Lymphomas and Leukemias??

[NRAI2001]

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I have an immuno final on Monday and I m still confused about a few tumor related concepts.

What is the differences between a leukemia vs lymphoma?

What is the difference between a acute leukemia vs a chronic leukemia?

What are the differences between a Hodgkins Lymphoma vs a non-Hodgkinds Lymphoma?

Our notes are decent overall but arent too great when it comes to explaining these topics. Wikipedia doesnt really explain the differences too well either.

THanks👍

 

[NRAI2001]

All I could decipher so far as the difference between a leukemia and lymphoma is that

-leukemia = progenitor cells & pre-b cell neoplasms
-lymphoma = mature b cell neoplasms

Any explanation to why this occurs or the significance of this?

Does BRS have an explanation?

Thanks!

 

[Water011]

Leukemia is when you have malignant proliferation of white blood cells in the blood, and lymphoma is when you have malignant proliferation of the same types of cells but in solid tissue, like lymph nodes. So they are basically the same thing, but they are in different places.

Just think of a lymphoma as a solid version of a leukemia.

There are a lot of differences between Hodgkin's vs. Non-Hodgkin's lymphomas. Like, Hodgkin's is just B cell proliferation, and Non-Hodgkin can involve B, T, or NK cells. And Non-Hodgkin's is more disseminated when it presents and found in a wide age range but mostly older people. Hodgkin's is found in younger people. They are just different diseases.

I try to remember to just think of Non-Hodgkin lymphomas as any lymphoma that isn't Hodgkins. I know that sounds really obvious, but Non-Hodgkin's lymphoma not just one disease, even though it may seem like that when people talk about it. For instance, a follicular center lymphoma is a Non-Hodgkin's, but so is a diffuse large B-cell lymphoma and a peripheral T cell lymphoma. And there are subtypes of Hodgkin's lymphoma, too. Does that make sense? I can't really list all the differences here because there are too many, and I don't know all of them, but they are just totally different diseases.

And, yeah, I would think BRS has better info in it than what I just wrote. I just wrote that from what I remember, and that information is not a full explanation, obviously. Do you have Robbin's? It has good information in it.

As for the maturity of the cells, I don't remember every detail about that stuff, but that has more to do with the different subtypes of the different leukemias and lymphomas. Some are well-differentiated, some are poorly differentiated, etc. It gets confusing.

 

[psipsina]

You could read about it in the hematology chapter of big Robbins if you have it which would probably clear things up for you.

 

[NRAI2001]

Leukemia is when you have malignant proliferation of white blood cells in the blood, and lymphoma is when you have malignant proliferation of the same types of cells but in solid tissue, like lymph nodes. So they are basically the same thing, but they are in different places.

Just think of a lymphoma as a solid version of a leukemia.

There are a lot of differences between Hodgkin's vs. Non-Hodgkin's lymphomas. Like, Hodgkin's is just B cell proliferation, and Non-Hodgkin can involve B, T, or NK cells. And Non-Hodgkin's is more disseminated when it presents and found in a wide age range but mostly older people. Hodgkin's is found in younger people. They are just different diseases.

I try to remember to just think of Non-Hodgkin lymphomas as any lymphoma that isn't Hodgkins. I know that sounds really obvious, but Non-Hodgkin's lymphoma not just one disease, even though it may seem like that when people talk about it. For instance, a follicular center lymphoma is a Non-Hodgkin's, but so is a diffuse large B-cell lymphoma and a peripheral T cell lymphoma. And there are subtypes of Hodgkin's lymphoma, too. Does that make sense? I can't really list all the differences here because there are too many, and I don't know all of them, but they are just totally different diseases.

And, yeah, I would think BRS has better info in it than what I just wrote. I just wrote that from what I remember, and that information is not a full explanation, obviously. Do you have Robbin's? It has good information in it.

As for the maturity of the cells, I don't remember every detail about that stuff, but that has more to do with the different subtypes of the different leukemias and lymphomas. Some are well-differentiated, some are poorly differentiated, etc. It gets confusing.

Thanks for the great reply👍

I havent taken path yet so I dont have robbins... this is an immunology course that I suppose will prep us for path next term. I dont think we are expected to know about leukemias and lymphomas to any great degree just yet, more of just know some of the more defining characteristics of each as an intro (I suppose the prof took this attitude too far and didnt really give much of an explanation at all besides that there exists two major categories of lymphoma).

I understand that a non-hodgkins lymphoma is any lymphoma that isnt hodgkins; so what actually defines a hodgkins lyphoma?

The notes dont define either, but a review sheet I got from a friend summarized each as:

Hodgkins lymphoma: lymphoid tumor, swollen lymph nodes and fever
Non-hodgkins lymphoma: nonspecific lymphoid tumor, low cd4+ count (as opposed to high cd4+ count in hodgkins lymphoma i guess???)

and thats all i got so far..?

 

[IHeartNerds]

The classic form of Hodgkins Lymphoma contains the Reed-Sternberg cell, which is a germinal center B cell of malignant behavior. You then see a reactive layer of cells as a "background" that are not malignant. However, it is not easily found in all forms of HL.

