ArticleProceedings of the National Academy of Sciences of the United States of America2009
Mutations in a gene encoding a midbody kelch protein in familial and sporadic classical Hodgkin lymphoma lead to binucleated cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- A genome-wide meta-analysis of nodular sclerosing Hodgkin lymphoma identifies risk loci at 6p21.32.Blood · 2012Pooled it
- Familial lymphoma and genetic predisposition: an updated review.BMC medical genomics · 2026Review
- Unfolding the enigma of familial Hodgkin lymphoma: Current insights.World journal of clinical cases · 2026Review
- Characteristics of the Kelch domain containing (KLHDC) subfamily and relationships with diseases.FEBS letters · 2025Review
- The art of war: using genetic insights to understand and harness radiation sensitivity in hematologic malignancies.Frontiers in oncology · 2024Review
- Deciphering the Genetic Complexity of Classical Hodgkin Lymphoma: Insights and Effective Strategies.Current genomics · 2024Review
- Article
- Discovery of novel predisposing coding and noncoding variants in familial Hodgkin lymphoma.Blood · 2023Article
- Gene and pathway based burden analyses in familial lymphoid cancer cases: Rare variants in immune pathway genes.PloS one · 2023Article
- Genetic lesions and targeted therapy in Hodgkin lymphoma.Therapeutic advances in hematology · 2023Review
- Review
- Promising drugs and treatment options for pediatric and adolescent patients with Hodgkin lymphoma.Frontiers in cell and developmental biology · 2022Review
- Plasma Extracellular Vesicle Long RNAs Have Potential as Biomarkers in Early Detection of Colorectal Cancer.Frontiers in oncology · 2022Article
- Lactate induced up-regulation of KLHDC8A (Kelch domain-containing 8A) contributes to the proliferation, migration and apoptosis of human glioma cells.Journal of cellular and molecular medicine · 2020Article
- Identification of Familial Hodgkin Lymphoma Predisposing Genes Using Whole Genome Sequencing.Frontiers in bioengineering and biotechnology · 2020Article
- Germline mutations in Protection of Telomeres 1 in two families with Hodgkin lymphoma.British journal of haematology · 2018Article
- Article
- Article
- Predispositions to Lymphoma: A Practical Review for Genetic Counselors.Journal of genetic counseling · 2016Review
- Whole exome sequencing in families at high risk for Hodgkin lymphoma: identification of a predisposing mutation in the KDR gene.Haematologica · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 8 institutions in 2 countries.
Funding
Abstract
Classical Hodgkin lymphoma (cHL) is a malignancy of B-cell origin in which the neoplastic cells, known as "Reed-Sternberg" (RS) cells, are characteristically binucleated. Here we describe a family where multiple individuals developing cHL have inherited a reciprocal translocation between chromosomes 2 and 3. The translocation disrupts KLHDC8B, an uncharacterized gene from a region (3p21.31) previously implicated in lymphoma and related malignancies, resulting in its loss of expression. We tested KLHDC8B as a candidate gene for cHL and found that a 5'-UTR polymorphism responsible for decreasing its translational expression is associated with cHL in probands from other families with cHL and segregates with disease in those pedigrees. In one of three informative sporadic cases of cHL, we detected loss of heterozygosity (LOH) for KLHDC8B in RS cells, but not reactive T lymphocytes, purified from a malignant lymph node. KLHDC8B encodes a protein predicted to contain seven kelch repeat domains. KLHDC8B is expressed during mitosis, where it localizes to the midbody structure connecting cells about to separate during cytokinesis, and it is degraded after cell division. Depletion of KLHDC8B through RNA interference leads to an increase in binucleated cells, implicating its reduced expression in the formation of cHL's signature RS cell.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.