowing Practice: Lymphoma - Learn English Speaking with Video

In this video, I will explain almost everything that you need to know about lymphomas.

So, as a brief overview, lymphomas are a heterogeneous group of malignancies that arise from clonal perforation of B cells,

T cells, and K cells at various stages of maturation.

Not to make it sound stupid or to dumb it down too much, but lymphocyte cancers equal lymphomas.

And so, if you understand the basic immunology and physiology of a lymphocyte,

it makes understanding lymphomas much more easy to understand.

So, I would encourage you, before you view this video, make sure that you understand the basics about all your different types of lymphocytes.

Now, lymphomas may arise from lymph nodes or extranodal tissue.

Non-Hodgkin lymphomas are much more common than Hodgkin lymphoma.

And if this is your first time learning about lymphomas, settle down because we will talk about the difference and the different types of lymphomas that fall into different categories.

So don't worry about this distinction just yet.

Note though that lymphomas arise most commonly from chromosomal translocations and or associations with various infections and more on that to come.

So broadly, when we talk about lymphoma, we separate them into two categories.

One category shown on the left is Hodgkin lymphoma or HL.

The other category shown on the right is non-Hodgkin lymphoma or NHL.

And this distinction is made pretty much by the presence of something called a Reed-Sternberg cell.

So, if there's a Reed-Sternberg cell, you're dealing with a Hodgkin lymphoma.

If there's no Reed-Sternberg cell, and alternatively, if you're mostly looking at lymphoid cells, then you're dealing with a non-Hodgkin lymphoma.

Reed-Sternberg cells are very important to know what they look like.

You will see this image either on your in-class exams or on step one or level one.

These are large binucleate, sometimes referred to as,

quote, allied giant lymphocytes that have eosinophilic nuclei and a lot of cytoplasm.

So stare at this image, burn this image into your brain.

This is a Reed Sternberg cell.

You have to know what this looks like because if the test writer shows you this picture, you have to infer that you're dealing with a type of Hodgkin lymphoma.

So when it comes to Hodgkin lymphoma, there are both classical and non-classical subtypes of Hodgkin lymphoma.

When it comes to non-Hodgkin lymphoma, we generally separate these into B-cell and T-cell non-Hodgkin lymphoma.

Now I want to pause for a second.

If you're watching this video because you are taking USMLE or Comlex,

the majority, I I would say 90% or more of your questions will come from the right hand part of this slide.

You need to know the non-Hodgkin lymphoma.

The B-cell non-Hodgkin lymphomas include Burkitt lymphoma, diffuse large B-cell lymphoma, follicular lymphoma,

mantle cell lymphoma, marginal zone lymphoma, and primary CNS lymphoma.

The T-cell non-Hodgkin lymphoma includes adult T-cell lymphoma and mycosis fungoides.

If you're watching this video, again, solely because you want to do well on step one or level one, this is what you need to understand.

And I'm not even going to bother talking about the different types of Hodgkin lymphoma, although I will type them out for completeness sake.

So this video will focus on the right hand part, the non-Hodgkin lymphomas, because that is 90%,

if not more, of all of the questions that you'll get on step one or level one.

So, let's go through these one at a time.

We'll talk about all the different types of non-Hodgkin lymphomas, and then at the end of this video, I'll talk about the clinical presentation,

the difference between Hodgkin and non-Hodgkin clinically, and then some associated syndromes that you need to know for USMLE and COMLEX.

So we'll begin with Burkitt lymphoma.

This is more common in children and young adults.

It is due to a chromosomal translocation 814.

This is a reciprocal translocation where the CMYK gene on eight and the heavy chain IG locus on 14 are involved.

So what happens here is after this translocation, you have increased activity of CMYK,

which is a proto-oncogene that increases transcription factors, which increases transcription.

So you have an increase in aerobic glycolysis and subsequent cell growth.

And that's how this cancer forms.

You have increased cell growth.

Now, Burkitt lymphoma is divided into several subtypes.

You have endemic, sporadic, and immunodeficiency.

On your exam, the one that you want to know is endemic.

This is associated with EBV.

It occurs most often in Africa and South America.

It classically involves the maxillary and mandibular area.