 

[Depakote]

The classic form of Hodgkins Lymphoma contains the Reed-Sternberg cell, which is a germinal center B cell of malignant behavior. You then see a reactive layer of cells as a "background" that are not malignant. However, it is not easily found in all forms of HL.

That was the only differentiating factor I had to know for Immuno... I'm sure I'll get a lot more detail when we get to hematology.

 

[Depakote]

Lymphoma- Solid B-Cell tumor- this can be anywhere you have a lymph node
Leukemia- disseminated blood borne tumor (usually a monoclonal expansion of a progenitor cell)
Myeloma- Tumor of a plasma cell clone. (distinct characteristic is you get a single Ab clone in disproportionate numbers)

 

[Depakote]

Acute leukemia hits hard and fast. You patients present acutely and will die quickly without treatment. Chronic leukemia can fester for years with only some minor hematologic abnormalities before it gets out of control.

Acute leukemias follow your typical cancer path, they're the result of multiple gene deletions leading to uncontrolled cell growth.

Your best example of a chronic leukemia is CML. The majority of patients with CML have a translocation of the philadelphia chromosome t(9:22). This single abnormality constituitively activates cell growth and division. It's less sporadic and while it does cause an increase in certain WBC populations, in the chronic phase it doesn't hijack the immune system to the degree that AML or ALL does.

 

[NRAI2001]

Acute leukemia hits hard and fast. You patients present acutely and will die quickly without treatment. Chronic leukemia can fester for years with only some minor hematologic abnormalities before it gets out of control.

Acute leukemias follow your typical cancer path, they're the result of multiple gene deletions leading to uncontrolled cell growth.

Your best example of a chronic leukemia is CML. The majority of patients with CML have a translocation of the philadelphia chromosome t(9:22). This single abnormality constituitively activates cell growth and division. It's less sporadic and while it does cause an increase in certain WBC populations, in the chronic phase it doesn't hijack the immune system to the degree that AML or ALL does.

Thanks👍

 

[NRAI2001]

Lymphoma- Solid B-Cell tumor- this can be anywhere you have a lymph node
Leukemia- disseminated blood borne tumor (usually a monoclonal expansion of a progenitor cell)
Myeloma- Tumor of a plasma cell clone. (distinct characteristic is you get a single Ab clone in disproportionate numbers)

👍

Are leukemias and lyphomas restricted to B cells? What about T-cells?

 

[silas2642]

👍

Are leukemias and lyphomas restricted to B cells? What about T-cells?

Seem to usually hit the B cells-- can hit the T cells as well, but more likely to affect the B cells. When you are differentiating the cancers always start off by asking yourself whether or not the disease is of the myeloid lineage or the lymphoid lineage, then ask yourself if it is chronic or acute. Chronic or acute actually (according to our heme/onc professor) refers to where the cell is in terms of hematopoietic differentiation. It used to refer to how long the patients lived, but with the changing therapies, it now refers to the cellular morphology.

The chronic lymphomas/leukemias are in their terminal stages of differentiation and look pretty much like mature lymphoid cells while the acute lymphomas/leukemias look like very immature progenitor cells.

Hope that made sense. Good luck on your final.

 

[NRAI2001]

So when you have autoimmune and inflammation diseases Th2 cytokines are often give as treatment..with a B-cell lymphoma/leukeima/myeloma can Th1 cytokines be given as a treatment? Or would this likely lead to increased incidence of autoimmunity?

As I was trying to understand the diffrenes between the Th1 pathway and Th2 pathways I kinda made an analogy back to neuro and physio for myself. The Th1 pathway is like the sympathetic pathway and is activated in times of need and it being activated chronically can lead to disease(autoimmunity and inflammation) as does chronic symph activation (cardiac hypertrophy, hypertension, edema, muscle decay..etc) so the parasymp kicks in once the need for sympathetic response is gone. Is it fair to make an analogy of this "rest/recoup" function of parasymp to the Th2 pathway? It doesnt seem as though the Th2 pathway has any real use in an infection situation other than to create plasma cells and memory b cells in preparation for the next infection as does the parasymp store energy for the next symp situation?? Is the major function of Th2 pathway to hault the Th1 pathway?

 

[mercaptovizadeh]

So when you have autoimmune and inflammation diseases Th2 cytokines are often give as treatment..with a B-cell lymphoma/leukeima/myeloma can Th1 cytokines be given as a treatment? Or would this likely lead to increased incidence of autoimmunity?

As I was trying to understand the diffrenes between the Th1 pathway and Th2 pathways I kinda made an analogy back to neuro and physio for myself. The Th1 pathway is like the sympathetic pathway and is activated in times of need and it being activated chronically can lead to disease(autoimmunity and inflammation) as does chronic symph activation (cardiac hypertrophy, hypertension, edema, muscle decay..etc) so the parasymp kicks in once the need for sympathetic response is gone. Is it fair to make an analogy of this "rest/recoup" function of parasymp to the Th2 pathway? It doesnt seem as though the Th2 pathway has any real use in an infection situation other than to create plasma cells and memory b cells in preparation for the next infection as does the parasymp store energy for the next symp situation?? Is the major function of Th2 pathway to hault the Th1 pathway?

