Thymic Neuroendocrine Tumours: What Patients Need to Know About the Science, Diagnosis and Treatment

Table of Contents

• Key Points
• Background: Why This Research Matters
• How the Review Was Conducted
• Pathology: How These Tumours Are Classified
• Genetic Alterations and Signalling Pathways
• Transcriptional and Epigenetic Control
• Clinical Characteristics and Management
• The Immune Microenvironment
• Treatment Approaches
• Clinical Implications for Patients
• Limitations of the Evidence
• Recommendations and Future Directions
• Frequently Asked Questions
• Source Information

Key Points

• T-NETs are exceptionally rare, with an annual incidence of about 0.01–0.02 per 100,000 people, and account for fewer than 5% of all thymic tumours.
• They are biologically distinct from other neuroendocrine tumours, so treatments borrowed from other NETs may not be optimal.
• High-grade tumours (LCNEC and SCC) are enriched for TP53/RB1 alterations and chromosomal instability; low-grade tumours generally have a low mutation burden.
• Surgical resection is the only curative option for localised disease; advanced disease treatments are extrapolated from other NETs.
• Improved care requires thymus-specific molecular and immune profiling, standardised diagnostic criteria, and prospective collaborative studies.

Background: Why This Research Matters

Thymic neuroendocrine tumours (T-NETs) are exceptionally rare malignancies. The annual incidence is approximately 0.01–0.02 per 100,000 people. These tumours account for fewer than 5% of all thymic neoplasms (tumours of the thymus gland).

T-NETs span a wide spectrum of disease. At one end are well-differentiated typical and atypical carcinoids. At the other end are poorly differentiated large-cell and small-cell neuroendocrine carcinomas (NECs). This spectrum aligns with the broader framework used for neuroendocrine neoplasms elsewhere in the body. However, T-NETs arise within the distinct anatomical and immunological environment of the thymus gland.

T-NETs often behave aggressively. They show early involvement of lymph nodes, frequent recurrence and distant metastasis (spread to other organs). These features support the recognition of T-NETs as a biologically distinct entity.

Clinically, the presentation of T-NETs is often nonspecific or delayed. Many patients are diagnosed only when the disease is locally advanced or has already metastasised. Institutional series and registry-based analyses report large primary tumours, frequent mediastinal lymph-node involvement and distant spread. These factors contribute to unfavourable outcomes relative to thymoma (a different, generally less aggressive thymic tumour).

Radiological features of T-NETs overlap with other anterior mediastinal tumours. Therefore, definitive diagnosis relies on histopathology (microscopic examination of tissue) and immunohistochemistry (IHC, a technique that uses antibodies to identify specific proteins in tissue). Small biopsies and intratumoural heterogeneity (differences between different areas of the same tumour) may limit grading accuracy. These factors can also complicate the distinction from thymic carcinoma or metastatic neuroendocrine tumours from other sites.

Recent molecular and immune studies have begun to refine the understanding of T-NETs, although cohort sizes remain small. Higher-grade tumours more often show disruption of the TP53 (tumour protein p53) and RB1 (retinoblastoma 1) pathways, along with chromosomal instability. Lineage-associated transcriptional programmes only partially overlap with pulmonary (lung) NEC paradigms.

Early immunophenotyping studies suggest heterogeneous PD-L1 (programmed death-ligand 1) and VISTA (V-domain Ig suppressor of T-cell activation) expression, along with variable immune-cell infiltration. This indicates that checkpoint markers should be interpreted within the broader immune context rather than as standalone biomarkers. These findings suggest that extrapolated management strategies may not fully capture thymus-specific biology. They underscore the need for disease-specific evidence.

Given the scarcity of prospective trials and the predominance of small retrospective studies, this review summarises current evidence on the pathological, molecular and immune landscape of T-NETs. The review also examines contemporary diagnostic and therapeutic approaches and outlines translational directions for biomarker-driven management.

How the Review Was Conducted

The authors conducted a structured narrative review of T-NETs and closely related thoracic NETs. They searched PubMed/Medline, Embase, Web of Science and Scopus for articles published between 1 January 2000 and 28 February 2026.

Search terms included:

• "thymic neuroendocrine tumor" and "thymic neuroendocrine neoplasm"
• "thymic carcinoid"
• "thymic large-cell neuroendocrine carcinoma" and "thymic small-cell carcinoma"
• "molecular", "genomic", "transcriptional" and "epigenetic"
• "immune microenvironment" and "immune checkpoint"
• "immunotherapy"
• "somatostatin receptor"
• "everolimus"
• "peptide receptor radionuclide therapy"
• "targeted therapy"

Reference lists of relevant articles were also screened manually.

