Distinct multiplex immunofluorescence-based immune and stromal marker expression profile of subcutaneously metastatic SMARCA4-deficient undifferentiated thoracic tumor: a case report

Introduction

The SMARCA4 gene is located on band 3 of region 1 on the long arm of chromosome 19, encoding the BRG1 protein, one of the core catalytic subunits of the switch (SWI)/sucrose nonfermenting (SNF) remodeling complex. The deletion of the SMARCA4 gene has been confirmed in a variety of malignant tumors, such as malignant lung tumors, malignant gastrointestinal tumors, and malignant uterine and ovarian tumors. The SMARCA4 gene and the SWI/SNF complex play a wide range of roles in tumor suppression, and the deletion of the SMARCA4 gene may affect a number of molecular pathways (1,2). Thoracic SMARCA4-deficient tumors can be classified into two types: thoracic SMARCA4-deficient undifferentiated tumor (SMARCA4-UT) and SMARCA4-deficient non-small cell lung cancer (SMARCA4-dNSCLC). SMARCA4-UT, formerly known as SMARCA4-deficient thoracic sarcoma or SMARCA4-deficient thoracic sarcomatoid tumor, is an aggressive thoracic tumor associated with rapid progression and a low survival rate. SMARCA4-UT is a unique clinicopathological entity recognized in the 2021 World Health Organization classification of thoracic tumors (3). The overall prognosis of patients with SMARCA4-UT is poor, with patients often experiencing metastases, including to the cervical lymph nodes, gastrointestinal tract, adrenal glands, abdominopelvic cavity, and bones. The median survival of patients with SMARCA4-UT is only 9.6 months (4), and given the dearth of clinically significant target gene mutations and its poor response to chemotherapy, treatment strategies are still being investigated.

In terms of treatment, SMARCA4-UT lacks specific driver mutations, which contribute to the limited efficacy of traditional chemotherapy and targeted therapy. Immunotherapy with agents such as programmed cell death protein 1 (PD-1)/programmed cell death ligand 1 (PD-L1) inhibitors has emerged as a potential therapeutic option, but its response rate is low and heterogeneous, which is closely related to the unique tumor microenvironment (TME) of SMARCA4-UT (5). Key immune and stromal markers play critical roles in regulating or indicating TME function and tumor metastasis: CD8⁺ T cells are core antitumor effector cells, CD68⁺ macrophages participate in TME remodeling, PD-1/PD-L1 is a classic immune checkpoint mediating immune escape, CD56 is a marker of activated stromal myofibroblasts that promote metastasis, and pan-CK reflects the epithelial characteristics of tumor cells (6,7).

The majority of studies on SMARCA4-UT have focused on primary lesions, and the expression of key immune/stromal markers in subcutaneous metastatic lesions, as well as their correlation with immunotherapeutic efficacy, have not been fully clarified. Subcutaneous metastasis has biological behaviors and TME features distinct from those of primary lesions, which may affect treatment response. In this report, we describe a case of SMARCA4-UT with subcutaneous metastasis, outline the diagnostic process and treatment outcome, and discuss the results of systematic multiplex immunofluorescence (mIF) staining depicting the expression profile of six key markers in the subcutaneous metastatic lesion. It is hoped these findings can provide insights into the diagnosis, TME characteristics, and individualized treatment of patients with SMARCA4-UT and subcutaneous metastasis. We present this article in accordance with the CARE reporting checklist (available at https://tlcr.amegroups.com/article/view/10.21037/tlcr-2026-0218/rc).

Case presentation

A 49-year-old man was admitted to the department of thoracic oncology due to painful swelling of the left lower limb lasting for over a month, which was accompanied by intermittent chest tightness and shortness of breath, intermittent pain in the chest and back, and hoarseness. The patient had no fever, cough or sputum production, abdominal pain or diarrhea, or generalized joint pain. Six months prior to the visit, the patient underwent coronary angiography, which revealed a coronary artery stenosis of approximately 70%. The patient took an unknown medication for 1 month but then discontinued doing so. He had no other chronic illnesses, denied any allergies, and was not taking any long-term medications. He reported drinking alcohol occasionally, and he had smoked 40 cigarettes a day (2 packs) for over 20 years but had quit one 1 year prior. The patient had no significant family medical history.

