Exploration of the immunogenetic landscape of hyperprogressive disease after combined immunotherapy in cancer patients

Gong, Caifeng; Zhang, Wen; Sun, Yangying; Shou, Jianzhong; Jiang, Zhichao; Liu, Tianyi; Wang, Shengzhou; Li, Jun; Yin, Sun; Zhou, Aiping

doi:10.1016/j.isci.2023.106720

Cited by 4 publications

(2 citation statements)

References 32 publications

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“…Genomic profiling emerges as a promising avenue for discerning HP disease, as evidenced by a case report study implicating EGFR alteration and MDM2 amplification as potential indicators for HPD in NSCLC) ( 90 , 91 ). Notably, MDM2/MDM4 amplification was universally detected in all hyper progressive patients, all experiencing cessation of immunotherapy merely two months post-treatment initiation.…”

Section: Hyper Progressive Diseasementioning

confidence: 99%

Further knowledge and developments in resistance mechanisms to immune checkpoint inhibitors

Berland,

Gabr,

Chang

et al. 2024

Front. Immunol.

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The past decade has witnessed a revolution in cancer treatment, shifting from conventional drugs (chemotherapies) towards targeted molecular therapies and immune-based therapies, in particular immune-checkpoint inhibitors (ICIs). These immunotherapies release the host’s immune system against the tumor and have shown unprecedented durable remission for patients with cancers that were thought incurable, such as metastatic melanoma, metastatic renal cell carcinoma (RCC), microsatellite instability (MSI) high colorectal cancer and late stages of non-small cell lung cancer (NSCLC). However, about 80% of the patients fail to respond to these immunotherapies and are therefore left with other less effective and potentially toxic treatments. Identifying and understanding the mechanisms that enable cancerous cells to adapt to and eventually overcome therapy can help circumvent resistance and improve treatment. In this review, we describe the recent discoveries on the onco-immunological processes which govern the tumor microenvironment and their impact on the resistance to PD-1/PD-L1 checkpoint blockade.

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Section: Hyper Progressive Diseasementioning

confidence: 99%

Further knowledge and developments in resistance mechanisms to immune checkpoint inhibitors

Berland,

Gabr,

Chang

et al. 2024

Front. Immunol.

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“…Several studies have indicated that HPD is associated with various factors, including older age, poor performance status, higher tumor burden, as well as amplification of EGFR or MDM2/4, and immune-cell biomarkers. 6 It is worth noting that patients older than 65 are more susceptible to developing HPD, and those with poor performance status (PS) are at a higher risk. 7 , 8 The mechanism connecting HPD and advanced age may be due to the immunosenescence, which causes a reduction generated by age-related thymic atrophy.…”

Section: Introductionmentioning

confidence: 99%

Exploration of genetic characterization in hyperprogressive disease after immunotherapy retreatment in a patient with LCNEC: A case report

Zhang,

Yang,

Shao

et al. 2024

Human Vaccines & Immunotherapeutics

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Immune checkpoint inhibitors (ICIs) have emerged as a promising therapeutic option for large cell neuroendocrine carcinoma (LCNEC). However, various studies have suggested a potential risk of hyperprogressive disease (HPD) in patients receiving ICI, which might be associated with gene alterations. Here, this is the first report on an unknown primary LCNEC patient who had achieved a long-term response from ICI treatment (atezolizumab), but developed HPD after tumor progression due to receiving another ICI agent (serplulimab). The mutation region of FAT4, SMARCA4, CYLD, CTNNB1, and KIT was altered prior to serplulimab treatment compared to before atezolizumab treatment. This case suggested a potential association between these mutated genes and HPD. Patients with the aforementioned genes should caution when selecting ICI treatment. These findings required further confirmation in a larger study cohort.

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Immunotherapy‐induced reprogramming of cancer‐associated fibroblasts can promote tumor progression

Yamashita,

Horiguchi,

Kadomatsu

et al. 2024

Genes to Cells

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Use of immune checkpoint inhibitors (ICIs) as cancer immunotherapy has advanced rapidly in the clinic; however, ICI initiation can also cause an unexpectedly rapid acceleration of cancer progression in some patients. Here, we used a murine syngeneic melanoma model to conduct mechanistic analysis of cancer‐associated fibroblast (CAF) function in cancer progression in the context of immunotherapy. We found that after ICI treatment CAFs acquire inflammatory properties, which can promote tumor progression. Mechanistically, we show that T‐cell‐derived interferon‐γ (IFN‐γ) stimulates production of tumor necrosis factor‐α (TNF‐α) by macrophages, facilitating CAF conversion to inflammatory CAFs. Our findings suggest that CAF/immune cell crosstalk plays an essential role in ICI‐associated tumor progression.

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Exploration of the immunogenetic landscape of hyperprogressive disease after combined immunotherapy in cancer patients

Cited by 4 publications

References 32 publications

Further knowledge and developments in resistance mechanisms to immune checkpoint inhibitors

Further knowledge and developments in resistance mechanisms to immune checkpoint inhibitors

Exploration of genetic characterization in hyperprogressive disease after immunotherapy retreatment in a patient with LCNEC: A case report

Immunotherapy‐induced reprogramming of cancer‐associated fibroblasts can promote tumor progression

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