No. The B-cell/plasma cell function is dysregulated internally and is unlikely to respond to something so "gentle" as a shift to Th1.

Th1 and Th2 counteract each other. Th1 promotes the cellular immune response whereas Th2 promotes the humoral immune response. Practically speaking, this means that Th1 is more useful in infections in which cellular immunity is the more important means of pathogen clearance, such as viral infections or mycobacterium tuberculosis infection. Th2 is more useful in infections in which the humoral response is the more important means of pathogen clearance, such as many extracellular bacterial infections, parasitic infections, and indeed viruses. Of course, most infections will involve both kinds of responses since this will provide for optimal clearance.

Note that Th2 is not "protective" in the autoimmune/hypersensitive sense. For instance, asthma, allergies, lupus, Graves' disease, pemphigus, and myasthenia gravis would be more Th2. Type 1 diabetes, DTH, and multiple sclerosis would be more Th1.

Note the interesting case of leprosy. If the response is more Th1, the infection is far better controlled and this is called lepromatous leprosy. If the response is more Th2, the infection is much more rampant and this is called tuberculoid leprosy. Clearly, mycobacterium leprae is better combatted by a Th1 response.

 

[NRAI2001]

No. The B-cell/plasma cell function is dysregulated internally and is unlikely to respond to something so "gentle" as a shift to Th1.

Th1 and Th2 counteract each other. Th1 promotes the cellular immune response whereas Th2 promotes the humoral immune response. Practically speaking, this means that Th1 is more useful in infections in which cellular immunity is the more important means of pathogen clearance, such as viral infections or mycobacterium tuberculosis infection. Th2 is more useful in infections in which the humoral response is the more important means of pathogen clearance, such as many extracellular bacterial infections, parasitic infections, and indeed viruses. Of course, most infections will involve both kinds of responses since this will provide for optimal clearance.

Note that Th2 is not "protective" in the autoimmune/hypersensitive sense. For instance, asthma, allergies, lupus, Graves' disease, pemphigus, and myasthenia gravis would be more Th2. Type 1 diabetes, DTH, and multiple sclerosis would be more Th1.

Note the interesting case of leprosy. If the response is more Th1, the infection is far better controlled and this is called lepromatous leprosy. If the response is more Th2, the infection is much more rampant and this is called tuberculoid leprosy. Clearly, mycobacterium leprae is better combatted by a Th1 response.

The humoral response is dependent upon past exposure and a past TH1 response.. so in a sense isnt the humoral response really just preparation for the next infection which was originally cleared??

Good point with the TH2 response and parasitic, extracellular infections.

 

[mercaptovizadeh]

The humoral response is dependent upon past exposure and a past TH1 response.. so in a sense isnt the humoral response really just preparation for the next infection which was originally cleared??

Good point with the TH2 response and parasitic, extracellular infections.

Not really. The humoral response depends on T helper cell assistance - Th2 help in this case. The humoral response may arrive in time during a primary infection to play an important role in clearing pathogen. If pathogen is cleared too quickly by the innate immune system, a humoral response may not develop. Clearly, the humoral response is much stronger on a secondary infection.

You should note that the T cell response is also much stronger on secondary infection. Although affinity maturation doesn't occur, an expansion in reactive clones does occur.

In the case of a vaccination, it's likely that most of the expanded clones would be Th2, not Th1, and that initial challenge, given sufficient antigen and proper kinetics, would be sufficient to mount a protective humoral response which would prevent or ameliorate secondary infections.

 

[NRAI2001]

Not really. The humoral response depends on T helper cell assistance - Th2 help in this case. The humoral response may arrive in time during a primary infection to play an important role in clearing pathogen. If pathogen is cleared too quickly by the innate immune system, a humoral response may not develop. Clearly, the humoral response is much stronger on a secondary infection.

You should note that the T cell response is also much stronger on secondary infection. Although affinity maturation doesn't occur, an expansion in reactive clones does occur.

In the case of a vaccination, it's likely that most of the expanded clones would be Th2, not Th1, and that initial challenge, given sufficient antigen and proper kinetics, would be sufficient to mount a protective humoral response which would prevent or ameliorate secondary infections.

Th2 vs Th1 response with vaccination would be dependent on the vaccination type. Live-attenuated virus will elicit a Th1 response, dna and recombinant vaccinations will also elicit a Th1 response; bacterial protein and toxoid vaccinations will elicit a Th2 response...if I m correct?

 

[mercaptovizadeh]

Th2 vs Th1 response with vaccination would be dependent on the vaccination type. Live-attenuated virus will elicit a Th1 response, dna and recombinant vaccinations will also elicit a Th1 response; bacterial protein and toxoid vaccinations will elicit a Th2 response...if I m correct?

I can't comment on DNA or recombinant vaccines, but yes, if it goes beyond merely presentation of pathogen protein and more closely mimics an actual viral infection, Th1 would become a relevant mechanism. Th2 would be important here as well.

In all honesty, most infections elicit both pathways, since the pathways complement and support each other. There's relatively few phenomena where you'd have a clearly skewed T cell response that could be characterized as "Th1" or "Th2."