SESSION 6: LYMPHOMA BIOLOGY 1
MOLECULAR SUBCLUSTERS OF FOLLICULAR LYMPHOMA: A REPORT FROM THE UK’S HAEMATOLOGICAL MALIGNANCY RESEARCH NETWORK abstract
S. Crouch, D. Painter, S. Barrans, E. Roman, et al.
The study authors conclude that their population-based analysis provides evidence for distinct mechanistic entities in FL, with aSHM burden and STAT6 mutation status providing key determinants of this heterogeneity. In contrast to DLBCL, they did not find evidence that tumor genetics provides a strong marker for predicting patient outcomes in FL. Instead, the authors speculate that factors related to the microenvironment or host immune system may have a greater influence on patient survival.
SOMATIC ALTERATIONS IN FOLLICULAR LYMPHOMA ASSOCIATE WITH UNIQUE TUMOR-CELL TRANCRIPTIONAL STATES AND TUMOR-IMMUNE MICROENVIRONMENTS. abstract
J. Krull, K. Wenzl, M. K. Manske, M. A. Hopper, et al.
The study authors conclude that using sing a multi-omic approach, three unique FL tumor B cell states were identified which are linked to specific genetic events and TME composition. Their study improves the understanding of the mechanisms driving FL tumors and motivates further investigation into transcriptional consequences of genetic events, as well as potential tumor intrinsic factors that may influence the TME.
CREBBP MEDIATED ACETYLATION OF KMT2D IN NORMAL AND TRANSFORMED GC B CELLS abstract
S. Vlasevska, L. Garcia-Ibanez, R. Duval, A.B. Holmes, et al
The study authors data reveal a physiologically relevant role for CREBBP in acetylating the KMT2D protein and suggest that this post-translational modification acts as a modulator of its activity. According to the authors, these findings imply that CREBBP mutant tumors bear KMT2D functional insufficiency, suggesting that CREBBP/KMT2D haploinsufficiency facilitates the expansion of the common precursor cell before acquisition of secondary genetic events leading to FL and/or DLBCL. They conclude, that CREBBP-targeted epigenetic therapies may add to the therapy in KMT2D mutated tumors.
GENETIC AND PHENOTYPIC ATTRIBUTES OF SPLENIC MARGINAL ZONE LYMPHOMA abstract
F. Bonfiglio, A. Bruscaggin, F. Guidetti, L. Terzi di Bergamo, et al.
The author's study highlights the complexity of SMZL. They conclude that the molecular framework provides an evolving understanding of the pathogenesis of SMZL, and can be regarded as a building block for further refining the classification of B-cell tumors of the spleen, and for aiding the development of rationally targeted treatments.
MONOMORPHIC EPITHELIOTROPIC INTESTINAL T-CELL LYMPHOMA (MEITL) : CLINICO-PATHOLOGICAL ANALYSIS OF A MULTICENTER EUROPEAN COHORT. abstract
D. Cavalieri, O. Tournilhac, E. Missiglia, C. Bonnet, et al.
The study authors expand in this large European cohort of MEITL the extremely poor prognosis related both to the complexity of clinical presentation and to primary resistance to CHOP-like polychemotherapy, with a negative impact of single and double-hit mutations of TP53 and STAT5B. They note, that Dynamic management including post-operative supportive care, chemotherapy attempt, and potential consolidation by auto- or even allograft is crucial.
RHOA G17V POTENTIATES CD28 T195P MUTATION INDUCED NFAT TRANSCRIPTIONAL ACTIVITY UPON CD3/CD28 STIMULATION abstract
D. Vallois, E. Missiaglia, B. Bisig, Mél. Favre Juilland, et al.
The study authors suggest with their results, that RHOA G17V expression does not involve increased phosphorylation of TCR signaling molecules but rather potentiates CD28 T195P-increased NFAT transactivation through VAV1 and P300 activities modulation, leading to a synergistic IL2 secretion.