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Journal Articles

Adult thymectomy is associated with increased mortality risk from cancer but not cardiovascular disease

Open Access
Kameron A. Kooshesh, Brody H. Foy, Richard A. Baylis, Karin Gustafsson, Daniel A. Zlotoff, Tomas G. Neilan, David T. Scadden
Journal: Blood Advances
Blood Adv (2025) 9 (21): 5449–5452.
https://doi.org/10.1182/bloodadvances.2024015286
Published: 2025
Includes: Supplemental data
Journal Articles

Familial forms of chronic lymphocytic leukemia have a worse prognosis than sporadic forms: an Italian case-control study

Open Access
Alberto Fresa, Idanna Innocenti, Annamaria Tomasso, Candida Vitale, Alessandro Sanna, Anna Maria Frustaci, Andrea Visentin, Azzurra Romeo, Paolo Sportoletti, Annamaria Giordano, Francesca Perutelli, Roberta Murru, Francesca Romana Mauro, Antonio Mosca, Francesca Morelli, Roberta Laureana, Andrea Galitzia, Ilaria Angeletti, Esmeralda Conte, Riccardo Moia, Giovanni D’Arena, Raffaella Pasquale, Francesco Autore, Jacopo Olivieri, Luca Stirparo, Giulia Benintende, Francesco Angotzi, Florenzia Vuono, Andrea Corbingi, Maria Ilaria Del Principe, Diana Giannarelli, Alessandra Tedeschi, Marta Coscia, Eugenio Sangiorgi, Dimitar G. Efremov, Luca Laurenti
Journal: Blood Advances
Blood Adv (2025) 9 (21): 5399–5408.
https://doi.org/10.1182/bloodadvances.2025016546
Published: 2025
Journal Articles

A disrupted adenosinergic axis facilitates platelet activation in APS: exploring a novel therapeutic target

Open Access
Somanathapura K. NaveenKumar, Thalia G. Newman, Bruna Mazetto Fonseca, Srilakshmi Yalavarthi, Mariane C. Flores Nascimento, Kaitlyn Sabb, Katarina Kmetova, Emily Chong, Kavya Sugur, Caroline H. Ranger, Megan P. Tompkins, Cyrus Sarosh, Jacqueline A. Madison, Ajay Tambralli, Jordan K. Schaefer, Michael Holinstat, Yu Zuo, Jason S. Knight
Journal: Blood Advances
Blood Adv (2025) 9 (21): 5423–5435.
https://doi.org/10.1182/bloodadvances.2025016162
Published: 2025
Includes: Supplemental data
Journal Articles

High-grade B-cell lymphoma, not otherwise specified: an LLMPP study

Open Access
Brett Collinge, Laura K. Hilton, Jasper Wong, Waleed Alduaij, Susana Ben-Neriah, Graham W. Slack, Pedro Farinha, Merrill Boyle, Barbara Meissner, James R. Cook, German Ott, Andreas Rosenwald, Elias Campo, Catalina Amador, Timothy C. Greiner, Philipp W. Raess, Joo Y. Song, Giorgio Inghirami, Sarah L. Ondrejka, Elaine S. Jaffe, Dennis D. Weisenburger, Wing C. Chan, Harald Holte, Klaus Beiske, Kai Fu, Jan Delabie, Stefania Pittaluga, Javeed Iqbal, George Wright, Kerry J. Savage, Andrew J. Mungall, Louis M. Staudt, Christian Steidl, Andrew L. Feldman, Ryan D. Morin, Lisa M. Rimsza, David W. Scott
Journal: Blood Advances
Blood Adv (2025) 9 (21): 5409–5422.
https://doi.org/10.1182/bloodadvances.2025016651
Published: 2025
Includes: Supplemental data
Journal Articles

HLA-E [pHLA-G] complex–specific monoclonal antibody enhancing NK activity in multiple myeloma

