ReviewCancers2017
The Role of PI3K Isoforms in Regulating Bone Marrow Microenvironment Signaling Focusing on Acute Myeloid Leukemia and Multiple Myeloma.
Review in Cancers, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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
23 citing papers in PubMed, 39 citations in OpenAlex.
- PI3Kδ inhibitor YY‑20394 is effective alone or in combination with Bcl‑2 inhibitor ABT199 in acute myeloid leukemia cells.Oncology reports · 2026Article
- Review
- Whole-Exome Sequencing, Mutational Signature Analysis, and Outcome in Multiple Myeloma-A Pilot Study.International journal of molecular sciences · 2024Article
- AC024896.1/miR-363-3p Axis Regulates the Malignant Progression of Acute Myeloid Leukemia by Cuproptosis-Related Gene MYO1B.Blood and lymphatic cancer : targets and therapy · 2024Article
- Alternative splicing in multiple myeloma is associated with the non-homologous end joining pathway.Blood cancer journal · 2023Article
- Natural products modulate cell apoptosis: a promising way for treating endometrial cancer.Frontiers in pharmacology · 2023Review
- Cellular senescence in cancers: relationship between bone marrow cancer and cellular senescence.Molecular biology reports · 2022Review
- Venetoclax-Resistant MV4-11 Leukemic Cells Activate PI3K/AKT Pathway for Metabolic Reprogramming and Redox Adaptation for Survival.Antioxidants (Basel, Switzerland) · 2022Article
- PI3K Targeting in Non-solid Cancer.Current topics in microbiology and immunology · 2022Review
- YBX1 promotes tumor progression via the PI3K/AKT signaling pathway in laryngeal squamous cell carcinoma.Translational cancer research · 2021Article
- Metabolic Disorders in Multiple Myeloma.International journal of molecular sciences · 2021Review
- Inhibition of the proteasome and proteaphagy enhances apoptosis in FLT3-ITD-driven acute myeloid leukemia.FEBS open bio · 2021Article
- The PI3K-Akt-mTOR Signaling Pathway in Human Acute Myeloid Leukemia (AML) Cells.International journal of molecular sciences · 2020Review
- Highly multiplexed proteomic assessment of human bone marrow in acute myeloid leukemia.Blood advances · 2020Article
- Metabolic Reprogramming Induces Immune Cell Dysfunction in the Tumor Microenvironment of Multiple Myeloma.Frontiers in oncology · 2020Review
- The role of Pim kinase in immunomodulation.American journal of cancer research · 2020Review
- Bone Marrow Senescence and the Microenvironment of Hematological Malignancies.Frontiers in oncology · 2020Review
- Co-targeting CK2α and YBX1 suppresses tumor progression by coordinated inhibition of the PI3K/AKT signaling pathway.Cell cycle (Georgetown, Tex.) · 2019Article
- Development of Multi-Target Chemometric Models for the Inhibition of Class I PI3K Enzyme Isoforms: A Case Study Using QSAR-Co Tool.International journal of molecular sciences · 2019Article
- Using Prognosis-Related Gene Expression Signature and Connectivity Map for Personalized Drug Repositioning in Multiple Myeloma.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite the development of novel treatments in the past 15 years, many blood cancers still remain ultimately fatal and difficult to treat, particularly acute myeloid leukaemia (AML) and multiple myeloma (MM). While significant progress has been made characterising small-scale genetic mutations and larger-scale chromosomal translocations that contribute to the development of various blood cancers, less is understood about the complex microenvironment of the bone marrow (BM), which is known to be a key player in the pathogenesis of chronic lymphocytic leukaemia (CLL), AML and MM. This niche acts as a sanctuary for the cancerous cells, protecting them from chemotherapeutics and encouraging clonal cell survival. It does this by upregulating a plethora of signalling cascades within the malignant cell, with the phosphatidylinositol-3-kinase (PI3K) pathway taking a critical role. This review will focus on how the PI3K pathway influences disease progression and the individualised role of the PI3K subunits. We will also summarise the current clinical trials for PI3K inhibitors and how these trials impact the treatment of blood cancers.
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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 Socratic graph.