Eligible studies included adult human studies of primary T-NETs. These studies reported clinicopathological features, diagnostic criteria, molecular or immune profiling, treatment outcomes, recurrence or survival. Relevant guidelines, consensus statements, systematic reviews and high-quality reviews were also included when they provided diagnostic, biological or clinical context.

Exclusion criteria were:

• Nonhuman studies
• Paediatric-only reports
• Duplicate or overlapping cohorts without complementary data
• Conference abstracts without sufficient methodological or outcome details
• Non-English-language articles without accessible full text
• Studies without extractable T-NET-specific information

Literature on nonthymic NETs was used only to contextualise shared biological pathways or treatment strategies. It was not used to estimate T-NET incidence, prognosis or treatment outcomes.

The selection process followed a simplified narrative-review workflow. This included database searching, title and abstract screening, full-text assessment, manual reference checking and qualitative thematic synthesis.

The final cited evidence base comprised 80 references. These included:

• 25 T-NET-specific original studies or case-based reports
• 13 T-NET-focused reviews, guidelines, consensus statements or systematic reviews
• 24 contextual studies from nonthymic or broader NETs
• 18 contextual studies related to thymic epithelial tumours (TETs), differential diagnosis, local therapy, imaging or immune checkpoint inhibitor safety

Within the T-NET-specific evidence base:

• 13 studies addressed epidemiology, clinicopathological features, endocrine syndromes or prognosis
• 6 addressed histopathology, diagnostic classification or imaging
• 5 addressed molecular, genomic, transcriptional or epigenetic features
• 2 addressed the immune microenvironment or immune checkpoint expression
• 10 addressed surgery, radiotherapy, systemic therapy, peptide receptor radionuclide therapy or other therapeutic strategies

Because some studies contributed to more than one thematic domain, these categories were not mutually exclusive. No formal meta-analysis was performed because of heterogeneous study designs and small T-NET cohorts. Direct T-NET evidence was distinguished from extrapolated or hypothesis-generating data throughout the review.

Pathology: How These Tumours Are Classified

T-NETs are classified in the 2021 World Health Organization (WHO) classification of thoracic tumours. They are classified in parallel with pulmonary NETs into four categories:

1. Typical carcinoid (TC)
2. Atypical carcinoid (AC)
3. Large-cell neuroendocrine carcinoma (LCNEC)
4. Small-cell carcinoma (SCC)

Histologically, T-NETs show classic neuroendocrine architecture. This includes organoid nesting, trabeculae, rosettes and peripheral palisading. They should be distinguished from thymomas and thymic carcinomas that lack unequivocal neuroendocrine differentiation.

TC and AC are well-differentiated neoplasms with relatively uniform cytology and preserved organoid architecture. In contrast, LCNEC and SCC are poorly differentiated tumours with marked atypia (abnormal cell appearance), high mitotic activity and extensive necrosis (tissue death).

As in pulmonary NETs, grading is primarily based on mitotic count and necrosis in standardised fields equivalent to 2mm²:

• TC: fewer than 2 mitoses per 2mm² and no necrosis
• AC: 2–10 mitoses per 2mm² and/or focal necrosis
• LCNEC/SCC: more than 10 mitoses per 2mm² with extensive geographic or confluent necrosis

However, thymic tumours may display overlapping features, particularly between AC and LCNEC. This makes classification challenging in limited specimens.

Immunohistochemistry (IHC) is essential to confirm neuroendocrine differentiation and thymic epithelial origin. T-NETs typically express synaptophysin and chromogranin A, with CD56 positivity in most cases.

INSM1 (insulinoma-associated protein 1) is a sensitive nuclear marker of neuroendocrine differentiation in T-NETs. However, INSM1 may also be expressed in some non-neuroendocrine thymic carcinomas. Therefore, it should be interpreted with morphology and a broader IHC panel.

Cytokeratin expression supports epithelial differentiation. Radiologic correlation and exclusion of thymoma-associated features help distinguish primary T-NETs from metastatic pulmonary or extrathoracic NETs.

The role of Ki-67 in T-NET grading remains unsettled. Ki-67 is a protein marker of cell division. Although Ki-67 is not formally incorporated into the 2021 WHO grading criteria for thoracic NETs, higher Ki-67 indices may correlate with adverse outcomes and refine prognostic stratification.