Physical examination was conducted on admission. On the medial side of the left lower limb, there was a protruding, approximately round mass 3 cm × 2 cm in size; it was firm in texture, had poor mobility, and was slightly tender on palpation. There was no redness, swelling, or ulceration on the surface, and the skin temperature was slightly elevated. No vascular engorgement was observed around it. No abnormalities were found in the left upper limb or the right limb, and no other abnormalities were found on physical examination.

The patient had visited a local hospital 1 month prior. The bronchoscopic biopsy showed a small amount of bronchial mucosal tissue and cartilage in the left pulmonary hilum, with a few atypical cells around it. Tumor could not be ruled out. Immunohistochemistry showed CK (AE1/AE3) positivity in epithelial cells, LCA positivity in lymphocytes, and negative TTF-1 expression. Under microscopy, the lung puncture biopsy tissue appeared with coagulation and lymphoid tissue, with regular distribution of B cells and T cells in the lymphoid tissue, and no abnormal expression in the immunophenotype. Reactive hyperplasia was considered, and no malignant components were found in the received specimens. Immunohistochemistry of the lung puncture biopsy showed CD5 and CD3 positivity in T cells, CD21 positivity in the follicular dendritic cell network, CD20 positivity in B cells, and high Ki-67 expression in germinal centers. TdT, CD30, CK (AE1/AE3), and TTF-1 were negative. In situ hybridization for EBER was also negative.

Moreover, the pathological analysis of the puncture biopsy from the left leg mass showed a few atypical epithelial cells in a small amount of fibrous connective tissue. Given the clinical condition, metastatic cancer was suspected. Immunohistochemistry showed focal positivity for CK (AE1/AE3) and EMA, positivity for CK7, along with approximately 1% Ki-67 positivity. CD34, S-100, SMA, desmin, CK20, p40, and TTF-1 were negative. Testing for PD-L1 was completed for reference purposes only; PD-L1 was negative, with a combined positive score of 0. There were a few tumor cells, and the cancer tissue could not be classified.

The findings from positron emission tomography-computed tomography (PET-CT) were as follows: (I) there was a high metabolic focus at the left pulmonary hilum and mediastinum (6.1 cm × 5.0 cm), suggesting a malignant tumor, and biopsy was recommended for confirmation. Moreover, there was a high metabolic nodule in the left adrenal gland, suggesting possible metastasis; a soft tissue mass on the medial side of the left calf (2.5 cm × 1.8 cm) with elevated metabolism, suggesting metastasis involving the tibia; thickening of the gastric antrum wall with increased metabolism and multiple high metabolic nodules in the descending colon and sigmoid colon, suggesting the need for endoscopic examination to rule out tumor lesions. (II) Cavitary cerebral infarction was apparent in the left frontal lobe and the basal ganglia area. (III) There was sinusitis of the left maxillary sinus and thickening of the oropharyngeal wall with increased metabolism, suggesting inflammatory uptake; high metabolism of the left vocal cord was also observed.

The patient was admitted to our department. Considering the clinical findings, the patient’s symptoms, and the PET-CT results, we continued to conduct relevant examinations for further treatment.

Laboratory abnormalities included a slightly elevated cancer antigen 125 (CA125) level of 66.96 U/mL (reference range 0–35 U/mL). However, there were no abnormalities in the lung cancer-specific tumor markers, complete blood count, urinalysis, fecal examination, or liver function tests. The glomerular filtration rate and creatinine values remained within the normal range.