Open Access
Muhammad Abu Ahmad, Olga Radinsky, Bar Kaufman, Kamran Waidha, Eman Gharra, Sharon Dim, Dinesh Babu Manikandan, Noa Ofir, Dirk Jäger, Marten Meyer, Moshe Elkabets, Kerry S. Campbell, Miri Zektser, Roi Gazit, Ory Rouvio, Frank Momburg, Angel Porgador
Journal: Blood Advances
Blood Adv (2025) 9 (21): 5436–5448.
https://doi.org/10.1182/bloodadvances.2025016276
Published: 2025
Includes: Supplemental data
Images
The effect of thymectomy on the risk of mortality, cancer, and MACE. (A) Panel A shows the 5-year relative risk of mortality, cancer, MACE (myocardial infarction, heart failure, and stroke), and MACE excluding patients with a previous history of CVD and ICA, among TMx as compared with control patients. (B-D) Kaplan-Meier curves for rates of mortality (B), cancer (C), and MACE (D) in 1071 TMx and 5355 control patients over 20 years after match. (E) Cox proportional hazard risk ratios of CVD, coronary artery bypass grafting, and percutaneous coronary intervention are illustrated, comparing 1071 TMx with 5355 control patients. HR, hazard ratio; ICA, infection, cancer, or autoimmunity; TMx, patients who had undergone thymectomy.

The effect of thymectomy on the risk of mortality, cancer, and MACE. (A) P...

Open Access
in Adult thymectomy is associated with increased mortality risk from cancer but not cardiovascular disease > Blood Advances
Published: 2025
Figure 1. The effect of thymectomy on the risk of mortality, cancer, and MACE. (A) Panel A shows the 5-year relative risk of mortality, cancer, MACE (myocardial infarction, heart failure, and stroke), and MACE excluding patients with a previous history of CVD and ICA, among TMx as compared with ... More about this image found in The effect of thymectomy on the risk of mortality, cancer, and MACE. (A) P...
Images
Characteristics of postthymectomy cancer mortality. To investigate the causes of death after thymectomy, a detailed medical record review was performed on all 112 patients who underwent a thymectomy procedure who died. Of these, 64 had adequate records available to adjudicate causes of death. Six patients had a genetic syndrome diagnosed (ie, multiple endocrine neoplasia, Lynch syndrome) and were excluded from the analysis, leaving a total of 58 patients who underwent a thymectomy procedure. Medical record review was also performed on 216 control patients who died, of whom 124 had adequate death records available for review. This analysis matched on postoperative rates of infection, malignancy, and autoimmune disease. (A) Among the patients who passed away, the causes of mortality were different between control (N = 124) and patients who underwent a thymectomy procedure (N = 58); 63.8% of mortality in patients who underwent a thymectomy procedure occurred because of cancer vs 29.8% in control patients (P < .001). Outside of cancer, autoimmunity (10.3%; P = .002) and infection (8.6%; P = .057) were the major drivers of mortality in patients who underwent a thymectomy procedure. (B) The types of cancers that directly caused death also differed between control and patients who underwent a thymectomy procedure, whereby patients who underwent a thymectomy procedure (N = 37 patients, 41 cancers) experienced a significant burden of thymoma, sarcoma, and rarer malignancies (eg, germ cell tumor) that were not observed in control patients (N = 37 patients, 37 cancers) who passed away. (C) Relapse after definitive therapy was significantly more frequent (P < .001) in patients who underwent a thymectomy procedure (among all 71 patients who underwent a thymectomy procedure who developed cancer of the total 112 surveyed that died) vs control patients (among all 69 control patients who developed cancer of the total 124 surveyed that died). The types of cancers that recurred in patients who underwent a thymectomy procedure who passed away were also different, featuring a burden of aggressive thymoma, sarcoma, leukemia, and lymphoma that was not observed in control patients.

Characteristics of postthymectomy cancer mortality. To investigate the cau...

Open Access
in Adult thymectomy is associated with increased mortality risk from cancer but not cardiovascular disease > Blood Advances
Published: 2025
Figure 2. Characteristics of postthymectomy cancer mortality. To investigate the causes of death after thymectomy, a detailed medical record review was performed on all 112 patients who underwent a thymectomy procedure who died. Of these, 64 had adequate records available to adjudicate causes of... More about this image found in Characteristics of postthymectomy cancer mortality. To investigate the cau...
Images
Kaplan-Meier of TTFT of familial and sporadic CLL.