DINTER and colleagues proposed a "Thy-NET G1–G3" morphomolecular grading concept. This concept integrates mitotic rate, Ki-67, necrosis and genomic features. This framework supports the recognition of a well-differentiated high-grade NET, or NET G3-like category, in the thymus. This category should be distinguished from poorly differentiated NEC, including LCNEC and SCC. This approach is consistent with the broader WHO 2022 neuroendocrine neoplasm framework.

To improve diagnostic reproducibility, the International Collaboration on Cancer Reporting recommends structured reporting of TETs, including T-NETs. Key elements include tumour type, mitotic count, necrosis, margin status and relevant IHC markers.

Genetic Alterations and Signalling Pathways

Comprehensive genomic profiling indicates that T-NETs have a relatively low single-nucleotide mutation burden. They show recurrent but mostly low-frequency alterations and substantial copy-number changes.

In contrast to pancreatic and many pulmonary NETs, classical NET-associated genes are only sporadically altered in T-NETs. These genes include MEN1 (multiple endocrine neoplasia type 1), ATRX (α-thalassemia/mental retardation syndrome X-linked) and DAXX (death domain-associated protein). This suggests site-specific molecular biology and a less prominent role for canonical telomere-maintenance pathways in T-NETs.

By contrast, TP53 and RB1 alterations are enriched in high-grade T-NETs. In the clinicogenomic study by STRÖBEL and colleagues, abnormal p53 expression and loss of Rb immunoreactivity were largely confined to LCNEC and SCC. These alterations were uncommon in TC and AC.

DINTER and colleagues further integrated copy-number, mutation and protein data. They proposed three morphomolecular "Thy-NET G1–G3" groups. These groups are characterised by increasing chromosomal instability and a gradual shift from carcinoid-like to NEC-like TP53/RB1 alterations.

These findings support a broad molecular distinction between:

• Low-mutational-burden, well-differentiated TC/AC
• High-grade LCNEC/SCC driven by TP53/RB1 inactivation and extensive aneuploidy (abnormal chromosome numbers)

At the pathway level, chromatin remodelling and PI3K (phosphatidylinositol 3-kinase)/AKT (AKT serine/threonine kinase 1)/mTOR (mechanistic target of rapamycin) signalling appear to be important molecular hubs. Thoracic carcinoids, including thymic primaries, are enriched for alterations in chromatin regulation and histone modification. Canonical oncogenic driver mutations are relatively infrequent.

Although prospective T-NET-specific therapeutic data remain limited, the involvement of PI3K/AKT/mTOR dysregulation provides biological support for mTOR inhibition in selected progressive well-differentiated T-NETs. This is supported by the established activity of everolimus in thoracic NETs and limited thymic experience.

Transcriptional and Epigenetic Control

Transcriptional profiling of T-NETs remains limited but has begun to identify lineage-associated transcription factor programmes. In a 16-case series, OMURA and colleagues found that ASCL1 (achaete-scute family bHLH transcription factor 1) was expressed in most thymic carcinoids. NEUROD1 (neuronal differentiation 1) and POU2F3 (POU class 2 homeobox 3) were uncommon. YAP1 (Yes-associated protein 1) expression was mainly observed in LCNEC, with ASCL1/YAP1 co-expression in this subset.

These findings suggest that well-differentiated thymic carcinoids frequently align with an ASCL1-high neuroendocrine programme. Some high-grade tumours may acquire YAP1-associated features. However, the four-factor transcriptional framework widely used in SCLC (small-cell lung cancer) cannot yet be directly applied to T-NETs without larger thymus-specific multi-omic validation.

Evidence on epigenetic regulation in T-NETs is even more limited. Epigenetic regulation refers to changes in gene activity that do not involve changes to the DNA sequence itself. Insights from pulmonary and gastroenteropancreatic NETs suggest that chromatin modifiers and DNA methylation programmes may contribute to neuroendocrine differentiation, lineage plasticity and treatment resistance.

Although T-NET-specific methylation cohorts are lacking, these broader data support further investigation of epigenetic mechanisms in thymic primaries. This is particularly relevant in relation to lineage state, tumour grade and differential diagnosis.

