Two-year treatment-free sustained remission after chemo-immunotherapy in a 52-year-old male with recurrent ARID1A-mutant lung adenocarcinoma: a case report

Introduction

Lung cancer is the second most frequently diagnosed malignancy worldwide and remains the leading cause of cancer-related mortality (1,2). Non-small cell lung cancer (NSCLC) comprises approximately 80–85% of all lung malignancies and is frequently diagnosed at an advanced stage, contributing to its unfavorable prognosis (3). The therapeutic landscape of advanced NSCLC has been substantially reshaped by precision oncology. This evolution is reflected in the numerous Food and Drug Administration (FDA) approvals for NSCLC granted during 2024 and 2025, which predominantly feature biomarker-directed tyrosine kinase inhibitors, bispecific antibodies, and antibody-drug conjugates (ADCs) targeting driver alterations such as epidermal growth factor receptor (EGFR) mutations, anaplastic lymphoma kinase (ALK) rearrangements, human epidermal growth factor receptor 2 (HER2) and c-MET mutations (4,5). While immune checkpoint inhibitors (ICIs) targeting programmed cell death protein 1 (PD-1) and its ligand (PD-L1) remain the cornerstone of treatment in the advanced and metastatic setting, identifying the genomic determinants of durable ICI response has acquired relevance in a period where standard-of-care is increasingly stratified by molecular phenotype.

The switch/sucrose non-fermentable (SWI/SNF) chromatin remodeling complex regulates gene expression through nucleosome repositioning and transcriptional control (6). SWI/SNF genes are frequently altered across malignancies, with somatic mutations present in nearly 25% of all cancers (7). However, the immunologic consequences of these mutations diverge depending on the specific subunit involved. Mutations in the SMARCA4 ATPase subunit are associated with aggressive clinical behavior, dedifferentiation, and an immunosuppressive tumor microenvironment (TME) characterized by reduced T-cell infiltration, increased regulatory T-cell density, and impaired antigen presentation (8,9). Accordingly, ICIs have demonstrated limited efficacy in SMARCA4-deficient NSCLC, with significantly shorter progression-free survival compared to SMARCA4-intact tumors (10). In contrast, loss-of-function alterations in the AT-rich interaction domain 1A (ARID1A) gene, encoding a DNA-binding subunit of the SWI/SNF complex and occurring in 5–10% of NSCLCs (11), have been identified as potential determinants of enhanced responsiveness to immunotherapy (IO) (12,13).

Despite this mechanistic rationale, to our knowledge, no prior case of sustained complete remission following IO has been reported in ARID1A-mutant NSCLC. Here, we describe a case of complete remission in a patient with ARID1A-mutant lung adenocarcinoma treated with carboplatin, pemetrexed and pembrolizumab at the time of locoregional recurrence, with longitudinal confirmation of the ARID1A-mutant clone across primary and recurrent disease and sustained treatment-free survival exceeding 2 years after therapy discontinuation. We present this case in accordance with the CARE reporting checklist (available at https://tlcr.amegroups.com/article/view/10.21037/tlcr-2026-1-0040/rc).

Case presentation (Figures 1,2)

Figure 1 Axial contrast-enhanced CT images and clinical course of the patient. At baseline, (A) with a lesion in the left lung (June 2019); (B) after completing neoadjuvant chemotherapy (partial response, October 2019); (C) after surgery and adjuvant chemotherapy, with no evidence of disease relapse (January 2020); (D) presenting an enlarged left superior mediastinal lymph node (yellow arrow) indicative of nodal recurrence (September 2021); (E) complete response following four cycles of chemo-immunotherapy, maintained afterwards. CR, complete response; CT, computed tomography; M, metastasis; N, node; PR, partial response; T, tumor.

Figure 2 Infiltrative component in the pulmonary lobectomy specimen (A) and detail of the tumoral glands (B); hematoxylin and eosin staining. Immunohistochemical staining of these glands shows cytoplasmic positivity for CK7 (C) and nuclear positivity for TTF-1 (D). Metastatic lymph node with near-complete replacement of nodal tissue by tumor (E), with a detail of the tumoral component and a thin rim of peripheral nodal tissue (F); hematoxylin and eosin staining. CK7, cytokeratin 7; TTF-1, thyroid transcription factor-1.

