• IGHV mutational status: Whether the leukaemia's antibody gene has been 'edited' by the immune system.
• LymphGen and the genetic clusters of large B-cell lymphoma: Sequencing shows that large B-cell lymphoma is at least seven diseases, each defined by which faults occur together.
• BTK C481S, PLCG2 and BCL2 G101V resistance mutations: When ibrutinib-type drugs stop working in CLL, the usual reason is a mutation at the exact spot the drug binds (BTK C481S) or just downstream (PLCG2); when venetoclax fails, a BCL2 G101V mutation loosens its grip.
• Transformation: when a slow lymphoma turns into a fast one: An indolent lymphoma can change into an aggressive one, usually by acquiring new genetic faults in the same clone.
• M-protein, immunofixation and serum free light chains: Myeloma cells are clones of one antibody-making cell, so they pour a single identical antibody, the M-protein, into the blood; measuring it (and the free light chains that go with it) is how myeloma is diagnosed, how deep a response is judged, and how relapse is caught before symptoms.
• MYD88 L265P and CXCR4 mutations: One letter change in MYD88 (L265P) keeps a B-cell survival signal permanently on; it is found in more than nine in ten Waldenström's macroglobulinaemia, most primary CNS and testicular lymphomas and a poor-risk group of DLBCL, and it predicts that BTK inhibitors will work, while a second mutation in CXCR4 predicts that they will work more slowly.
• Vaccinations around lymphoma treatment: the ones to have first, and the ones not to have at all: Inactivated vaccines work best when they are given at least two weeks before immunosuppressive treatment begins, and live vaccines are generally not given to someone whose immune system is suppressed.
• The surveillance schedule, and the evidence that routine scans do not find relapse first: Most people expect regular scans after lymphoma treatment and are unsettled when they are not offered.
• Living with an indolent lymphoma rather than being cured of one: Slow-growing lymphomas are usually controlled rather than cured: treatment works, the disease goes away for a while, and at some point it comes back and is treated again.
• Going back to work after lymphoma, and the money in the meantime: Some people work through lymphoma treatment and some cannot, and the difference is mostly the job rather than the person.

Biomarker results to ask for: MYD88 L265P (AS-PCR/NGS), CXCR4 mutation (S338X and others), Serum IgM and viscosity, IPSSWM / rIPSSWM, Anti-MAG antibodies (neuropathy), Cryoglobulins, cold agglutinins.

Scans and tests linked to this cancer: Active surveillance, Comprehensive genomic profiling, Multidisciplinary tumour boards, Multiparameter flow cytometry MRD.

Bring copies of scan reports, pathology and blood results, and a list of every medicine and supplement.

• Asymptomatic: Observation; treat on symptoms, cytopenias, hyperviscosity or neuropathy, not on IgM level alone. (Active surveillance)
• Symptomatic, first line: Bendamustine-rituximab or dexamethasone-rituximab-cyclophosphamide for fixed duration; or zanubrutinib / ibrutinib (± rituximab) continuously; plasmapheresis first for hyperviscosity. (Bendamustine, Rituximab, Zanubrutinib, Ibrutinib)
• Waldenstrom macroglobulinaemia: what to test before treatment, and why the genotype matters: A lymphoplasmacytic lymphoma that secretes IgM. Two mutations, found by allele-specific PCR on a marrow aspirate, shape the whole plan. MYD88 L265P is present in more than 90 per cent and predicts response to BTK inhibitors; MYD88 wild-type disease responds much less well to them. CXCR4 mutations, present in about a third, predict slower and shallower responses to ibrutinib and a higher risk of a rise in IgM when treatment starts. Two complications need to be looked for because they change the urgency. Hyperviscosity, from a very high IgM, causes headache, blurred vision, nosebleeds and confusion, is confirmed on fundoscopy, and is treated with plasma exchange before anything else. IgM-related peripheral neuropathy, often anti-MAG positive, is a reason to treat even when other criteria are not met, because nerve damage does not reverse. Rituximab causes a transient rise in IgM, an IgM flare, in about half of patients, which can precipitate hyperviscosity; it is therefore held back or given after plasma exchange where the IgM is very high. (Somatic mutations in MYD88 and CXCR4 are determinants of clinical presentation and overall survival in Waldenstrom macroglobulinemia, Rituximab, Ibrutinib, Zanubrutinib)
• Waldenstrom macroglobulinaemia, first treatment: BTK inhibitor or chemoimmunotherapy: Treatment is for symptoms, not for a number: anaemia, thrombocytopenia, constitutional symptoms, symptomatic organ or node enlargement, hyperviscosity, neuropathy, cryoglobulinaemia or amyloidosis. An asymptomatic patient is watched. Two routes. Fixed-duration chemoimmunotherapy, usually bendamustine with rituximab for four to six cycles, gives deep responses and a treatment-free interval afterwards, and is the preference of many patients and many British units. Continuous BTK inhibition with zanubrutinib or ibrutinib gives high response rates without chemotherapy but is taken indefinitely. ASPEN, the only head-to-head trial, randomised 201 patients with MYD88-mutated disease to zanubrutinib or ibrutinib: the complete or very good partial response rate by independent review was 28.4 against 19.2 per cent, which did not reach statistical significance, but zanubrutinib caused markedly less atrial fibrillation, hypertension, bleeding and diarrhoea. A separate cohort treated MYD88 wild-type disease with zanubrutinib. Where a BTK inhibitor is chosen, zanubrutinib is therefore preferred. Rituximab with cyclophosphamide and dexamethasone is an alternative chemoimmunotherapy for patients in whom bendamustine is unsuitable. Proteasome-inhibitor regimens containing bortezomib are used where a rapid response is needed and neuropathy is absent. (ASPEN (Waldenström macroglobulinaemia), Zanubrutinib, Ibrutinib, Bendamustine, Rituximab, Cyclophosphamide, Dexamethasone, Bortezomib, Watch and wait in lymphoma: when the right treatment is none yet, A randomized phase 3 trial of zanubrutinib vs ibrutinib in symptomatic Waldenström macroglobulinemia: the ASPEN study)
• Relapsed: Switch class (BTKi ↔ chemo-immunotherapy); bortezomib- or carfilzomib-based regimens; venetoclax; pirtobrutinib after covalent BTKi; autologous transplant in selected young patients. (Bortezomib, Carfilzomib, Venetoclax, Pirtobrutinib, Autologous stem cell transplant (high-dose therapy))
• Relapsed Waldenstrom macroglobulinaemia: The choice turns on what was used first and how long the remission lasted. After fixed-duration chemoimmunotherapy with a remission of two years or more, the same regimen can be repeated, or a BTK inhibitor started. After a BTK inhibitor, options are a different BTK inhibitor including the non-covalent pirtobrutinib, venetoclax, which has activity in this disease, proteasome-inhibitor regimens, chemoimmunotherapy if not previously used, and a clinical trial. Autologous transplant is occasionally used in younger patients with chemosensitive disease and multiple relapses. Transformation to diffuse large B-cell lymphoma is treated as aggressive lymphoma. Plasma exchange remains the immediate treatment for symptomatic hyperviscosity at any point. (Zanubrutinib, Ibrutinib, Pirtobrutinib, Venetoclax, Bortezomib, Bendamustine, Rituximab, Autologous stem cell transplant (high-dose therapy), Stem cell transplant in lymphoma: what it is still for)

From the standard of care recorded for this cancer; which apply depends on your stage and biomarkers. Ask which the team recommends and why.