And this occurs predominantly in areas where there is malaria.

And what happens here is that malaria decreases one's resistance to EBV, and therefore EBV is associated with Burkitt lymphoma.

Know for completeness sake, of course, that we have a sporadic subtype where the abdomen and pelvis is involved.

This actually is the most common subtype, but on your exam, chances are the exam writer is going to go after endemic, and I'll tell you why in just a moment.

And then lastly, there's an immunodeficiency subtype, which is associated with HIV and patients who are post-transplant.

Again, if you're just taking USMLE or Comlex, you got to know endemic.

And the reason you need to know that is because the maxillary

and mandibular involvement has a classical image that looks like this.

So if you see this image, you have to know Burkitt lymphoma.

This image equals Burkitt lymphoma.

So again, if you're looking at this slide, endemic, highest yield, second highest yield,

immunodeficiency, third highest yield, which interestingly enough happens to be the most common, but on exams, not that important.

So what I want you to take away so far, Burkitt lymphoma equals 814 translocation,

increased activity of CMYK, endemic subtype associated with EBV in areas of the world where malaria is present

because that decreases one's resistance to EBV.

And this image equals Burkitt lymphoma because this is the endemic subtype that involves the face.

Now histologically you're going to see something called a starry sky pattern and this has become quite a hot buzzword.

If you see starry sky, the answer is Burkitt lymphoma.

Now the description that you could see are tangible body-laden macrophages with phagocytized tumor cells that may or may not show up,

but starry sky is the buzzword that gets thrown around all the time.

So know that that equals Burkitt lymphoma.

Now there are two mnemonics that I can offer you that might help you on your exam.

When I think Burkitt lymphoma, I think Burk-8 lymphoma instead of Burk-it.

So Burk-it, Burk-8.

And that cues my brain that I'm dealing with an 814 chromosomal translocation because unfortunately,

sometimes the exam writer wants you to pick the chromosomal translocation associated with whatever lymphoma they're describing.

And because you have all of these translocations, as you'll see as I go through this video, it's kind of difficult to memorize.

Luckily, I have a mnemonic for almost all of these.

And then lastly, you can remember the E's with Burkitt lymphoma.

E for endemic, E associated with EBV, and E for eating, which reminds me of that facial involvement.

E, endemic, EBV, eating.

The most important thing from this slide again though is Burkate lymphoma, 8, 814, translocation.

Now let's talk about diffuse large B-cell lymphoma.

This is most common, this is the most common non-Hodgkin lymphoma in adults.

And this one is the one where you don't need to memorize a chromosomal translocation

because it's due to a mutation in BCL2, BCL8, and P53.

Now just recall, we won't go too deep into this, but recall that BCL2 is a proto-oncogene gene that is involved in apoptosis regulation.

BCL-6 is a transcriptional repressor that regulates cell maturation.

And P53 is a tumor suppressor gene.

So when you mutate these things, obviously, you're going to affect cell function, cell division, cell regulation.

And when you have that at an unchecked level, you get cancer.

And that's what you're dealing with here.

Now, luckily, there's not a whole lot you need to memorize for exams.

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When I think DLBL for diffuse large B-cell lymphoma, DLBL, that kind of sounds like BCL.

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There's a lot of L's and B's and it doesn't rhyme, but it almost rhymes.

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DLBL, BCL.

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And that just, you know, in my brain makes the association that with DLBL, we're dealing with things like BCL2 and BCL6.

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And if you can take that one step further, perhaps you can memorize P53.

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But if that doesn't seem worthwhile to memorize, you know, if you're cramped for brain space, or you're just like, dude,

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I can't memorize anything that I don't 100% need to know that's super high yield, then just move right on to follicular lymphoma.

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Follicular lymphoma is the most common low-grade B-cell lymphoma.

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It is due to a chromosomal translocation between 14 and 18.

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So you have the heavy chain IG on 14 and BCL2 on 18.

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And what happens is when you translocate, then you have BCL2 increasing or overexpressing its product.

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And when that happens, you have decreased apoptosis, which prolongs cell survival.

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Anytime you pathologically prolong cell survival, you get subsequent malignant progression.

