ReviewBiochemical pharmacology2010
Inflammation and survival pathways: chronic lymphocytic leukemia as a model system.
Review in Biochemical pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.
- Recent trends in research on the role of cholesterol in leukemia: a bibliometric and visualization study.Frontiers in immunology · 2025Pooled it
- Evaluation of the anti-leukemia activity and underlying mechanisms of the novel perinucleolar compartment inhibitor CTI-2 in acute myeloid leukemia.Investigational new drugs · 2025Article
- Molecular Regulation of SASP in Cellular Senescence: Therapeutic Implications and Translational Challenges.Cells · 2025Review
- Evaluation of the anti-leukemia activity and underlying mechanisms of the novel perinucleolar compartment inhibitor CTI-2 in acute myeloid leukemia.Investigational new drugs · 2025Article
- The Quest for Eternal Youth: Hallmarks of Aging and Rejuvenating Therapeutic Strategies.Biomedicines · 2024Review
- Ageing microenvironment mediates lymphocyte carcinogenesis and lymphoma drug resistance: From mechanisms to clinical therapy (Review).International journal of oncology · 2024Review
- Targeting vascular senescence in cardiovascular disease with aging.The journal of cardiovascular aging · 2024Article
- PIM3 Kinase: A Promising Novel Target in Solid Cancers.Cancers · 2024Review
- The potential for senotherapy as a novel approach to extend life quality in veterinary medicine.Frontiers in veterinary science · 2024Review
- Therapy-induced senescence in breast cancer: an overview.Exploration of targeted anti-tumor therapy · 2024Review
- Low plateletcrit is associated with reduced progression: Free and overall survival in chronic lymphocytic leukemia.Journal of medical biochemistry · 2023Article
- Article
- Cellular senescence and senolytics: the path to the clinic.Nature medicine · 2022Review
- Insights Into the Role of Mortalin in Alzheimer's Disease, Parkinson's Disease, and HIV-1-Associated Neurocognitive Disorders.Frontiers in cell and developmental biology · 2022Review
- BH3-mimetics: recent developments in cancer therapy.Journal of experimental & clinical cancer research : CR · 2021Review
- PIM Kinases in Multiple Myeloma.Cancers · 2021Review
- Comparison of the mRNA expression profile of B-cell receptor components in normal CD5-high B-lymphocytes and chronic lymphocytic leukemia: a key role of ZAP70.Cancer medicine · 2017Article
- Broad targeting of resistance to apoptosis in cancer.Seminars in cancer biology · 2015Review
- Pre-clinical evidence of PIM kinase inhibitor activity in BCR-ABL1 unmutated and mutated Philadelphia chromosome-positive (Ph+) leukemias.Oncotarget · 2015Article
- Regulation of Mcl-1 expression in context to bone marrow stromal microenvironment in chronic lymphocytic leukemia.Neoplasia (New York, N.Y.) · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
A primary response to inflammation is an increased survival of the target cell. Several pathways have been identified that promote maintenance of the cell. The principal mechanism for the extended survival is through induction of anti-apoptotic Bcl-2 family proteins. Bcl-2 was the founding member of this family with five additional members, Bcl-X(L), Bcl-W, Bcl-B, Bfl-1, and Mcl-1, discovered mostly in hematological malignancies. Another mechanism that could add to cell survival is the Pim kinase pathway. This family of enzymes is associated with Myc-driven transcription, cell cycle regulation, degradation of pro-apoptotic proteins, and protein translation. Chronic lymphocytic leukemia serves as an optimal model to understand the mechanism by which these two protein families provide survival advantage to cells. In addition, since this malignancy is known to be maintained by microenvironment milieu, this further adds advantage to investigate mechanisms by which these pro-survival proteins are induced in the presence of stromal support. Multiple mechanisms exists that result in increase in transcript and protein level of anti-apoptotic Bcl-2 family members. Following these inductions, post-translational modifications occur resulting in increased stability of pro-survival proteins, while Pim-mediated phosphorylation inhibits pro-apoptotic protein activity. Furthermore, there is a cross-talk between these two (Bcl-2 family proteins and Pim family proteins) pathways that co-operate with each other for CLL cell survival and maintenance. Vigorous efforts are being made to create small molecules that affect these proteins directly or indirectly. Several of these pharmacological inhibitors are in early clinical trials for patients with hematological malignancies.
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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.