Evidence map›Paper›PMID 36758208›Full record

ReviewBlood2023

Richter syndrome: novel insights into the biology of transformation.

Erin M Parry, Elisa Ten Hacken, Catherine J Wu

Open access · greenAbstract readReview
In one paragraph

Review in Blood, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
9.8field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. The Evolving Therapeutic Landscape of Richter Transformation.Current hematologic malignancy reports · 2025
    Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Chromoplexy: A Pathway to Genomic Complexity and Cancer Development.International journal of molecular sciences · 2025
    Review
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Erin M ParryDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA.ORCID 0000-0002-3382-9769
Elisa Ten HackenDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA.ORCID 0000-0003-1573-8799
Catherine J WuDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA.ORCID 0000-0002-3348-5054
Broad Institute · USHarvard University · US

Funding

ProteomicsP01CA206978 · NCI · DANA-FARBER CANCER INST · PI WU, CATHERINE JU-YING · 2016 to 2025
$17.0M
ITSC for Leukemia: Novel Molecular Strategies for NCTN: "Individualized" TherapieU10CA180861 · NCI · OHIO STATE UNIVERSITY · PI BLOOMFIELD, CLARA D, MARCUCCI, GUIDO · 2014 to 2018
$3.4M
Tracing the Evolution of Chronic Lymphocytic Leukemia to Richter's Syndrome: Defining TransformationK08CA270085 · NCI · DANA-FARBER CANCER INST · PI Erin M Parry · 2022 to 2026
$945k
NCI NIH HHS K08 CA270085NCI NIH HHS P01 CA206978NCI NIH HHS U10 CA180861
6 · The paper itself

Abstract

Although the genetic landscape of chronic lymphocytic leukemia (CLL) has been broadly profiled by large-scale sequencing studies performed over the past decade, the molecular basis of the transformation of CLL into aggressive lymphoma, or Richter syndrome (RS), has remained incompletely characterized. Recent advances in computational methods of clonal deconvolution, as well as extensive sample collection efforts in this rapidly progressive malignancy, have now enabled comprehensive analysis of paired CLL and RS samples and have led to multiple new studies investigating the genetic, transcriptomic, and epigenetic origins of RS. In parallel, new genetically engineered and xenograft mouse models have provided the opportunity for gleaning fresh biological and mechanistic insights into RS development and stepwise evolution from antecedent CLL. Altogether, these studies have defined RS driver lesions and CLL risk lesions and identified pathways dysregulated in transformation. Moreover, unique molecular subtypes of RS have been revealed, including a disease marked by profound genomic instability with chromothripsis/chromoplexy and whole genome duplication. Novel profiling approaches, including single-cell DNA and transcriptome sequencing of RS biopsy specimens and cell-free DNA profiling of patient plasma, demonstrate promise for the timely identification of RS clones and may translate to noninvasive identification and early diagnosis of RS. This review summarizes the recent scientific advances in RS and supports the integrated study of human genomics with mouse modeling to provide an advanced understanding of the biological underpinnings of transformation. These recent studies have major implications for much-needed novel therapeutic strategies for this still largely incurable malignancy.

Indexed as

Cell Transformation, NeoplasticLeukemia, Lymphocytic, Chronic, B-CellLymphoma, Large B-Cell, DiffuseAnimalsGenome, HumanHumansMiceXenograft Model Antitumor Assays

Identifiers

PMID36758208
PMCPMC10356575
OpenAlexW4319661445

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.