Lymphoblasts Express Hemostatic Factors: A Mechanism for Hypercoagulability in Pediatric Acute Lymphoblastic Leukemia
Bibliographic record
Abstract
Venous thromboembolism (VTE) is a serious complication of pediatric acute lymphoblastic leukemia (ALL), primarily occurring during induction therapy and associated with acquired hemostatic abnormalities. However, the contribution of leukemic lymphoblasts to hypercoagulability remains unexplored. This study aimed to determine whether leukemic lymphoblasts express hemostatic factors that promote a hypercoagulable state and to assess the functional impact of lysed lymphoblasts on thrombin and fibrin generation.We examined the expression of 28 hemostatic factors at both mRNA and protein levels in four pediatric leukemic cell lines (T-ALL and B-ALL) and normal lymphocytes using RT-PCR and immunoblotting. To evaluate the overall functional effect, we conducted thrombin and fibrin generation assays by adding cell lysates to platelet-poor plasma in the absence of exogenous tissue factor or phospholipids.Leukemic lymphoblasts constitutively expressed the procoagulants tissue factor, factor VIII and factor XIIIa; the coagulation inhibitors antithrombin, ADAMTS13 and TFPI; and the pro-fibrinolytic and antifibrinolytic proteins uPA, TAFI, and α2-AP. Lysed, but not intact, leukemic lymphoblasts enhanced thrombin and fibrin generation, indicating a procoagulant state. Additionally, leukemic lysates exhibited a hypo-fibrinolytic state, as evidenced by prolonged fibrin clot lysis times.These findings suggest that leukemic lymphoblasts actively contribute to a hypercoagulable state in pediatric ALL by simultaneously increasing procoagulant activity and impairing fibrinolysis. This study provides novel insights into the mechanisms underlying VTE risk in pediatric ALL, highlighting the role of leukemic lymphoblasts in disrupting the hemostatic balance. · Leukemic lymphoblasts express hemostatic system factors at gene and protein levels.. · Leukemic lymphoblasts lysis directly contributes to hypercoagulability and hypofibrinolysis in thrombin and fibrin generation assays..
Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.
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 | 0.000 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.000 | 0.000 |
| Bibliometrics | 0.000 | 0.000 |
| 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) | 0.001 | 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".