Kaplan-Meier of TTFT of familial and sporadic CLL.

Open Access
in Familial forms of chronic lymphocytic leukemia have a worse prognosis than sporadic forms: an Italian case-control study > Blood Advances
Published: 2025
Figure 1. Kaplan-Meier of TTFT of familial and sporadic CLL. More about this image found in Kaplan-Meier of TTFT of familial and sporadic CLL.
Images
Kaplan-Meier of TTNT of familial and sporadic CLL.

Kaplan-Meier of TTNT of familial and sporadic CLL.

Open Access
in Familial forms of chronic lymphocytic leukemia have a worse prognosis than sporadic forms: an Italian case-control study > Blood Advances
Published: 2025
Figure 2. Kaplan-Meier of TTNT of familial and sporadic CLL. More about this image found in Kaplan-Meier of TTNT of familial and sporadic CLL.
Images
Kaplan-Meier of OS from diagnosis of familial and sporadic CLL.

Kaplan-Meier of OS from diagnosis of familial and sporadic CLL.

Open Access
in Familial forms of chronic lymphocytic leukemia have a worse prognosis than sporadic forms: an Italian case-control study > Blood Advances
Published: 2025
Figure 3. Kaplan-Meier of OS from diagnosis of familial and sporadic CLL. More about this image found in Kaplan-Meier of OS from diagnosis of familial and sporadic CLL.
Images
Kaplan-Meier of OS from the first treatment received of familial and sporadic CLL.

Kaplan-Meier of OS from the first treatment received of familial and sporad...

Open Access
in Familial forms of chronic lymphocytic leukemia have a worse prognosis than sporadic forms: an Italian case-control study > Blood Advances
Published: 2025
Figure 4. Kaplan-Meier of OS from the first treatment received of familial and sporadic CLL. More about this image found in Kaplan-Meier of OS from the first treatment received of familial and sporad...
Images
Relationship between platelet activation and low cAMP levels in patients with aPL+. (A) Estimation of cAMP in platelets (2 × 105/μL) purified from the fresh blood of healthy controls (n = 20), patients who are aPL+ (n = 38), and patients with aPL-negative VTE [VTE (aPL−), n = 8]. (B) Flow cytometric evaluation of platelet surface P selectin (CD62P+ events within the CD41+ population) and (C) activated αIIbβ3 receptor (PAC-1+ events within the CD41+ population) in fresh blood. (D) ELISA-based estimation of plasma PF4. Spearman correlation for platelet cAMP of aPL+ patients with surface CD62P (E), activated αIIbβ3 receptor (F), plasma PF4 (G), and anti-PS/PT IgG (H). Data represent mean ± standard deviation (SD). ∗P < .05, ∗∗P < .01, ∗∗∗∗P < .0001, and nonsignificant (ns) by 1-way analysis of variance (ANOVA) with the Tukey multiple comparisons correction. MFI, Mean Fluorescence Intensity.

Relationship between platelet activation and low cAMP levels in patients wi...

Open Access
in A disrupted adenosinergic axis facilitates platelet activation in APS: exploring a novel therapeutic target > Blood Advances
Published: 2025
Figure 1. Relationship between platelet activation and low cAMP levels in patients with aPL + . (A) Estimation of cAMP in platelets (2 × 10 5 /μL) purified from the fresh blood of healthy controls (n = 20), patients who are aPL + (n = 38), and patients with aPL-negative VTE [VTE (aPL − ), n = 8... More about this image found in Relationship between platelet activation and low cAMP levels in patients wi...
Images
FcγRIIa-mediated platelet activation and lowering of cAMP by IgG purified from APS plasma. (A) Purified platelets obtained from healthy volunteers (n = 4) were treated with various concentrations of control IgG (cont IgG) or APS IgG for 1 hour, and cAMP was measured by assay kit. Platelets pretreated with either a monoclonal anti-FcγRIIa antibody (aFcγRIIa, clone IV.3, 1μg) or U73122 (PLC-i, 1μM), followed by stimulation with 100 μg/mL APS IgG for 1 hour. Platelets were evaluated for surface CD62P (α-granules) using a flow cytometer (B), released ATP (dense granule) using luminescent-based assay (C), and cellular cAMP using an assay kit (D). (E-H) CD62P and cAMP were measured in platelets pretreated with aFcγRIIa (1 μg) or PLC-i (1 μM). After incubation, platelets were stimulated with affinity-purified aβ2GPI IgG (20 μg/mL) or affinity-purified aPT IgG (10 μg/mL) for 1 hour. Data represent mean ± SD. ∗P < .05, ∗∗P < .01, ∗∗∗P < .001, ∗∗∗∗P < .0001, and ns by a 1-way ANOVA with the Tukey multiple comparisons correction (n = 4). PLC-I, phospholipase C-inhibitor.

