ArticleCancer research2018
Inhibition of the Stromal p38MAPK/MK2 Pathway Limits Breast Cancer Metastases and Chemotherapy-Induced Bone Loss.
Article in Cancer research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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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.
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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.
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Who cites it
42 citing papers in PubMed, 66 citations in OpenAlex.
- Disruption of CDK4/6-RARα-NF-κB axis attenuates senescence-associated inflammation and improves function during aging and following chemotherapy.Nature aging · 2026Article
- Review
- p38 blockade reverses the immune suppressive tumor microenvironment in metastatic breast cancer.Research square · 2025Article
- Stromal senescence contributes to age-related increases in cancer.Nature reviews. Cancer · 2025Review
- Cancer treatments accelerate ageing.Nature reviews. Cancer · 2025Article
- Targeting Senescence in Oncology: An Emerging Therapeutic Avenue for Cancer.Current oncology (Toronto, Ont.) · 2025Review
- MK2 promotes p16 negative head and neck cancer migration, invasion, and metastasis.Cancer letters · 2025Article
- Targeted delivery of liposomal senolytics to alleviate cellular senescence-induced bone loss.Fundamental research · 2025Article
- Review
- Neuronal p38 MAPK Signaling Contributes to Cisplatin-Induced Peripheral Neuropathy.Antioxidants (Basel, Switzerland) · 2025Article
- Role, mechanisms and effects ofOncology letters · 2025Review
- Harnessing the interaction between redox signaling and senescence to restrain tumor drug resistance.Frontiers in cell and developmental biology · 2025Review
- MK2-mediated AKT/MYC signaling activation promotes epithelial-mesenchymal transition in lung adenocarcinoma.Frontiers in genetics · 2025Article
- Collagen Mineralization Decreases NK Cell-Mediated Cytotoxicity of Breast Cancer Cells via Increased Glycocalyx Thickness.Advanced materials (Deerfield Beach, Fla.) · 2024Article
- Targeting senescence-associated secretory phenotypes to remodel the tumour microenvironment and modulate tumour outcomes.Clinical and translational medicine · 2024Review
- Therapy-induced senescence through the redox lens.Redox biology · 2024Review
- Senescent CAFs Mediate Immunosuppression and Drive Breast Cancer Progression.Cancer discovery · 2024Article
- COLLAGEN MINERALIZATION DECREASES NK CELL-MEDIATED CYTOTOXICITY OF BREAST CANCER CELLS VIA INCREASED GLYCOCALYX THICKNESS.bioRxiv : the preprint server for biology · 2024Article
- MAPK-activated protein kinase 2 is associated with poor prognosis of glioma patients and immune inhibition in glioma.Frontiers in oncology · 2024Article
- p38MAPKα Stromal Reprogramming Sensitizes Metastatic Breast Cancer to Immunotherapy.Cancer discovery · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 3 institutions in 2 countries.
Funding
Abstract
The role of the stromal compartment in tumor progression is best illustrated in breast cancer bone metastases, where the stromal compartment supports tumor growth, albeit through poorly defined mechanisms. p38MAPKα is frequently expressed in tumor cells and surrounding stromal cells, and its expression levels correlate with poor prognosis. This observation led us to investigate whether inhibition of p38MAPKα could reduce breast cancer metastases in a clinically relevant model. Orally administered, small-molecule inhibitors of p38MAPKα or its downstream kinase MK2 each limited outgrowth of metastatic breast cancer cells in the bone and visceral organs. This effect was primarily mediated by inhibition of the p38MAPKα pathway within the stromal compartment. Beyond effectively limiting metastatic tumor growth, these inhibitors reduced tumor-associated and chemotherapy-induced bone loss, which is a devastating comorbidity that drastically affects quality of life for patients with cancer. These data underscore the vital role played by stromal-derived factors in tumor progression and identify the p38MAPK-MK2 pathway as a promising therapeutic target for metastatic disease and prevention of tumor-induced bone loss.
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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.