This clinicopathological study reports eight cases of aggressive B‑cell lymphoma (ABCL) characterized by MYC gene cluster amplification. The aim was to define clinical features, histomorphology, immunophenotype, molecular genetic changes, treatments, and outcomes in this molecularly defined subset.
Eight cases were collected between July 2018 and August 2025: six cases diagnosed at the Department of Pathology, the First Affiliated Hospital, Zhejiang University School of Medicine, and two consultation cases from outside hospitals. The analysis included assessment of histomorphology, immunohistochemistry, and molecular genetic testing. Clinical follow‑up and a literature review were also performed. The abstract does not provide full details on specific laboratory methods, treatment protocols, or extent of genomic testing for all cases beyond the reported FISH and chromosomal microarray results.
Among the eight patients, six were male and two female. The reported central tendency for age was 71.5 years (interquartile range 61.7–74.2 years). All six in‑house patients presented with abdominal pain at onset and did not have systemic B symptoms. Most patients presented with advanced disease, staged as Ann Arbor III–IV. One patient had a history of immunosuppression after renal transplantation. Initial bone marrow biopsies for the in‑house patients showed no evidence of lymphoma involvement.
Morphologically, two cases displayed features consistent with diffuse large B‑cell lymphoma (DLBCL). The remaining six cases had high‑grade morphology; within this group three cases exhibited Burkitt lymphoma‑like features. One case represented a blastoid variant of mantle cell lymphoma. Immunophenotypic profiling showed that six of seven evaluable cases demonstrated a germinal center B‑cell phenotype. The six in‑house cases tested by fluorescence in situ hybridization (FISH) were negative for bcl‑2 and bcl‑6 rearrangements.
All cases included in the series were defined by the presence of MYC gene cluster amplification. In addition, seven of eight cases had detectable alterations on chromosome 11q: five demonstrated combined gain and loss-type 11q changes and two showed isolated 11q gain. One of the two 11q gain cases that underwent chromosomal microarray analysis did not demonstrate telomeric loss of heterozygosity. The abstract does not report additional recurrent copy number changes or whole‑genome sequencing data.
Initial bone marrow biopsies from the in‑house cohort showed no lymphoma infiltration. Extranodal disease was common: five of six in‑house patients had extranodal involvement, with the gastrointestinal tract being the predominant site (4 of 5 extranodal cases). These findings indicate a predilection for abdominal and gastrointestinal presentation in this case series.
Follow‑up duration across the cohort ranged from 5.9 to 55.5 months. At the end of the reported follow‑up period, five patients were alive. The abstract states that antineoplastic combined chemotherapy protocols are relevant MeSH terms, but it does not provide case‑level details of specific chemotherapy regimens, dose intensity, responses, or causes of death. Therefore, treatment regimens and detailed outcome measures were not reported in the abstract.
In this small series, ABCL with MYC gene cluster amplification frequently demonstrated high‑grade histology, often with gastrointestinal involvement, and a strong association with 11q alterations. Despite high‑grade morphology, the cohort appeared to have a relatively favorable mid‑term outcome, with most patients alive at last follow‑up. The authors highlight that the combination of high‑grade morphology and gastrointestinal presentation should raise suspicion for 11q abnormalities in the setting of MYC cluster amplification.
The published abstract provides a concise summary but omits several specific details: exact chemotherapy regimens and responses for individual patients, comprehensive genomic profiling beyond 11q and MYC amplification, and cause‑specific survival or progression‑free survival metrics. The small sample size (n=8) and inclusion of consultation cases limit broad generalizability. These limitations are inherent to the dataset as reported in the abstract.
All authors declared no conflicts of interest.
When encountering aggressive B‑cell lymphomas with marked MYC gene cluster amplification, pathologists and clinicians should be aware of the frequent association with 11q alterations, the tendency toward high‑grade morphology (including Burkitt‑like features), and common gastrointestinal involvement. Detailed molecular testing, including assessment of 11q, may be informative. The limited case series suggests a more favorable prognosis than might be expected from morphology alone, but larger series with treatment and outcome details are needed to define optimal management.