Lymphoma
The AIDS-defining cancers are Kaposi sarcoma, certain lymphomas and cervical cancer.
What our notes say
- The AIDS-defining cancers are Kaposi sarcoma, certain lymphomas and cervical cancer. (Internal Medicine (MBIM 4100) main exam, Paper One: 3 July 2019)
- This is endemic Burkitt lymphoma, linked to Epstein-Barr virus and chronic malaria. (Paediatrics end of fourth year main exam: 1 July 2019, Paper One, 99 of 100 MCQs)
- | Nephrotic syndrome, hypoalbuminaemia | Malignancy (lung, breast, lymphoma, mesothelioma, metastases) | (Pleural Effusion)
- Exudates: tuberculosis, pneumonia (parapneumonic effusion, empyema), malignancy (lung, breast, lymphoma, mesothelioma), pulmonary embolism, rheumatoid arthritis and lupus, pancreatitis, asbestos exposure, drugs, chylothorax and haemothorax. (Junior Clerkship in Internal Medicine (MBIM4100) main exam, Paper One: 31 Januar)
- Malaria (chronic, with splenomegaly), tropical splenomegaly syndrome, schistosomiasis, typhoid and brucellosis, tuberculosis, HIV and AIDS, lymphoma and leukaemia (chronic myeloid), histoplasmosis, and hepatosplenic causes such as chronic liver disease with portal hypertension. (Junior Clerkship in Internal Medicine (MBIM4100) main exam, Paper One: 31 Januar)
- Topics tested: respiratory disease, sickle cell disease and anaemias, rheumatic fever, diabetes, TB, pulmonary embolism, connective tissue disease, HIV, gastroenterology, thyroid disease, gout, leukaemia and lymphoma, kidney disease and stroke. (Internal Medicine (MBIM 4100) main exam, Paper One: 3 July 2019)
Study material on Lymphoma
- Lymphoma Overview and Classification
- Non-Hodgkin Lymphoma: Classification, Symptoms, Diagnosis, and Treatment
- Pathology Spot Exam Revision: Lymphoma, Adenoma, Appendicitis, FISH
- White Cell Disorders — Must-Know Notes
- hematopathology
- Hematology MCQs
- Here are all 45 questions, complete with full stems, choices, and answers.
- Haematology Exam 2025: MCQs on Anaemia, Leukaemia & Clotting
- Hematologic Malignancies and Bleeding Disorders
- Haematopathology MCQs: Blood Disorders & Anemia Explained
- Non-Hodgkin Lymphoma: Classification, Symptoms, Diagnosis, and Treatment — Practice Questions
- Non-Hodgkin Lymphoma: Classification, Symptoms, Diagnosis, and Treatment — Practice Questions
- Non-Hodgkin Lymphoma: Classification, Symptoms, Diagnosis, and Treatment — Practice Questions
- Non-Hodgkin Lymphoma: Classification, Symptoms, Diagnosis, and Treatment — Practice Questions
- Non-Hodgkin Lymphoma: Classification, Symptoms, Diagnosis, and Treatment — Practice Questions
- Non-Hodgkin Lymphoma: Classification, Symptoms, Diagnosis, and Treatment — Practice Questions
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Practice questions on Lymphoma
The anti-apoptotic effect of BCL-2 overexpression in follicular lymphoma occurs due to:
- Activation of caspases.
- Inhibition of pro-apoptotic proteins like BAX and BAK.
- Increased DNA damage.
- Stimulation of the extrinsic apoptotic pathway.
Answer: B. BCL-2 is an anti-apoptotic protein. Overexpression of BCL-2, as seen in follicular lymphoma (often due to the t(14;18) translocation), prevents the activation of pro-apoptotic proteins (like BAX and BAK) and thus inhibits the intrinsic pathway of apoptosis, leading to increased cell survival.
The anti-apoptotic effect of BCL-2 overexpression in follicular lymphoma occurs due to:
- Direct inhibition of pro-apoptotic proteins like Bax and Bak
- Activation of caspase cascades
- Increased DNA damage
- Promotion of cell cycle arrest
Answer: A. BCL-2 is an anti-apoptotic protein. Overexpression of BCL-2, often due to the t(14;18) translocation in follicular lymphoma, inhibits the function of pro-apoptotic proteins (like Bax and Bak), thereby preventing the intrinsic pathway of apoptosis and allowing malignant B cells to survive.
The anti-apoptotic effect of BCL-2 overexpression in follicular lymphoma occurs due to:
- Inhibition of the intrinsic pathway of apoptosis
- Activation of caspase cascades
- Increased DNA fragmentation
- Autocrine production of death ligands
Answer: A. BCL-2 is a proto-oncogene that acts as an inhibitor of apoptosis. Overexpression of BCL-2, as seen in follicular lymphoma (often due to t(14;18) translocation), blocks the intrinsic pathway of apoptosis by preventing the release of cytochrome c from mitochondria, thereby promoting cell survival.
The anti-apoptotic effect of BCL-2 overexpression in follicular lymphoma occurs due to:
- Inhibition of mitochondrial outer membrane permeabilization
- Activation of caspases
- Increased DNA fragmentation
- Release of cytochrome c from the nucleus
Answer: A. BCL-2 is an anti-apoptotic protein. Overexpression of BCL-2 prevents the release of pro-apoptotic factors, such as cytochrome c, from the mitochondria by inhibiting the permeabilization of the outer mitochondrial membrane. This blocks the activation of caspases, thereby inhibiting apoptosis and promoting tumor cell survival. Cyt c is released from the mitochondria, not the nucleus.
The anti-apoptotic effect of BCL-2 overexpression in follicular lymphoma occurs due to:
- Inhibition of the intrinsic apoptotic pathway by preventing mitochondrial outer membrane permeabilization
- Activation of caspases that cleave cellular substrates
- Upregulation of pro-apoptotic proteins like BAX
- Increased DNA repair, leading to cell survival
Answer: A. BCL-2 is an anti-apoptotic protein. Overexpression of BCL-2, often due to a translocation in follicular lymphoma (t(14;18)), prevents the release of cytochrome c from the mitochondria, thereby inhibiting the intrinsic apoptotic pathway and promoting cell survival.
The anti-apoptotic effect of BCL-2 overexpression in follicular lymphoma occurs due to:
- Activation of caspase cascades.
- Inhibition of mitochondrial outer membrane permeabilization.
- Cleavage of PARP.
- Release of cytochrome c from the nucleus.
Answer: B. BCL-2 is an anti-apoptotic protein. Overexpression of BCL-2 inhibits apoptosis by preventing the release of pro-apoptotic factors, such as cytochrome c, from the mitochondria into the cytoplasm. This process is crucial for the initiation of caspase cascades, which execute the apoptotic program. Therefore, BCL-2 overexpression blocks mitochondrial outer membrane permeabilization.