A 52-year-old Caucasian male, former 15-pack-year smoker with a 3-month history of mild irritative cough and no significant comorbidities or relevant findings on physical examination, was referred for a chest computed tomography (CT) scan in June 2019. Imaging revealed a mass in the upper lobe of the left lung with infiltration of the main pulmonary artery and left parahilar lymphadenopathies (Figure 1A). A tissue biopsy confirmed lung adenocarcinoma with thyroid transcription factor 1 (TTF-1) positivity by immunohistochemistry (IHC; Figure 2A-2D). Magnetic resonance imaging (MRI) ruled out intracranial dissemination, and ¹⁸F-fluorodeoxyglucose (¹⁸F-FDG) positron emission tomography (PET)/CT confirmed a stage IIB disease (cT2bN1M0) according to the 9^th edition of the tumor-node-metastasis (TNM) staging system. PD-L1 immunohistochemistry (IHC) using the Dako pharmDx 22C3 clone showed a tumor proportion score (TPS) of 30%. Fluorescence in situ hybridization (FISH) excluded ALK and ROS proto-oncogene 1 (ROS1) rearrangements. Polymerase chain reaction (PCR) testing ruled out mutations in EGFR, v-RAF murine sarcoma viral oncogene homolog B (BRAF), and Kirsten rat sarcoma viral oncogene homologue (KRAS). All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

The multidisciplinary tumor board considered the tumor initially unresectable due to vascular infiltration and recommended neoadjuvant chemotherapy with three cycles of cisplatin (75 mg/m², day 1) and pemetrexed (500 mg/m², day 1). Treatment was completed in October 2019 with excellent tolerance. Post-treatment CT scan showed a partial response in both the primary tumor and the lymph nodes (Figure 1B), and a left upper lobectomy with lymphadenectomy was subsequently performed. The surgical specimen demonstrated pT2aN1 adenocarcinoma [IHC: TTF-1⁺, cytokeratin 7 (CK7)⁺, napsin A⁺, p40^–; Figure 2A], free resection margins (R0), and visceral pleural invasion involving both elastic layers (PL2). In view of these findings, the patient received two additional cycles of adjuvant cisplatin and pemetrexed, completed in January 2020 (Figure 1C).

Follow-up visits and CT scans were performed every 3 months during the first year and every 6 months thereafter. In September 2021, surveillance imaging identified new mediastinal lymphadenopathies (Figure 1D). The differential diagnosis at that juncture included locoregional relapse of the original adenocarcinoma, a metachronous second primary lung malignancy, lymphoma involving mediastinal nodes, sarcoidosis, and infectious mediastinal lymphadenitis. Mediastinoscopy confirmed recurrent adenocarcinoma with PD-L1 TPS of 30% (Figure 2E,2F). Histopathologic examination demonstrated an identical TTF-1-positive, CK7-positive immunophenotype to the 2019 surgical specimen, without evidence of lymphoid proliferation, granuloma formation, or microbiologic organisms on special stains, thereby excluding lymphoproliferative and granulomatous etiologies. The anatomic continuity with the prior surgical field and the absence of morphologic features suggestive of a different histologic subtype further supported the diagnosis of recurrence over a metachronous primary.

Next-generation sequencing (NGS) was performed on the 2019 diagnostic specimen using the Oncomine Precision GX5-Solid Tumor DNA and Fusions panel (version w3.2.0, Genexus Integrated Sequencer, Thermo Fisher Scientific), identifying a somatic, pathogenic ARID1A c.2109del p.(Ala704ProfsTer38) frameshift mutation in exon 5 with a variant allele fraction (VAF) of 13.86%. NGS of the 2021 recurrence sample detected the same ARID1A mutation (VAF 12.66%) and a TP53 c.730G>T p.(Gly244Cys) pathogenic variant in exon 7 (VAF 17.28%). No microsatellite instability, structural variants, germline alterations, or copy number variations were detected. The persistence of the identical ARID1A frameshift variant across both specimens, separated by a 26-month interval, confirmed clonal continuity and provided molecular evidence that the mediastinal recurrence originated from the resected primary adenocarcinoma rather than representing a de novo malignancy.