FcγRIIa-mediated platelet activation and lowering of cAMP by IgG purified f...

Open Access
in A disrupted adenosinergic axis facilitates platelet activation in APS: exploring a novel therapeutic target > Blood Advances
Published: 2025
Figure 2. FcγRIIa-mediated platelet activation and lowering of cAMP by IgG purified from APS plasma. (A) Purified platelets obtained from healthy volunteers (n = 4) were treated with various concentrations of control IgG (cont IgG) or APS IgG for 1 hour, and cAMP was measured by assay kit. Plate... More about this image found in FcγRIIa-mediated platelet activation and lowering of cAMP by IgG purified f...
Images
Induction of A2AR reduces platelet activation by enhancing cAMP. (A) Healthy platelets were pretreated with either vehicle or CGS21680 (A2AR-a, 5μM) or BAY 60-6583 (A2BR-a, 5μM), followed by stimulation with thrombin (0.05 U/mL) for 15 minutes. CD62P was assessed using flow cytometry. (B-C) Flow cytometric analysis of surface CD62P in platelets preincubated with vehicle or A2AR inhibitor (SCH-442416, 5μM) for 20 minutes, followed by A2AR-a and thrombin (0.05 U/mL) stimulation. (D) Quantification of released ATP in A2AR-a and thrombin-treated platelets. (E-F) A2AR-a (1μM and 5μM) pretreated platelets were stimulated with either convulxin (20 ng/mL) or (G-H) U46619 (5μM) and assessed for surface CD62P using a flow cytometer. (I) Purified platelets were pretreated with vehicle or A2AR-a for 15 minutes before stimulation with thrombin (0.05 U/ml), or convulxin (20 ng/mL), or U46619 (5μM) for 15 minutes. The representative immunoblots show the phosphorylated-Akt (pAkt, Ser 473), total Akt, (pGSK3β, Ser9), and total GSK3β. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) was also used as an internal loading control for all the samples. Data represent mean ± SD. ∗∗∗P < .001, ∗∗∗∗P < .0001, and ns by a 1-way ANOVA with the Tukey multiple comparisons correction (n = 4).

Induction of A 2A R reduces platelet activation by enhancing cAMP. (A) Hea...

