Targeting signaling pathways in multiple myeloma: Pathogenesis and implication for treatments
Abstract
Multiple myeloma (MM), which is characterized by osteolytic bone lesions, anemia, hypercalcemia, and renal failure, accounts for approximately 10% of all hematologic malignancies. Although the therapeutic landscape of MM has evolved spectacularly over the past decades with 5-year median survival over 50%, most of these patients relapse eventually. The widely recognized therapeutic approaches include chemotherapy, radiation, stem cell transplant, and monoclonal antibody therapy. Former studies have implied that the proliferation, survival, migration and drug resistance of MM cells are in association with the activation of several signaling pathways. In this review, we intended to focus on the major signaling pathways such as PI3K/Akt/mTOR, Ras/Raf/MEK/MAPK, JAK/STAT, NF-κB, Wnt/β-catenin, and RANK/RANKL/OPG, that contribute to the pathogenesis of the MM and the therapeutic approaches developed to target them.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The pathogenesis of multiple myeloma involves interaction between MM cells and the bone marrow microenvironment through soluble cytokines and cell adhesion molecules, activating PI3K/AKT/mTOR, RAS/MAPK, JAK/STAT, Wnt/β-catenin, and NF-κB pathways.
“The pathogenesis of MM involves the interaction between MM cells and the bone marrow microenvironment through soluble cytokines and cell adhesion molecules, which activate various signaling pathways such as PI3K/AKT/mTOR, RAS/MAPK, JAK/STAT, Wnt/β-catenin, and NF-κB pathways.”
From Multiple myeloma: signaling pathways and targeted therapy (2024) · cites this paper as [31]
Cites
1 retracted
RETRACTED: Targeting MEK induces myeloma-cell cytotoxicity and inhibits osteoclastogenesis
Tai, Y.-T., Fulciniti, M., Hideshima, T., Song, W., Leiba, M., Li, X.-F., Rumizen, M., Burger, P., Morrison, A., Podar, K., et al. (2007) · Blood · doi:10.1182/blood-2007-03-081240 · Cited by 109 · see citing works
RetractedDarnell, J. E., Kerr, L. M., & Stark, G. R. (1994) · Science · doi:10.1126/science.8197455 · Cited by 6,080 · see citing works
Wnt/β-catenin signaling and disease
Clevers, H., & Nusse, R. (2012) · Cell · doi:10.1016/j.cell.2012.05.012 · Cited by 5,554 · see citing works
Elotuzumab Therapy for Relapsed or Refractory Multiple Myeloma
Lonial, S., Dimopoulos, M., Palumbo, A., White, D., Grosicki, S., Spicka, I., Walter-Croneck, A., Moreau, P., Mateos, M.-V., Magen, H., et al. (2015) · New England Journal of Medicine · doi:10.1056/nejmoa1505654 · Cited by 1,322 · see citing works
Body, J.-J., Greipp, P., Coleman, R. E., Facon, T., Geurs, F., Fermand, J.-P., Harousseau, J.-L., Lipton, A., Mariette, X., Williams, C. D., et al. (2003) · Cancer · doi:10.1002/cncr.11138 · Cited by 383 · see citing works
Bone marrow mesenchymal stem cells are abnormal in multiple myeloma
Corre, J., Mahtouk, K., Attal, M., Gadelorge, M., Huynh, A., Fleury-Cappellesso, S., Danho, C., Laharrague, P., Klein, B., Rème, T., et al. (2007) · Leukemia · doi:10.1038/sj.leu.2404621 · Cited by 328 · see citing works
Spencer, A., Yoon, S.-S., Harrison, S. J., Morris, S. R., Smith, D. A., Brigandi, R. A., Gauvin, J., Kumar, R., Opalinska, J. B., & Chen, C. (2014) · Blood · doi:10.1182/blood-2014-03-559963 · Cited by 142 · see citing works
Flagged first, then by citations
Cited by
Sorted by citations
Multiple myeloma: signaling pathways and targeted therapy
Lu, Q., Yang, D., Li, H., Niu, T., & Tong, A. (2024) · Molecular biomedicine · doi:10.1186/s43556-024-00188-w · Cited by 90 · see citing works
- Authors
- Hu, J., & Hu, W.-X.
- Affiliations
- Central South University (CN)
- Corresponding author
- Hu, Jingping
- Hu, Wei-Xin
- ORCID
- Hu, Jingping
- Venue
- Cancer Letters
- Publisher
- Elsevier BV
- Published
- 2018-02
- Volume
- 414
- Pages
- 214-221
- ISSN
- 0304-3835 (ISSN-L)
- OpenAlex
- W2770054994
- Cited by
- 84
- References
- 7
- Citations by year
- 2026: 5 · 2025: 7 · 2024: 10 · 2023: 13 · 2022: 8 · 2021: 15 · 2020: 10 · 2019: 13 · 2018: 3
- FWCI
- 1.14
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Cancer Letters (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (81400819, 81372538)
- Topics
- Health Sciences › Medicine › Hematology › Multiple Myeloma Research and Treatments
- Health Sciences › Medicine › Genetics › Chronic Lymphocytic Leukemia Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Keywords
- multiple myeloma, signaling pathways, PI3K/AKT/mTOR pathway, JAK/STAT signaling, NF-κB, Wnt/β-catenin signaling, drug resistance, myeloma pathogenesis, targeted therapy, monoclonal antibodies, stem cell transplantation
- MeSH terms
- Phosphoinositide-3 Kinase Inhibitors, Antineoplastic Agents, Humans, Multiple Myeloma, Signal Transduction, Phosphatidylinositol 3-Kinases, MAP Kinase Signaling System, Proto-Oncogene Proteins c-akt, TOR Serine-Threonine Kinases, Molecular Targeted Therapy
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