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So that's follicular lymphoma.

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Now, histologically, you need to know that there's going to be the presence of something called centricites.

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These centricites have small cleaved nuclei.

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Occasionally, they might really throw you a curveball and give you a centroblast.

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Centroblasts are large lymphocytes, but do not have the cleaving.

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So if you see either of these terminologies, centrocyte or centroblast, think follicular lymphoma.

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If you see small cleaved nuclei, think follicular lymphoma.

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Now, when I think of follicular lymphoma, the way that I've always memorized 14-18 translocation is follicular 14.

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14 begins with F, follicular 14.

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Keep it simple because this is the only translocation where the first number in the translocation is 14.

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Now let's talk about mantle cell lymphoma.

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This is most common in adult males, and this is due to a chromosomal translocation between 11 and 14.

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Pause for a second.

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I just told you in follicular lymphoma, no other translocation had 14 as the first number, but here you see 14 as the second number.

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So just keep that straight in your brain.

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This involves cyclin D1 on 11 and the heavy chain IG on 14.

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When you increase the activity pathologically of cyclin D1,

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you increase replication because you're essentially going through into S phase more than you should.

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This increases cell proliferation, and we have pathological malignant progression.

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Now, usually when it comes to mantle cell lymphoma,

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this spreads pretty rapidly, so it unfortunately generally gets diagnosed when it's already reached an advanced stage.

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But for USMLE or COMLEX, you really just need to know the chromosomal translocation, not a whole lot of other high yield details.

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That's mantle cell lymphoma.

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I have a mnemonic for you, but we'll come back to it after we talk about marginal zone lymphoma.

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So marginal zone lymphoma is due to a chromosomal translocation between 11 and 18.

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Now, occasionally they'll write out something after the 1118 translocation

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and it might say q21 q21 don't worry about

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that this is an 1118 translocation that's what you need to know

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if you're studying for boards now marginal zone lymphoma is very high yield

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because it is associated with autoimmune inflammation

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and something called a gastric malt lymphoma now this confuses medical students

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so let's just say what malt is malt m-a-l-t stands for mucosa associated lymphoid tissue

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and basically in certain mucosal tissues there's this submucosal lining and

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that that material is actually lymphoid it serves a lymph function

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and so in this instance gastric malt lymphoma is a lymphoma specifically associated

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with that mucosal associated lymphoid tissue in the stomach so

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because of that it is highly associated with h pylori gastritis

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so in patients who have h pylori infections

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and h pylori gastritis there's some connection between that inflammation and

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that malt tissue becoming cancerous

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and the important thing to know is one there's the simple

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association where gastric lymphoma is a type of marginal zone lymphoma and it's associated with H pylori, but what's high yield to know,

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especially if you're taking step two, level two and beyond, is that this lymphoma actually may remit if the H pylori is treated.

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So that's high yield for step two, level two, and beyond.

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For step one, level one, just know that gastric malt lymphoma is a subtype of marginal zone lymphoma in

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that mucosa-associated lymphoid tissue in the stomach connected somehow to H pylori inflammation.

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As far as the autoimmune association goes, marginal zone lymphoma is associated with Hashimoto thyroiditis and Sjogren's syndrome.

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So this is a really tricky opportunity where the test writer can start you off on a question

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that maybe gives you labs or buzzwords that have to do with thyroiditis or Sjogren.

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And then they'll ask you which of the following is the patient at increased risk for?

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And the answer is going to be marginal zone lymphoma.

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So you're going to have to connect lymphoma with these and more endocrine rheumatological diseases.

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Now the mnemonic for both marginal and mantle, because if we go back to mantle,

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mantle starts the chromosomal translocation starts with 11 and in marginal it also starts with 11.

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These are the only two translocations that begin with 11.

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And so what I want you to think about when you think about 11 is if you've ever seen stranger things.

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There's a character named Eleven, and Eleven is played by Millie Bobby Brown.

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Millie beginning with M, so both mantle and marginal begin with M.

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Both mantle and marginal begin with Eleven in their translocation.

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So I associate Millie the M in Millie Bobby Brown with the character that she plays Eleven and the two chromosomal translocations.

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Now let's talk about primary CNS lymphoma.

