Impact Factor
4.53
Journal Citation Impact
Estimated influence, citation density, publishing volume, and citation integrity from the analytics table.
Citation rate
7.01
4,618 total citations
h5-index
83
h5 depth signal
Cited share
86.9%
595 of 685
Total citations
4,618
Citation footprint
Metric signal
7.75
External metric anchor
Self-citation
3.6%
164 self-citations
Citations Trend
Monthly Publications Cadence
Citing Geographic Demographics
United States
1,777
Germany
1,040
United Kingdom
650
Italy
586
France
568
Citing Fields of Research
Hematology
2,503
Lymphomas
1,113
Immunology
616
Oncology
387
Cancer & Development
343
Publishing Activity & Reach
Volume, recency, access pattern, and citing-community signals from the journal analytics record.
All-time article footprint
11,636
Articles tracked across the journal lifetime
Indexed publication set
685
595 cited publications
Last 12 months
367
30.6 publications/month
Open access share
63.8%
234 OA publications in the last year
Leading citing country
United States
1,777 citing publications
Leading citing field
Hematology
2,503 citing publications
Latest tracked publication
19 October 2026
10 recent records available
Coverage & Indexing History
v1n1,Jan. 1987-
v1n1,Jan. 1987-
Active Coverage
Research Focus & Classification
Indexed Subjects
Hematology
Lymphomas
Immunology
Issuing & Sponsoring Bodies
Contributor
Leukemia Society of America
Contributor
Leukaemia Research Fund
Contributor
Sven-Aage Killmann Leukemia Foundation
Broad Categories
Hematology
Neoplasms
Lymphomas
MeSH Descriptors
Leukemia
Latest Publications
Recent article records with DOI-first linking and condensed abstracts.
01
02
DOI 10.1038/s41375-026-03177-w
Open DOI
Predicting long-term survival in primary myelofibrosis
03
04
DOI 10.1038/s41375-026-03157-0
Open DOI
Targeting the eIF4F translation initiation complex disrupts BCR::ABL1 translation and overcomes drug resistance in CML
Chronic myeloid leukemia (CML) is driven by the constitutively active BCR::ABL1 kinase, which promotes uncontrolled cell proliferation. Although protein-tyrosine kinase inhibitors (TKIs) have revolutionized CML treatment, resistance rema...
05
DOI 10.1038/s41375-026-03169-w
Open DOI
Neoantigenic receptor ROR1 promotes cell growth through diverse and complementary mechanisms
06
DOI 10.1038/s41375-026-03143-6
Open DOI
Fibroblast growth factor receptor-signaling confers stroma-mediated drug resistance in malignant B cells
07
DOI 10.1038/s41375-026-03160-5
Open DOI
Inhibition of PHB2/PINK1-mediated mitophagy potentiates venetoclax activity in acute myeloid leukemia
Acute myeloid leukemia (AML) cells are highly dependent on mitochondrial activity for survival, with this metabolic reliance driven in part by BCL-2, which is therapeutically targeted by venetoclax-based therapies. The regulation of mito...
08
DOI 10.1038/s41375-026-03159-y
Open DOI
Combating CD24 to overcome CD19 CAR-T resistance via induction of innate and adaptive immunity in B-cell malignancies
CD24 is highly expressed in aggressive B-cell malignancies and represents a novel immunologic vulnerability to overcome resistance to CD19 chimeric antigen receptor T-cell (CAR-T) therapy. We developed a CD24 × CD3 bispecific antibody (C...
09
DOI 10.1038/s41375-026-03151-6
Open DOI
Marrow hypercellularity is common and clinically neutral in essential thrombocythemia
10
DOI 10.1038/s41375-026-03171-2
Open DOI
PHI-101: a novel FLT3 inhibitor with potent activity against the F691L gatekeeper resistance mutation
Bibliographical & Catalog Notes
Title from cover.
Some vols. have supplements.
Also issued online.
Issues for Jan. 1991- are published on behalf of the Sven-Aage Killmann Leukemia Foundation.
Vol. 5, no. 1 (1991)19920825 Notice published Printed on acid-free paper that meets the full ANSI standard for Permanent Paper