Polymorphisms in cell cycle pathway genes and risk of non-Hodgkin’s lymphoma
Bibliographic record
Abstract
2558 Cell cycle genes, responsible for cell cycle checkpoints and apoptotic process, have been documented to be involved in the development and progression of many human cancers. Genetic variations in cell cycle genes may alter cell cycle function, resulting in the accumulation of genetic damage and consequently promoting tumorigenesis. Here, we test the hypothesis that genetic polymorphisms in several major cell cycle pathway genes may be associated with non-Hodgkin’s lymphoma (NHL) risk in a population-based case-control study in Connecticut women involving 518 cases and 597 controls who donated either blood or buccal cell samples. High-throughput genotyping was conducted on an ABI 7900HT sequence detection system at the Core Genotyping Facility of the National Cancer Institute (http://snp500cancer.nci.nih.gov). We examined associations between nine single nucleotide polymorphisms (SNPs) in six cell cycle genes and NHL risk: BCL6, TP53, CCNH, CCND1, CHEK1, and CDKN2A. A SNP (rs1056932) in the B cell lymphoma 6 (BCL6) gene showed a significantly increased risk for all NHL (OR=2.1, 95%CI: 1.4-3.2), for all B-cell lymphomas (OR=2.0, 95%CI: 1.3,3.1), and T-cell lymphomas (OR=5.1, 95%CI: 2.0,13.0) for the C/C compared to the T/T genotype. Significantly increased risk was similarly observed for the following B cell subtypes: B-cell chronic lymphatic leukemia/prolymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) (OR=3.5, 95%CI: 1.6,7.9), diffuse large B-cell lymphoma (OR=2.0, 95%CI: 1.1,3.5), and follicular lymphoma (OR=2.0, 95%CI: 1.1,3.7). The tumor suppressor TP53 polymorphism (rs1042522) was associated with a reduced risk of T-cell lymphoma (OR=0.4, 95%CI: 0.2,0.9) for C/C and C/G combined genotypes compared to the G/G genotype. A significantly reduced risk of CLL/SLL was also observed for the combined C/C and C/T genotypes of the CCNH gene (rs2266690) compared to the T/T genotype (OR=0.4, 95%CI: 0.2,0.9). There were no significant associations found between SNPs in the CCND1, CHEK1, or CDKN2A genes and risk of NHL overall and by subtype. Our results support the hypothesis that genetic variation in cell cycle genes play a role in the etiology of NHL and support the need for more intensive investigation of this pathway as a factor in lymphomagenesis.
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.000 | 0.001 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.000 | 0.000 |
| Bibliometrics | 0.001 | 0.001 |
| Science and technology studies | 0.000 | 0.000 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.000 | 0.000 |
| Insufficient payload (model declined to judge) | 0.002 | 0.000 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".