Given the disease-free interval exceeding 20 months since adjuvant chemotherapy, regarded as sufficient to permit platinum re-exposure, the biologic rationale for incorporating PD-1 blockade, and the lack of approved alternatives such as datopotamab deruxtecan at that time, the tumor board proposed systemic therapy with carboplatin [area under the curve (AUC) 5, day 1], pemetrexed (500 mg/m², day 1), and pembrolizumab (200 mg fixed dose, day 1), which was initiated in November 2021. After four cycles, a CT scan performed in January 2022 demonstrated a complete response (Figure 1E). Treatment-related adverse events included a single episode of grade 1 anterior uveitis according to the Common Terminology Criteria for Adverse Events (CTCAE) in April 2022, successfully managed with topical dexamethasone. The patient subsequently developed persistent diarrhea, consisting of four to five depositions daily without hematochezia. Flexible colonoscopy revealed mild patchy erythema confined to the sigmoid colon and rectum without ulceration or luminal hemorrhage, whereas histopathologic examination demonstrated intraepithelial lymphocytosis and focal cryptitis in one fragment, consistent with lymphocytic colitis and focal active colitis; the clinical features, together with the endoscopic and pathologic findings, led to the diagnosis of grade 2 immune-related colitis. Given the absence of deep ulcerations, proximal colonic involvement, and systemic manifestations, a conservative approach with loperamide and dietary modification was adopted, achieving adequate symptom control.

Maintenance therapy was administered every 3 weeks for 20 months (27 cycles), after which treatment was discontinued in January 2024 per patient preference despite a sustained metabolic response. After 2 years off treatment, he remains asymptomatic with no radiologic evidence of relapse.

Discussion

To our knowledge, this is the first reported case of sustained and complete remission following chemo-immunotherapy administered for locoregional recurrence in a patient with ARID1A-mutant lung adenocarcinoma. The 24-month period of disease control observed after therapy cessation represents a clinically meaningful treatment-free survival, an endpoint adopted in recent IO trials to capture benefit beyond progression-free and overall survival (14). This outcome carries favorable prognostic implications: in KEYNOTE-189, the progression-free rate 3 years after completing 35 cycles of pembrolizumab was 56.2%, reinforcing that sustained off-treatment disease control of this magnitude remains uncommon and has been associated with durable immune surveillance (15). Taken together, these observations raise the possibility that the underlying ARID1A mutation contributed to an immunologically favorable tumor phenotype, a hypothesis supported by the mechanistic evidence discussed below.

ARID1A encodes a DNA-binding subunit of the canonical BRG1/BRM-associated factor (cBAF) chromatin-remodeling complex, which regulates chromatin accessibility and multiple DNA-dependent processes including transcription and DNA repair (16). Mechanistically, loss of ARID1A disrupts the resolution of transcription-associated RNA-DNA hybrids (R-loops), leading to replication stress and accumulation of cytosolic DNA fragments, which activate the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway, triggering a type I interferon transcriptional program that enhances tumor immunogenicity (17). This immune activation promotes antigen presentation, chemokine expression, and recruitment of cytotoxic lymphocytes, resulting in increased infiltration by CD8⁺ T and natural killer cells and the establishment of a more inflamed TME that may convert immunologically “cold” tumors into “hot” tumors, more sensitive to ICI therapy (17).

Most patients with advanced NSCLC lack guideline-recognized, druggable driver alterations with approved targeted therapies (18). In this setting, prediction of clinical benefit from ICIs has relied predominantly on the semiquantitative PD-L1 expression assessed by IHC on baseline tumor tissue (19,20). More recently, genomic biomarkers such as tumor mutational burden (TMB) and mismatch-repair deficiency/microsatellite instability-high (MMRd/MSI-H) have been explored as complementary predictors of response, although their clinical utility remains variable and context-dependent (21-23). In this context, ARID1A alterations have emerged as a candidate determinant of ICI responsiveness: despite their association with adverse clinicopathologic features, such as poorer differentiation, higher rates of nodal and distant metastasis, and more advanced staging, they correlate with increased TMB, MSI, high neoantigen load, and elevated PD-L1 expression (16,24,25). In our patient, the combination of intermediate PD-L1 expression and an ARID1A frameshift mutation may have contributed to the observed profound response, although the absence of TMB data limits mechanistic interpretation. The TP53 pathogenic variant may also be relevant, as retrospective analyses link TP53 co-mutations in SWI/SNF-altered NSCLC to inflamed TME and improved ICI responsiveness (26).