Overall, current evidence supports a cautious model. In this model, T-NETs are characterised by:

• Low overall mutational burden
• TP53/RB1 alterations and chromosomal instability in high-grade LCNEC/SCC
• ASCL1-dominant transcriptional programmes with possible YAP1 involvement in a subset of high-grade tumours
• Incompletely defined epigenetic regulation

Larger thymus-specific multi-omics cohorts are needed before these findings can be translated into routine molecular subtyping or treatment selection.

Clinical Characteristics and Management

T-NETs are among the rarest thoracic malignancies, as shown by population-based Surveillance, Epidemiology, and End Results datasets. Although they account for fewer than 5% of thymic tumours, they are among the most aggressive thymic malignancies. They are associated with substantial risks of recurrence, metastasis and unfavourable survival.

Most cohorts report a male predominance of approximately 70% and a median age at onset in the fifth to sixth decades of life. In MEN1 (multiple endocrine neoplasia type 1) syndrome, T-NETs occur in approximately 3–8% of patients. They often show a strong male predominance and account for almost 20% of MEN1-associated mortality despite their rarity.

Clinical presentation is often delayed because the anterior mediastinum (the front part of the chest cavity between the lungs) permits substantial tumour growth before symptoms appear. Many patients present with locally advanced disease. In a 26-patient cohort, 61.5% had Masaoka–Koga stage III–IV disease and 23.1% had stage IVb disease at diagnosis.

Symptoms are usually nonspecific and related to mediastinal mass effect. These include:

• Chest pain or tightness
• Cough
• Dyspnoea (shortness of breath)
• Superior vena cava syndrome (compression of the large vein returning blood from the upper body)

Endocrine or paraneoplastic manifestations occur in a clinically meaningful minority, reported in up to 20–30% of cases. The most common are ectopic adrenocorticotropic hormone (ACTH)-dependent Cushing syndrome and MEN1-associated disease. Classic carcinoid syndrome is rare.

Biochemical assessment should therefore be guided by clinical presentation. In patients with suspected functional disease, syndrome-directed hormone testing may support diagnosis and follow-up. This includes ACTH/cortisol evaluation and selected gut hormone profiles.

Chromogranin A can aid disease monitoring in selected patients. However, its specificity is limited. Levels may be affected by renal dysfunction, proton-pump inhibitor use and other non-neoplastic conditions. Neuron-specific enolase may provide additional information in high-grade NECs. However, it should be interpreted as a supportive rather than diagnostic marker.

T-NETs show a marked propensity for nodal and distant spread. The lungs and bones are frequent metastatic sites, whereas liver involvement appears less common. In a systematic review of 162 cases of ectopic Cushing syndrome due to T-NETs, most patients presented with locally invasive or advanced disease. The median survival was approximately 38 months. This underscores the aggressive course of hormone-secreting T-NETs.

The Immune Microenvironment

The immune microenvironment of T-NETs is predominantly "inflamed". This means that immune cells are present within the tumour. However, the immune response is often restrained by a myeloid-rich stroma (connective tissue containing many immune cells of the myeloid lineage).

PD-L1 (programmed death-ligand 1) and VISTA (V-domain Ig suppressor of T-cell activation) expression is heterogeneous. T-cell infiltration is variable. These findings indicate that checkpoint markers should be interpreted within the broader immune context rather than as standalone biomarkers.

This immune landscape suggests that immunotherapy and novel combinations represent emerging investigational avenues. However, the complex immune environment means that simple checkpoint marker testing may not be sufficient to predict which patients will respond to immunotherapy.

Treatment Approaches

For localised disease, surgical resection (surgery to remove the tumour) is curative. This is the mainstay of treatment when the tumour has not spread.

In advanced stages, therapy is extrapolated from other NETs. Current options include:

• Somatostatin analogues for somatostatin receptor-positive tumours
• Everolimus (an mTOR inhibitor)
• Temozolomide-based regimens (chemotherapy)
• Peptide receptor radionuclide therapy in selected cases

Immunotherapy and novel combinations represent emerging investigational avenues. The authors note that PI3K/AKT/mTOR dysregulation is involved in these tumours. Everolimus has established activity in thoracic NETs, and thymic experience is limited. Together, these factors provide biological support for mTOR inhibition in selected progressive well-differentiated T-NETs.

The authors emphasise that current management is extrapolated from other neuroendocrine tumours. This highlights a critical need for a synthesised understanding of the unique molecular and immune landscape of T-NETs.

Clinical Implications for Patients

This review has several important implications for patients with T-NETs and their families.

First, T-NETs are biologically distinct thymic malignancies. They are not simply the same as neuroendocrine tumours arising in other parts of the body. This means that treatment approaches borrowed from other NETs may not be optimal.