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And I want to point out that depending on the textbook

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that you read or the lecturer that teaches you at your school,

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this technically is a subtype of diffuse large B-cell lymphoma,

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but it kind of gets carved out because it's its own thing.

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So what you need to know for your exams is that primary CNS lymphoma is associated with EBV and HIV AIDS.

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Now EBV infection may be required for pathogenesis in immunocompromised individuals.

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So it's not like it's associated necessarily with one or the other.

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It is highly associated with both EBV and HIV AIDS almost concurrently.

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And what you see here is a neuropsychiatric presentation.

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That is important to know.

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What I think is even more high yield for USMLE or COMLEX is being able to do a differential diagnosis between toxoplasmosis,

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CNS lymphoma, abscess, and metastasis.

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And I've tried as best as I can to simplify this for you, but admittedly, it's not an exact science and the test writer is going to try to trick you.

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But when it comes to looking at these differentials,

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the reason that you need to know this is because these all cause ring enhancing lesions in the brain.

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So you're going to be taking your exam.

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They're going to give you the results of imaging, and there's going to be one or more ring enhancing lesions.

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And then they're going to ask you which of the following is responsible for this presentation.

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And all four of these things are going to be potential answer choices.

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And so how you can think about this, and again, not an exact science, so this isn't a 100% way to get this correct.

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But in general, you can think about someone's immunocompromised or not status and then other associations.

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So with CNS lymphoma, chances are on the exam, the patient's going to be immunocompromised because again, it's associated with HIV AIDS.

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There is a chance that they will give you a patient with autoimmune disease.

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And if the test writer really wants you to pick CNS lymphoma, they're going to tell you that the patient was tried on treatment for toxoplasmosis,

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but failed that treatment.

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Some people think that when it's a solitary or single ring enhancing lesion, that the answer is CNS lymphoma.

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And that's not really helpful on exams anymore because they can give you one and it could still be an answer choice.

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That's not CNS lymphoma, or they could give you multiple and you just don't know.

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Toxoplasmosis chances are on the exam, the patient will be immunocompromised because that's associated with HIV AIDS.

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On the exam, if the test writer wants you to pick toxo,

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they're very likely going to give you associated risk factors or exposures to things like cat feces, raw meat, or goat's milk.

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So your classic buzzwords associated with toxo.

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They don't have to, but generally they do.

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If the test writer wants you to pick an abscess, you can't go by the immunostatus because the patient could be immunocompromised or immunocompetent,

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what they will give you in most instances is

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that the patient had a recent infection

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and it's the entry of the pathogen through that infectious route that leads eventually to the abscess.

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Lastly, for metastasis, chances are on the exam, the patient will be immunocompetent.

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So they're not, they're very unlikely to have HIV AIDS on your exam.

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And if If they want you to pick metastasis on the exam, they will either give you that there are multiple ring enhancing lesions.

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Although again, solitary versus multiple doesn't really necessarily tell you metastasis, but metastasis is usually multiple lesions.

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And usually they will either give you the cancer history or insinuate very strongly that the patient has a history of cancer.

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So again, not a complete science, but as far as differentiating CNS lymphoma versus toxo versus abscess versus metastasis.

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This is a very broad way to conceptualize this.

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Now let's talk about mycosis fungoides.

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So to be clear, we've talked about the B-cell lymphomas, and now we're moving into the few T-cell lymphomas that you need to know.

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Mycosis fungoides is the most common low-grade T-cell lymphoma.

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It involves malignant CD4 plus T-cell infiltration of the skin.

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So because of that, the clinical presentation is pretty unique.

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You see patches, plaques, and nodules.

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So a lot of dermatological findings.

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And what you will see described are cesare cells.

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Now cesare cells, you see an image here, they have cerebriform nuclei.

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That is a very hot buzzword.

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Don't worry about the term cesare cell, no cerebriform nuclei.

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You can also see So basically that is a fancy way of saying that in the epidermis,

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there's aggregations of cells and those are called, I may be butchering the pronunciation here, potriae micro abscesses.

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If mycosis fungoides involves the blood, it is termed Cesare syndrome.

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So that is a leukemic form of mycosis fungoides.