In our case, ARID1A mutational status was identified at the moment of recurrence rather than at diagnosis, which may have delayed trial consideration and limited the scope of individualized risk stratification. This observation reinforces the value of early comprehensive genomic profiling in advanced NSCLC to detect actionable driver alterations and support enrollment in biomarker-driven studies, while also capturing genomic features that may influence IO responsiveness (27,28). Incorporating ARID1A, SMARCA4, and other SWI/SNF subunits into routine profiling panels could facilitate early recognition of tumors with increased immunogenic potential and, if validated prospectively, help identify patients achieving deep metabolic responses who might benefit from discontinuing treatment.

Ongoing translational research targeting ARID1A-deficient tumors is preliminary but promising. Early-phase clinical trials are exploring ICI efficacy in ARID1A-deficient tumors. For example, NCT04957615 is a phase II study evaluating nivolumab in patients with ARID1A-mutant, chemokine (C-X-C motif) ligand 13 (CXCL13)-expressing unresectable or metastatic solid tumors; it will report objective response rate and survival outcomes (29). Complementary to IO, synthetic lethality approaches are being evaluated in clinical trials to target pathways rendered essential by ARID1A loss, including poly (ADP-ribose) polymerase (PARP), enhancer of zeste homolog 2 (EZH2), and ataxia telangiectasia and Rad3-related protein (ATR) inhibition (30). Of note, JAB-2485, a small-molecule inhibitor targeting Aurora kinase A (AURKA), has demonstrated potent and highly selective inhibition of this protein in preclinical studies (31), and is being evaluated on an ongoing phase 1/2a trial (NCT05490472) (32).

This case report had several limitations. First, as a single case report, its findings cannot be generalized to a broader population. Second, the absence of a comparative control group limits the ability to draw definitive conclusions regarding the relative efficacy of the treatment regimen in ARID1A-mutant NSCLC. Third, TMB was not assessed, which would have been of interest given that ARID1A alterations have been associated with hypermutated phenotypes (33). Finally, the lack of functional analysis of the detected mutations hinders a comprehensive understanding of the mechanisms underlying the observed sensitivity to IO.

Prospective cohort studies and randomized trials are needed to validate ARID1A mutations as a predictive biomarker for ICI clinical benefit. Given the pan-tumor distribution of ARID1A alterations, platform or basket trials and coordinated registries may efficiently evaluate targeted strategies.

Patient perspective

“When I was first told that the cancer had returned, I felt devastated because I had endured the surgery and the chemotherapy believing it was over. Starting the new treatment was emotionally tough, but the medical team explained what the molecular tests meant and why they believed this combination could work for me specifically. The 22 months of maintenance were demanding; the hospital visits every 3 weeks affected my work schedule and personal life, and the episodes of diarrhea were uncomfortable and unpredictable, although manageable. However, learning that the scans showed no remaining disease gave me the strength to continue. When the time came to decide whether to stop treatment, I was anxious about the cancer returning, but I trusted my oncologist’s judgment that the benefits of continued therapy no longer outweighed the toll it was taking. Two years later, I feel well and am grateful for the outcome.”

Conclusions

This case report supports a potential association between ARID1A alterations and enhanced sensitivity to immune checkpoint inhibition in NSCLC. The plausibility of this association is reinforced by emerging evidence linking ARID1A loss to increased tumor immunogenicity, including higher mutational load, neoantigen generation, and a more inflamed TME, all of which may potentiate ICI responsiveness. Our findings advocate the incorporation of ARID1A testing into comprehensive genomic profiling, which could enable earlier recognition of SWI/SNF-altered tumors with immunologic vulnerability. Further validation research is required to confirm its role as a predictive biomarker of response to ICI.

Acknowledgments

We acknowledge the patient and his family for providing consent for publication.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://tlcr.amegroups.com/article/view/10.21037/tlcr-2026-1-0040/rc

Peer Review File: Available at https://tlcr.amegroups.com/article/view/10.21037/tlcr-2026-1-0040/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://tlcr.amegroups.com/article/view/10.21037/tlcr-2026-1-0040/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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