Gastroscopy revealed chronic gastritis and duodenal bulb inflammation, while colonoscopy revealed colonic polyps. Pathological testing of the colonic tissue indicated a tubular adenoma with low-grade intraepithelial neoplasia. Laryngoscopy showed paralysis of the left vocal cord, and no definite mass was found. There were no abnormalities in the multilead electrocardiogram, echocardiography with color Doppler ultrasound, or the pulmonary function test.

Pathological testing of the left lower leg puncture biopsy indicated a malignant tumor, which was considered to be poorly differentiated metastatic carcinoma. Immunohistochemistry results were as follows: CK8/18 positive, TTF-1 negative, napsin A negative, p40 negative, CK5/6 negative, Ki-67 positive (about 5%), Syn negative, and CD56 negative.

In light of the existing examination and laboratory results, as well as the patient’s condition, primary lung adenocarcinoma with subcutaneous metastasis in the left lower limb was considered. To further clarify whether there were any mutation targets of therapeutic significance, the patient underwent genetic testing for cancer. The result revealed potentially clinically significant variants: CDKN2A exon 2 frame shift mutation N71Rfs at 29.41%, SMARCA4 splicing mutation 1943+1 dup at 33.59%, TP53 exon 8 frameshift mutation P301Q at 27.22%, and TSC1 intron 4 210+1 deletion at 27:02%. The tumor mutation burden was 28.8 mutations/Mb, and microsatellite instability-high status was not indicated.

After obtaining the results of the genetic testing, we contacted the pathology department for a consultation to review the patient’s pathological results. The pathologist soon provided a supplementary pathology report. The combined results from immunohistochemistry and clinical genetics indicated SMARCA4-UT. The medical history was consistent with metastatic disease. The immunohistochemical findings were as follows: BRG negative, CK7 positive, CK20 focally positive, villin partially positive, CDX-2 positive, MUC1 positive, MUC2 negative, and MUC5AC negative. The histological findings under microscopy and BRG1 staining results of the patient are shown in Figure 1.

Figure 1 The histological findings under microscopy and BRG1 staining results of the patient. (A-C) The tumor cells appeared diffusely arranged in sheets or nests, with round or oval shapes. The cytoplasm was abundant and eosinophilic, and the nuclei were vesicular with prominent nucleoli. Hematoxylin and eosin staining: (A) ×40; (B) ×100; (C) ×400. (D-F) SMARCA4/BRG1-negative tumor cells. Immunohistochemistry: (D) ×40; (E) ×100; (F) ×400.

According to the 2021 World Health Organization classification of thoracic tumors, the diagnosis of this type of lung cancer primarily relies on pathology and immunohistochemistry. The presence of typical epithelioid structures (such as gland formation) and the absence of SMARCA4 (BRG1) expression in immunohistochemistry can inform diagnosis (8). Ultimately, our diagnosis of this patient was SMARCA4-UT with subcutaneous metastasis in the left lower limb and metastasis to the left adrenal gland (T3N2M1c, IVB).

With a clear diagnosis, the patient’s physical condition was comprehensively assessed, and after communication with the patient and his family, a treatment plan of immunotherapy combined with chemotherapy was decided upon. Specifically, tislelizumab [200 mg; d1, intravenous (IV), every 3 weeks (Q3W)] was combined with albumin-bound paclitaxel (260 mg/m²; d1, IV, Q3W), and carboplatin {area under the curve at 5× [creatinine clearance (mL/min) + 25] (maximum dose of 750 mg); d1, IV, Q3W}. During the treatment, the patient experienced no significant discomfort and had good compliance. The grade I anemia resolved on its own. After four cycles, the therapeutic effect was evaluated as stable disease. Tislelizumab monotherapy was then administered for maintenance, and the patient completed four maintenance cycles and discontinued medication due to grade II rash. The best therapeutic effect was evaluated as partial response. The treatment outcome was good, with significant relief of pain in the chest, back, and left lower limb.