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So high yield to know that this T cell lymphoma has, it basically can be leukemia because it can involve the blood.

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It can progress to that form.

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Now let's wrap up by talking about adult T cell lymphoma.

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So this is neoplastic proliferation of mature CD4 plus T cells.

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What you need to know when it comes to adult T cell lymphoma are its associations with HTLV-1 and IV drug abuse.

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That's really important to know.

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On your exam, if the test writer is going to give you a vignette or a presentation with adult T cell lymphoma,

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they'll give you either the HTLV-1 or a history of IV drug abuse, and then they'll give you some labs and clinical findings.

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The labs will be an elevated lactate dehydrogenase, elevated calcium level, and all the symptoms that come with that,

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hepatosplenomegaly, and of course, because we're dealing with lymphoma, likely they'll give you lymph adenopathy.

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So know the elevated calcium and the elevated LDH.

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Of course, know all of your symptoms of hypercalcemia, in particular, those lytic or punched out lesions.

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Now, we've just gone through a number of different lymphomas this

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is sort of the summary of how this looks clinically

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so clinically you really can't distinguish hodgkin versus non-hodgkin lymphomas on the basis of symptoms

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because generally these present with what are known as b symptoms

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fever night sweats unintentional weight loss where you can differentiate these are what you see in age cells spread

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and associations so in age Hodgkin lymphoma tends to be more bimodal

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so young adults and those age 55

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and older whereas non-Hodgkin lymphoma on your exam it's very likely the patient will be 55

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or older but the risk increases with age the cells we already talked about really high yield to know

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that Hodgkin you see Reed Sternberg cells non-Hodgkin you see lymphoid cells spread This is one

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that can really help you get the answer correct

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if the test writer describes clinical findings or physical exam findings or nodal findings.

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And when I say nodal findings, I mean what lymph nodes are involved and where are they located on the body.

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So in Hodgkin lymphoma, it's more localized.

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The spread is contiguous, so it's kind of node to local node, and the prognosis is better.

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In non-Hodgkin lymphoma, it tends to be more extranodal.

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It's non-contiguous, so it's not really localized, and for these reasons, the prognosis is worse.

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Associations, Hodgkin tends to be more associated with immunosuppression and EBV,

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although clearly, we've talked about immunosuppression and EBV in non-Hodgkin, so this is one that you can't really go off this to get the answer correct.

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In non-Hodgkin, we're dealing with chromosomal translocations, very high yield, as I pointed out, autoimmunity, and not only EBV,

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but also things like HTLV1 and HIV.

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This is your high yield clinical summary.

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Now, I want to finish this video by talking about some associated clinical syndromes.

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These include tumor lysis syndrome and superior vena cava syndrome.

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And so on your exam, the test rater might give you findings of these syndromes because these syndromes are associated with lymphomas.

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Now, to be clear, it's not just limited to lymphomas these findings, these syndromes are also associated with other malignancies,

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but I'll include them here because they do tend to show up

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and they can get lumped in with the big package of symptoms that you'll get on your exam.

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So tumor lysis syndrome is a syndrome that occurs after cytotoxic tumor cell destruction.

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So let's just simplify this.

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You've got a tumor cell, the patient gets treated, the tumor cell explodes and it releases its intracellular components.

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It is the release of those intracellular components that causes tumor lysis syndrome.

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The big three are phosphate, potassium, and nucleic acids.

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Now, with an increased phosphate, phosphate will bind up all the free calcium and cause calcium phosphate crystals.

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With potassium, increased levels of potassium alter the resting membrane potential, which can cause cardiac arrhythmia.

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And with nucleic acids, these get converted to uric acid, which causes hyperuricemia.

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Now, what you'll see on your exam, of course, on the left here, we've got our lab findings.

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And on the right, we have some associated clinical features.

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On the left, we deal, like I said, increased levels of phosphate, increased potassium, increased nucleic acids,

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and by extension, increased uric acid, and decreased free calcium.

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Again, that phosphate binds up the calcium, so you actually get hypocalcemia if you're looking at labs.

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This can present very heterogeneously, so it's not just these symptoms, but I've included the big six, so to say.