Second, the molecular drivers of T-NETs are grade-specific. High-grade tumours (LCNEC and SCC) are enriched for TP53/RB1 alterations and chromosomal instability. Low-grade tumours (TC and AC) generally have a low mutation burden and occasional MEN1 alterations. This distinction has implications for prognosis and potentially for treatment selection.

Third, the immune microenvironment is complex. PD-L1 and VISTA expression is heterogeneous, and T-cell infiltration is often restrained by a myeloid-rich stroma. This means that checkpoint markers alone may not reliably predict response to immunotherapy.

Fourth, current treatment options for advanced disease are limited and extrapolated from other NETs. Surgical resection remains the only curative option for localised disease.

Fifth, improved care will require thymus-specific molecular and immune profiling, standardised diagnostic criteria and prospective collaborative studies. This means that patients may benefit from enrolment in clinical trials and from treatment at centres with expertise in rare thymic malignancies.

Limitations of the Evidence

The authors acknowledge several important limitations of the current evidence base.

First, T-NETs are exceptionally rare. This makes it difficult to conduct large prospective trials. Most available evidence comes from small retrospective studies and case reports.

Second, cohort sizes in molecular and immune studies remain small. This limits the statistical power of these studies and the generalisability of their findings.

Third, no formal meta-analysis was performed because of heterogeneous study designs and small T-NET cohorts. This means that the review provides a qualitative synthesis rather than a quantitative pooled analysis.

Fourth, direct T-NET evidence is limited in several domains. For example, only two studies addressed the immune microenvironment or immune checkpoint expression. Only five addressed molecular, genomic, transcriptional or epigenetic features.

Fifth, much of the evidence on treatment outcomes is extrapolated from nonthymic NETs. The authors explicitly state that literature on nonthymic NETs was used only to contextualise shared biological pathways or treatment strategies. It was not used to estimate T-NET incidence, prognosis or treatment outcomes.

Sixth, T-NET-specific methylation cohorts are lacking. Evidence on epigenetic regulation in T-NETs is even more limited than evidence on genetic alterations.

Seventh, the four-factor transcriptional framework widely used in SCLC cannot yet be directly applied to T-NETs without larger thymus-specific multi-omic validation.

Eighth, the role of Ki-67 in T-NET grading remains unsettled. Although higher Ki-67 indices may correlate with adverse outcomes, Ki-67 is not formally incorporated into the 2021 WHO grading criteria for thoracic NETs.

Ninth, thymic tumours may display overlapping features, particularly between AC and LCNEC. This makes classification challenging in limited specimens.

Recommendations and Future Directions

The authors conclude that T-NETs are biologically distinct thymic malignancies. Improved care will require several key steps.

1. Thymus-specific molecular and immune profiling: Larger thymus-specific multi-omics cohorts are needed before findings can be translated into routine molecular subtyping or treatment selection.
2. Standardised diagnostic criteria: Structured reporting of TETs, including T-NETs, is recommended to improve diagnostic reproducibility. Key elements include tumour type, mitotic count, necrosis, margin status and relevant IHC markers.
3. Prospective collaborative studies: Given the rarity of T-NETs, collaborative studies are essential to move beyond extrapolated treatment paradigms.
4. Biomarker-guided combinations: Thymus-specific molecular subtyping plus spatial immune profiling can move care beyond extrapolated regimens toward biomarker-guided combinations and dedicated trials.
5. Further investigation of epigenetic mechanisms: Although T-NET-specific methylation cohorts are lacking, broader data support further investigation of epigenetic mechanisms in thymic primaries.
6. Validation of the Thy-NET G1–G3 framework: The diagnostic and clinical relevance of the proposed well-differentiated high-grade NET or NET G3-like category in the thymus requires further validation.

For patients, these recommendations translate into several practical considerations:

• Ask your healthcare team about molecular and immune profiling of your tumour.
• Discuss whether enrolment in a clinical trial is appropriate for your situation.
• Seek care at a centre with expertise in rare thymic malignancies.
• Discuss the role of surgical resection if your disease is localised.
• Ask about the full range of systemic therapy options for advanced disease, including somatostatin analogues, everolimus, temozolomide-based regimens and peptide receptor radionuclide therapy.
• Discuss whether immunotherapy or novel combinations might be appropriate for your case.

Frequently Asked Questions

What are thymic neuroendocrine tumours (T-NETs)?