Open Access
in A disrupted adenosinergic axis facilitates platelet activation in APS: exploring a novel therapeutic target > Blood Advances
Published: 2025
Figure 3. Induction of A 2A R reduces platelet activation by enhancing cAMP. (A) Healthy platelets were pretreated with either vehicle or CGS21680 (A 2A R-a, 5μM) or BAY 60-6583 (A 2B R-a, 5μM), followed by stimulation with thrombin (0.05 U/mL) for 15 minutes. CD62P was assessed using flow cytom... More about this image found in Induction of A 2A R reduces platelet activation by enhancing cAMP. (A) Hea...
Images
Inhibition of APS IgG–accelerated platelet activation, clot retraction, and procoagulant platelet formation by an A2AR agonist. (A) Purified platelets were pretreated with A2AR-a (5 μM) and A2BR-a (5 μM), followed by stimulation with 100 μg/mL cont IgG or APS IgG for 1 hour, and surface CD62P was assessed using flow cytometry. (B-C) Using assay kits, released ATP in supernatant and cellular cAMP were measured in platelets pretreated with A2AR-a (5 μM) followed by stimulation with 100 μg/mL of cont IgG or APS IgG for 1 hour. Forskolin (1 μM) was used as a positive cont for cAMP quantification. (D-E) Flow cytometric quantification of PS exposure along with CD62P in platelets treated with either vehicle or various concentrations of A2AR-a, followed by stimulation with 100 μg/mL cont IgG or APS IgG. (F) The representative images show the clot retraction was measured for 1 hour in platelet-rich plasma, supplemented with red blood cells, incubated with 50 μg/mL of cont IgG or APS IgG in the presence or absence of A2AR-a (5 μM) before adding thrombin (0.25 U/mL). (G) Quantified clot size over time and the values are presented as mean ± standard error of the mean (SEM). Statistical significance was determined by 2-way ANOVA with Tukey multiple comparisons tests, n = 3 individual donors per group. Data represent mean ± SD. ∗P <.05, ∗∗P < .01, ∗∗∗P < .001, ∗∗∗∗P < .0001, and ns by a 1-way ANOVA with the Tukey multiple comparisons test (n = 4).

Inhibition of APS IgG–accelerated platelet activation, clot retraction, and...

Open Access
in A disrupted adenosinergic axis facilitates platelet activation in APS: exploring a novel therapeutic target > Blood Advances
Published: 2025
Figure 4. Inhibition of APS IgG–accelerated platelet activation, clot retraction, and procoagulant platelet formation by an A 2A R agonist. (A) Purified platelets were pretreated with A 2A R-a (5 μM) and A 2B R-a (5 μM), followed by stimulation with 100 μg/mL cont IgG or APS IgG for 1 hour, and ... More about this image found in Inhibition of APS IgG–accelerated platelet activation, clot retraction, and...
Images
cAMP inducers decrease APS IgG–induced platelet activation and aggregation. Purified platelets were preincubated with A2AR-i (5μM), A2AR-a (5 μM), dibutyryl-cAMP (Dibut-cAMP, 0.5 mM), 8-Br-cAMP (1 mM), or forskolin (1 μM) for 20 minutes, followed by stimulation with 100 μg/mL cont IgG or APS IgG for 1 hour. (A-B) Platelets were then assessed for surface CD62P using flow cytometry, and (C) released ATP in the supernatant from the treated platelets using the luminescence-based assay. ∗P < .05, ∗∗P < .01, ∗∗∗P < .001, and ∗∗∗∗P < .0001, by a 1-way ANOVA with the Tukey multiple comparisons test (n = 4). (D) Representative immunoblots for (pAkt, Ser 473), total Akt, and GAPDH in the treated platelets (n = 3). (E and F) Representative curves and quantification of washed platelet aggregation in response to 100 μg/mL cont IgG or APS IgG treatment in the presence or absence of cAMP inducers, followed by stimulation with ADP (Effective concentration of 5-10 μM). Data represent mean ± SD. ∗∗∗∗P < .0001 and ns by a 1-way ANOVA with the Tukey multiple comparisons test (n = 5).

cAMP inducers decrease APS IgG–induced platelet activation and aggregation....