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So you could see cardiac arrhythmias from your elevated potassium.

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Because of your calcium, you could see tetany, trosteic sign, trousseau sign.

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You could have seizures and because of various pathways that ultimately cause kidney injury,

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right, hyperuricemia and calcium phosphate crystals, you get obstructive uropathy.

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So these are things you want to look for on your exam.

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Each of these clinical findings will have third order findings and third order symptoms.

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So tumor lysis syndrome, it's really a big thing that they could go after on USMLE or COMLEX.

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Lastly, we have superior vena cava syndrome.

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So as the name implies, this is a syndrome that occurs when the SVC is blocked or congested because the malignancy,

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the cancer is locally kind of either pushing on that area

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or metastasizing to that area or involving the blood flow through that area.

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And so what you see are symptoms where you have decreased flow in that region.

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So things like upper extremity and facial edema, jugular venous distension, orthostatic hypotension.

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You can get neurological symptoms, including headache, difficulty with vision,

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altered mental status, and things like renal failure and a host of ENT symptoms.

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If you're looking at this now, I think tumor lysis syndrome is a lot more high yield than SVC syndrome, but both of these, again,

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can be associated with lymphoma and other malignancies.

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So that was a pretty long one.

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A lot of good information that I think you should know for your exams.

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Know the chromosomal translocations.

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Know what a Reed-Sternberg cell looks like.

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Know some of the more buzzy words in there.

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But that is lymphoma.

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Who Is This Video For?

This video is perfect for English learners ready to level up their english speaking practice while exploring academic topics. Whether you’re prepping for IELTS speaking practice or just want to sound more confident discussing complex ideas, the clear, conversational tone makes it ideal. It’s great for intermediate learners who want to mix science knowledge with language growth—you’ll pick up medical terms *and* everyday phrases that work in any conversation.

Words & Idioms Worth Stealing

Boost your vocabulary with standout phrases from the video:

"Heterogeneous group" – A mix of different types (great for describing categories in essays or speeches).
"Burn this image into your brain" – Remember something deeply (casual, impactful for everyday use).
"Settle down" – Relax, don’t worry (perfect for calming someone or staying calm yourself).
"Reciprocal translocation" – A specific scientific term, but the structure "reciprocal [noun]" works in other contexts (e.g., "reciprocal agreement").

These phrases add depth to your speech and work in both casual and formal settings—steal them for your next shadow speak session!

How to Get the Accent Right

The speaker uses a clear, instructional tone with natural pauses—ideal for shadowspeak practice. Focus on:

Stress on key terms: Words like "lymphomas," "Reed-Sternberg," and "translocation" get extra emphasis. Copy this to make your speech more engaging.
Rhythm of explanations: Notice how the speaker slows down for complex ideas ("So, if there's a Reed-Sternberg cell...") and speeds up for simpler points. Mimic this to sound more natural.
Casual contractions: "Don’t worry," "it’s" – these make your speech flow. Avoid over-pronouncing; keep it relaxed, like you’re chatting with a friend.

Practice repeating short sections—you’ll improve your pronunciation *and* learn to explain tricky topics clearly. It’s a win-win for learn english with videos!

Grammar in this video

The structures the speaker uses most, with the exact words from the video:

Structure	In the video
Present perfect have/has + past participle — a past action that still matters now	have increased · has become · have decreased
Passive voice be + past participle — the focus is on what happens, not who does it	is made · are involved · is divided
Relative clauses who / which + clause — extra information about a person or thing	subtype, which is · potential, which can

What is the Shadowing Technique?

Shadowing is a science-backed language learning technique originally developed for professional interpreter training and popularized by polyglot Dr. Alexander Arguelles. The method is simple but powerful: you listen to native English audio and immediately repeat it out loud — like a shadow following the speaker with just a 1–2 second delay. Unlike passive listening or grammar drills, shadowing forces your brain and mouth muscles to simultaneously process and reproduce real speech patterns. Research shows it significantly improves pronunciation accuracy, intonation, rhythm, connected speech, listening comprehension, and speaking fluency — making it one of the most effective methods for IELTS Speaking preparation and real-world English communication.

Shadowing technique: read the full step-by-step guide →

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