Biology as vulnerability in follicular lymphoma: genetics, epigenetics, and immunogenetics

Follicular lymphoma (FL) represents a heterogeneous group of B-cell neoplasms with distinct genetic, epigenetic, microenvironmental, and clinical features. It is the most prevalent indolent non-Hodgkin lymphoma, characterized by a relapsing course and risk of transformation to aggressive diffuse large B-cell lymphoma. Recent advances in high-throughput sequencing, spatial transcriptomics, and imaging technologies uncovered genetic, epigenetic, and immunogenetic features underpinning FL, offering insights into its biology and potential therapeutic vulnerabilities. Although FL is primarily driven by the hallmark t(14;18) translocation involving BCL2, its pathogenesis requires additional oncogenic mutations, particularly in genes regulating chromatin and histone modifications. These early genetic and epigenetic alterations promote the persistence and evolution of cancer precursor cells, setting the stage for lymphomagenesis. The tumor microenvironment is also crucial in FL progression and patient prognosis, with T cells, stromal cells, and macrophages playing pivotal roles in facilitating tumor immune escape. Targeted therapies, including B-cell lymphoma 2 (BCL2) inhibitors, epigenetic modulators, and immunotherapies, have emerged from this deeper understanding of FL biology. Achieving a cure for FL will require targeted therapies that selectively eliminate cancer precursor cells with minimal impact on normal cells, thus preventing relapse and avoiding harmful side effects. Eradicating minimal residual disease should be a primary objective rather than waiting for clinical relapse. Future research must prioritize the development of accurate experimental models, the elucidation of FL precursors, and a deeper understanding of its heterogeneity, dependencies, progression, and mechanisms driving transformation. Implementing targeted therapies at FL early stages, instead of the current "watch and wait" approach, will be essential to improve patient outcomes.

Authors

Institutions

Publication Details

Journal
Blood
Published
2025-03-16
DOI
https://doi.org/10.1182/blood.2024026020
Citations
6
Primary Topic
Lymphoma Diagnosis and Treatment
Type
article
Field-Weighted Citation Impact
8.83
Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

Biology as vulnerability in follicular lymphoma: genetics, epigenetics, and immunogenetics

Ferran Araujo‐Ayala, Wendy Béguelin
6 citations
Blood
Lymphoma Diagnosis and Treatment
8.83
article

Biology as vulnerability in follicular lymphoma: genetics, epigenetics, and immunogenetics

Ferran Araujo‐Ayala, Wendy Béguelin
article en
6 citations

Abstract

Follicular lymphoma (FL) represents a heterogeneous group of B-cell neoplasms with distinct genetic, epigenetic, microenvironmental, and clinical features. It is the most prevalent indolent non-Hodgkin lymphoma, characterized by a relapsing course and risk of transformation to aggressive diffuse large B-cell lymphoma. Recent advances in high-throughput sequencing, spatial transcriptomics, and imaging technologies uncovered genetic, epigenetic, and immunogenetic features underpinning FL, offering insights into its biology and potential therapeutic vulnerabilities. Although FL is primarily driven by the hallmark t(14;18) translocation involving BCL2, its pathogenesis requires additional oncogenic mutations, particularly in genes regulating chromatin and histone modifications. These early genetic and epigenetic alterations promote the persistence and evolution of cancer precursor cells, setting the stage for lymphomagenesis. The tumor microenvironment is also crucial in FL progression and patient prognosis, with T cells, stromal cells, and macrophages playing pivotal roles in facilitating tumor immune escape. Targeted therapies, including B-cell lymphoma 2 (BCL2) inhibitors, epigenetic modulators, and immunotherapies, have emerged from this deeper understanding of FL biology. Achieving a cure for FL will require targeted therapies that selectively eliminate cancer precursor cells with minimal impact on normal cells, thus preventing relapse and avoiding harmful side effects. Eradicating minimal residual disease should be a primary objective rather than waiting for clinical relapse. Future research must prioritize the development of accurate experimental models, the elucidation of FL precursors, and a deeper understanding of its heterogeneity, dependencies, progression, and mechanisms driving transformation. Implementing targeted therapies at FL early stages, instead of the current "watch and wait" approach, will be essential to improve patient outcomes.

BloodVol. 146(15)
Cornell University (US), Fundació Clínic per a la Recerca Biomèdica (ES), Consorci Institut D'Investigacions Biomediques August Pi I Sunyer (ES), Weill Cornell Medicine (US)
Good health and well-being
Openalex Percentile: Top 2%
Lymphoma Diagnosis and Treatment
8.83
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.