Open Access
in A disrupted adenosinergic axis facilitates platelet activation in APS: exploring a novel therapeutic target > Blood Advances
Published: 2025
Figure 5. cAMP inducers decrease APS IgG–induced platelet activation and aggregation. Purified platelets were preincubated with A 2A R-i (5μM), A 2A R-a (5 μM), dibutyryl-cAMP (Dibut-cAMP, 0.5 mM), 8-Br-cAMP (1 mM), or forskolin (1 μM) for 20 minutes, followed by stimulation with 100 μg/mL cont ... More about this image found in cAMP inducers decrease APS IgG–induced platelet activation and aggregation....
Images
Inhibition of PDE3 ameliorates APS IgG–induced platelet activation by increasing cAMP. (A-B) Surface CD62P, (C) released ATP, and (D) cellular cAMP were measured in platelets treated with cilostazol (PDE3-i, 10 μM) and BAY 60-7550 (PDE2-i, 10 μM) before stimulation with 100 μg/mL cont IgG or APS IgG. ∗∗P < .01, ∗∗∗P < .001, and ns by a 1-way ANOVA with the Tukey multiple comparisons test (n = 4). (E) Representative immunoblots for (pVASP, Ser 157), total VASP, and GAPDH in platelets treated with A2AR-i (5μM), A2AR-a (5 μM), dibutyryl-cAMP (0.5 mM), 8-Br-cAMP (1 mM), forskolin (1 μM), PDE3-i (10 μM), or PDE2-i (10 μM) for 20 minutes, followed by stimulation with 100 μg/mL of either cont IgG or APS IgG for 1 hour (n = 3). (F-G) Flow cytometric evaluation of surface CD62P in platelets pretreated with A2AR-a (5 μM), forskolin (1 μM), or PDE3-i (10 μM), followed by stimulation with affinity-purified (F) aβ2GPI IgG (20 μg/mL) or (G) aPT IgG (10 μg/mL) for 1 hour. (H-I) Quantification and representative images of platelet adhesion and accumulation in human whole blood stained with DiOC6 and treated with 100 μg/mL cont IgG or APS IgG along with A2AR-a (5 μM), dibutyryl-cAMP (0.5 mM), 8-Br-cAMP (1 mM), PDE3-i (10 μM) perfused through a collagen-coated chamber at arterial shear (n = 5). Data represent mean ± SEM. Two-way ANOVA. Scale bars represent 100 μm. Data represent mean ± SD for panels A-G. ∗∗P < .01, ∗∗∗P < .001, and ∗∗∗∗P < .0001, by a 1-way ANOVA with the Tukey multiple comparisons test (n = 5). MFI, Mean fluorescence intensity; UT, Untreated.

Inhibition of PDE3 ameliorates APS IgG–induced platelet activation by incre...

Open Access
in A disrupted adenosinergic axis facilitates platelet activation in APS: exploring a novel therapeutic target > Blood Advances
Published: 2025
Figure 6. Inhibition of PDE3 ameliorates APS IgG–induced platelet activation by increasing cAMP. (A-B) Surface CD62P, (C) released ATP, and (D) cellular cAMP were measured in platelets treated with cilostazol (PDE3-i, 10 μM) and BAY 60-7550 (PDE2-i, 10 μM) before stimulation with 100 μg/mL cont ... More about this image found in Inhibition of PDE3 ameliorates APS IgG–induced platelet activation by incre...
Images
Association between platelet hyperactivity and low CD73 activity in APS. (A) Estimation of ectonucleotidase activity by measuring free inorganic phosphate (μM) using the Malachite Green assay kit, after the addition of AMP (100 μM) to purified platelets from the fresh blood of healthy controls (n = 20), patients who are aPL+ (n = 38), or patients with aPL-negative VTE disease [VTE (aPL−), n = 8]. (B) Spearman correlation of CD73 activity with cAMP level and (C) surface CD62P for aPL+ patients as indicated. ∗∗∗∗P < .0001 and ns by a 1-way ANOVA with the Tukey multiple comparisons test. (D) Flow cytometric evaluation of surface expression of CD73 on platelets treated with 100 μg/mL cont IgG or APS IgG. ∗P < .05 by unpaired t test (n = 4). (E) Evaluation of CD73 expression using flow cytometer in platelets treated with aFcγRIIa (1 μg) or PLC-i (1 μM) before inducing 100 μg/mL of APS IgG for 1 hour (n = 4). (F) Schematic representation of healthy platelets treated with affinity-purified antibodies followed by AMP to measure surface CD73 activity. (G-H) Platelets were pretreated with aFcγRIIa (1 μg) or PLC-i (1 μM). Platelets were then stimulated with affinity-purified aβ2GPI IgG (20 μg/mL) (G) or affinity-purified aPT IgG (10 μg/mL) (H) for 1 hour. Platelet surface CD73 activity was measured using the Malachite Green assay kit after adding AMP (100 μM). (I) Schematic representation of the degradation of AMP to adenosine by CD73, including inhibition of CD73 by the selective inhibitor PSB 12379. (J) Platelet CD62P measured on PSB 12379 (20 μM) treated platelets in the presence or absence of APS IgG (100 μg/mL) (n = 5). Data represent mean ± SD. ∗P < .05, ∗∗P < .01, ∗∗∗P < .001, ∗∗∗∗P < .0001, and ns by a 1-way ANOVA with the Tukey multiple comparisons test (n = 4).

