July 2026 Research Update

This month added reassurance that some early, marginal zone-like B-cell conditions often move slowly and only sometimes develop into splenic marginal zone lymphoma. In a multicenter study of 98 people with CD5-negative clonal B-cell lymphocytosis of marginal zone origin, progression to splenic marginal zone lymphoma was uncommon, and most people stayed treatment-free for long periods. The same study also pointed to specific lab or bone marrow features that were linked to a higher chance of needing treatment over time. [1]

Within this group, two factors stood out as signals of a higher likelihood of needing therapy: having 50% or more bone marrow involvement and having a higher LDH blood test. The authors also described two clinical patterns, including one where a blood protein (paraprotein) was present more often and another with a more "leukemia-like" blood picture and more frequent low antibody levels. These details help explain why people with similar-sounding diagnoses can have different follow-up paths. [1]

For patients and caregivers, this mainly adds context about what an early marginal zone-type clonal B-cell finding can look like over time: in this cohort, most people did not quickly progress, and only about 5% later developed splenic marginal zone lymphoma. It also helps clarify that certain findings in bloodwork or bone marrow may relate to how closely someone is followed and whether treatment is eventually needed, although this study does not prove what will happen to any one person. This information may matter most during discussions about prognosis and follow-up planning, and it needs confirmation in other groups because the data were collected retrospectively over many years. [1]

This month included two case reports showing that splenic marginal zone lymphoma can sometimes appear alongside unexpected immune-related problems, especially around B-cell targeted therapy. One report described a bleeding disorder (acquired hemophilia A) that led to discovering an underlying lymphoma, and both conditions improved after rituximab. Another report described hepatitis B virus reactivation after rituximab-based chemotherapy, even though the person had hepatitis B surface antibodies at baseline. [2] [3]

In the acquired hemophilia A case, a 77-year-old man had spontaneous bruising and blood in the urine and was found to have very low factor VIII activity with an inhibitor. After initial measures for bleeding and prednisone, he received rituximab alone and the report described normalization of clotting tests, stopping of bleeding, and sustained clinical stability without evidence of lymphoma progression during follow-up. The authors also noted a significant infection-related complication (neutropenic diverticulitis) that required antibiotics and growth factor support. [2]

In the hepatitis B reactivation case, a 63-year-old man with splenic marginal zone lymphoma had negative hepatitis B surface antigen and detectable surface antibodies before treatment, with no detectable viral DNA. After rituximab-based chemotherapy, the report described a return of hepatitis B surface antigen and a high viral load along with marked liver enzyme elevation, which later resolved after tenofovir with ongoing viral suppression at last follow-up. The authors emphasized that having surface antibodies did not fully prevent reactivation during B-cell depleting therapy in this single patient. [3]

For patients, these reports mainly broaden the picture of what can happen in rare situations rather than describing what is typical. They help clarify that unusual bleeding due to an acquired clotting factor inhibitor can sometimes be a clue to an underlying lymphoma, and that hepatitis B can reactivate during rituximab-based treatment even when some protective antibodies are present. Because these are single-patient reports, they cannot predict risk for others, but they may matter as background information when discussing symptoms, safety monitoring, and past infection history during lymphoma care. [2] [3]