T-NETs are exceptionally rare cancers of the thymus gland, with an annual incidence of about 0.01–0.02 per 100,000 people. They account for fewer than 5% of all thymic tumours. They range from well-differentiated typical and atypical carcinoids to poorly differentiated large-cell and small-cell neuroendocrine carcinomas, and they often behave aggressively.

How are T-NETs diagnosed?

Definitive diagnosis relies on histopathology (microscopic examination of tissue) and immunohistochemistry (IHC), which uses antibodies to identify specific proteins. T-NETs typically express synaptophysin and chromogranin A, with CD56 positivity in most cases. INSM1 is a sensitive marker but may also appear in some non-neuroendocrine thymic carcinomas, so it is interpreted with morphology and a broader panel.

What symptoms do T-NETs cause?

Symptoms are usually nonspecific and related to mediastinal mass effect. They include chest pain or tightness, cough, dyspnoea (shortness of breath), and superior vena cava syndrome (compression of the large vein returning blood from the upper body). Endocrine or paraneoplastic manifestations occur in up to 20–30% of cases, most commonly ectopic ACTH-dependent Cushing syndrome and MEN1-associated disease.

What does the mitotic count mean in T-NET grading?

Grading is primarily based on mitotic count and necrosis in standardised fields equivalent to 2mm². Typical carcinoid has fewer than 2 mitoses per 2mm² and no necrosis. Atypical carcinoid has 2–10 mitoses per 2mm² and/or focal necrosis. Large-cell and small-cell neuroendocrine carcinomas have more than 10 mitoses per 2mm² with extensive geographic or confluent necrosis.

What treatments are available for T-NETs?

For localised disease, surgical resection is curative and is the mainstay when the tumour has not spread. In advanced stages, therapy is extrapolated from other neuroendocrine tumours. Options include somatostatin analogues for somatostatin receptor-positive tumours, everolimus (an mTOR inhibitor), temozolomide-based regimens, and peptide receptor radionuclide therapy in selected cases. Immunotherapy and novel combinations are emerging investigational avenues.

Are T-NETs hereditary or linked to MEN1?

In MEN1 (multiple endocrine neoplasia type 1) syndrome, T-NETs occur in approximately 3–8% of patients. They often show a strong male predominance and account for almost 20% of MEN1-associated mortality despite their rarity. Most cohorts report a male predominance of approximately 70% and a median age at onset in the fifth to sixth decades of life.

What is the prognosis for T-NETs?

T-NETs are among the most aggressive thymic malignancies, with substantial risks of recurrence, metastasis and unfavourable survival. In a systematic review of 162 cases of ectopic Cushing syndrome due to T-NETs, most patients presented with locally invasive or advanced disease, and median survival was approximately 38 months. This underscores the aggressive course of hormone-secreting T-NETs.

When should a patient with a newly diagnosed thymic neuroendocrine tumour seek a second opinion?

A second opinion is worth considering when the diagnosis rests on a small biopsy, because thymic tumours can show overlapping features, particularly between atypical carcinoid and large-cell neuroendocrine carcinoma, making classification challenging in limited specimens. Review of pathology, immunohistochemistry and imaging can clarify tumour type, grade, mitotic count and necrosis. Because advanced disease treatment is extrapolated from other neuroendocrine tumours and several options exist, including somatostatin analogues, everolimus, temozolomide-based regimens and peptide receptor radionuclide therapy, expert review can help confirm the plan and identify clinical trials. Diagnostic Detectives Network provides independent expert second opinions.

Source Information

Original article title: Thymic neuroendocrine tumours: molecular landscape, immune microenvironment and therapeutic perspectives.

Authors: Ding J, Leng X, Han Y, Lin T.

Author affiliations: Department of Medical Oncology, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Hospital and Institute, Sichuan Cancer Center, University of Electronic Science and Technology of China, Chengdu, China; Division of Thoracic Surgery, Sichuan Cancer Hospital and Institute, Sichuan Cancer Center, University of Electronic Science and Technology of China, Chengdu, China

Corresponding author: Tongyu Lin (linty@sysucc.org.cn)

Publication: European Respiratory Review, 2026; volume 35, article 260016

DOI: 10.1183/16000617.0016-2026

Received: 14 January 2026

Accepted: 3 July 2026

Copyright: © The authors 2026. This version is distributed under the terms of the Creative Commons Attribution Non-Commercial Licence 4.0.

This patient-friendly article is based on peer-reviewed research.