Association between platelet hyperactivity and low CD73 activity in APS. (...

Open Access
in A disrupted adenosinergic axis facilitates platelet activation in APS: exploring a novel therapeutic target > Blood Advances
Published: 2025
Figure 7. Association between platelet hyperactivity and low CD73 activity in APS. (A) Estimation of ectonucleotidase activity by measuring free inorganic phosphate (μM) using the Malachite Green assay kit, after the addition of AMP (100 μM) to purified platelets from the fresh blood of healthy ... More about this image found in Association between platelet hyperactivity and low CD73 activity in APS. (...
Images
Clinical and molecular features of HGBCL-NOS. (A) Heat map of molecular features of the 92 HGBCL-NOS tumors included in the study, grouped by morphological subtype. MYC, BCL2, and BCL6 rearrangement status were determined by FISH. Tumors with a negative (or missing) MYC or BCL2 FISH result for which a rearrangement was identified by sequencing are indicated with a red dot. (B) Comparison of clinical and molecular features in HGBCL-NOS with those of DLBCL-NOS. P values were calculated by the Fisher exact test for comparisons of clinical, FISH, and IHC data, and by χ2 test for refined COO and LymphGen comparisons. (C) Distribution of COO and refined COO subtypes in HGBCL-NOS. ∗P < .05; ∗∗P < .01; ∗∗∗P < .001; ∗∗∗∗P < .0001.

Clinical and molecular features of HGBCL-NOS. (A) Heat map of molecular fe...

Open Access
in High-grade B-cell lymphoma, not otherwise specified: an LLMPP study > Blood Advances
Published: 2025
Figure 1. Clinical and molecular features of HGBCL-NOS. (A) Heat map of molecular features of the 92 HGBCL-NOS tumors included in the study, grouped by morphological subtype. MYC , BCL2 , and BCL6 rearrangement status were determined by FISH. Tumors with a negative (or missing) MYC or BCL... More about this image found in Clinical and molecular features of HGBCL-NOS. (A) Heat map of molecular fe...
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The genetic landscape of HGBCL-NOS. (A) The architecture of MYC rearrangements and the observed frequency of IGH, IGK, IGL, and non-IG rearrangement partners. The outermost ring shows the chromosome ideogram, followed by a genomic coordinate scale and gene coordinate track. The innermost lines show the linkages between MYC and the corresponding rearrangement partner for each sample. (B) The architecture of IGH::MYC rearrangements and the frequency of breakpoints occurring at the indicated regions of the IGH locus. Eμ and 3′ regulatory region enhancers are included in the gene coordinate track (red). (C) Copy number profile of HGBCL-NOS. The proportion of tumors with a copy number gain (red) or deletion (blue) is plotted across each chromosome. (D) Oncoplot showing the mutation status of the most frequently mutated genes in HGBCL-NOS for each patient tumor. Genes included in the plot were mutated in at least 10% of HGBCL-NOS samples and identified as a significantly mutated gene in HGBCL-NOS, DLBCL-NOS, or BL. (E) PCA of RNA sequencing data. COMP, composite; NA, not available.

The genetic landscape of HGBCL-NOS. (A) The architecture of MYC rearrang...

Open Access
in High-grade B-cell lymphoma, not otherwise specified: an LLMPP study > Blood Advances
Published: 2025
Figure 2. The genetic landscape of HGBCL-NOS. (A) The architecture of MYC rearrangements and the observed frequency of IGH, IGK, IGL, and non-IG rearrangement partners. The outermost ring shows the chromosome ideogram, followed by a genomic coordinate scale and gene coordinate track. The inner... More about this image found in The genetic landscape of HGBCL-NOS. (A) The architecture of MYC rearrang...