ArticleBMC cancer2022
Inhibition of hyperprogressive cancer disease induced by immune-checkpoint blockade upon co-treatment with meta-tyrosine and p38 pathway inhibitor.
Article in BMC cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- Sex and risk of hyperprogressive disease in cancer patients receiving immune checkpoint inhibitors: a systematic review and meta-analysis.Frontiers in immunology · 2026Pooled it
- Evidence that non-cognate proteinogenic amino acids generate immunogenic neoepitopes.The Journal of biological chemistry · 2026Review
- Gompertz growth with a shared carrying capacity optimally simulates primary and metastatic tumor growth dynamics.British journal of cancer · 2026Article
- Neoadjuvant chemoimmunotherapy in patients with locally advanced squamous head and neck cancer: A retrospective study.Frontiers in oncology · 2025Article
- Neoadjuvant treatment in locally advanced thyroid cancer: a single institution experience.Frontiers in oncology · 2025Article
- Resistance against the development of diethylnitrosamine-induced hepatocellular carcinoma in female C3H mice: an experimental model.Experimental animals · 2024Article
- Prediction model for hyperprogressive disease in patients with advanced solid tumors received immune-checkpoint inhibitors: a pan-cancer study.Cancer cell international · 2023Article
- Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlthough immune-checkpoint inhibitors (ICI) are overall promissory for cancer treatment, they entail, in some cases, an undesired side-effect called hyperprogressive-cancer disease (HPD) associated with acceleration of tumor growth and shortened survival.
methodsTo understand the mechanisms of HPD we assayed the ICI therapy on two murine tumors widely different regarding immunogenicity and, subsequently, on models of local recurrences and metastases of these tumors. To potentiate the immune response (IR), we combined ICI with meta-tyrosine-that counteracts immune-suppressive signals-and a selective inhibitor of p38 pathway that proved to counteract the phenomenon of tumor-immunostimulation.
resultsICI were therapeutically effective against both tumor models (proportionally to their immunogenicity) but only when they faced incipient tumors. In contrast, ICI produced acceleration of large and residual tumors. The combined treatment strongly inhibited the growth of large tumors and it managed to cure 80% of mice with local recurrences and 60% of mice bearing residual metastases.
conclusionsTumor enhancement was paradoxically correlated to a weak increase of the antitumor IR suggesting that a weak IR - different from a strong tumor-inhibitory one-may produce stimulation of tumor growth, mimicking the HPD observed in some clinical settings.
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