The patient underwent regular imaging follow-up during treatment for evaluation of therapeutic efficacy (Figure 2). At the time of writing, the patient has a grade 1 rash and persistent hoarseness without significant changes, indicating a stable condition. In accordance with the patient’s personal preference, close monitoring of disease progression is being conducted, and no antitumor therapy has been initiated. All procedures performed in this study were in accordance with the Declaration of Helsinki and its subsequent amendments. Approval for this study was provided by the ethics committee of Tianjin Medical University Cancer Institute and Hospital (No. E20250575). Written informed consent was obtained from patient’s family for 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.

Figure 2 Computed tomography images of the patient. Red arrows indicate tumor lesions.

Materials and methods for mIF staining

mIF staining was performed to detect the expression and spatial distribution of target proteins in formalin-fixed paraffin-embedded tissue sections, with the entire experimental procedure being conducted via the fully automated AlphaXPainter Automated Staining System (AlphaX Bio, Beijing, China). All incubation time and temperature parameters were precisely controlled and standardized by the instrument to ensure experimental reproducibility.

Briefly, deparaffinization and antigen retrieval were sequentially conducted to fully expose the antigenic epitopes of target proteins in tissue sections for subsequent specific antibody binding. The target markers included CD20, CD56, CD8, PD-1, CD68, and pan-CK; a cyclic antibody labeling strategy with fluorophores was adopted for mIF staining. The staining cycle was repeated for all target markers, which included three key steps: primary antibody incubation for specific antigen-antibody binding, secondary antibody incubation for targeted conjugation to the primary antibody, and fluorophore conjugation to the secondary antibody for the fluorescent labeling of target proteins. After completion of cyclic fluorescent labeling for all markers, 4',6-diamidino-2-phenylindole (DAPI) was used for nuclear counterstaining. Subsequently, the stained tissue sections were mounted with an antifade mounting medium to prevent fluorescent signal quenching and preserve staining stability.

Fluorescent images of the stained sections were acquired with a fluorescent scanning imaging system. The expression levels, positive staining localization, and spatial distribution characteristics of CD20, CD56, CD8, PD-1, CD68, and pan-CK proteins in the samples were further subjected to qualitative and quantitative analysis via HALO 3.5 (Indica Labs, Albuquerque, NM, USA) and ZEN (Zeiss, Oberkochen, Germany) analysis software.

Results

mIF staining was performed to evaluate the expression patterns of six target molecules (CD20, CD56, CD8,
PD-1, CD68, and pan-CK) in SMARCA4-UT tissue sections, and positive staining signals with varying intensities were observed for all detected markers.

Quantitative and qualitative analyses with ZEN image analysis software further verified the differential expression profiles of these markers. Specifically, CD56, PD-1, and pan-CK were highly expressed, as evidenced by strong fluorescence intensity and a high percentage of positive cells in the tumor tissues. In contrast, CD8, CD68, and CD20 had low expression levels, characterized by weak fluorescence signals and a low proportion of positive cells among the studied specimens (Figure 3).

Figure 3 Multiplex immunofluorescence staining of SMARCA4-deficient undifferentiated thoracic tumor tissues showing the expression patterns of CD20, CD56, CD8, PD-1, CD68, and pan-CK. CD56, PD-1, and pan-CK exhibited high expression with strong fluorescent signals, while CD8, CD68, and CD20 exhibited low expression with weak fluorescent signals. Nuclei were counterstained with DAPI (blue). Scale bar =200 µm. DAPI, 4',6-diamidino-2-phenylindole; PD-1, programmed cell death protein 1.

Discussion

The majority of patients SMARCA4-UT have metastatic disease, with the commonly affected sites being the lymph nodes, bones, adrenal glands, liver, gastrointestinal tract, central nervous system, and kidneys. The patient described in our report had involvement in the subcutaneous tissue of the left lower limb, which, to our knowledge, has not been reported in the literature thus far, although one study has reported subcutaneous metastasis in a patient with SMARCA4-dNSCLC (9). In our patient, the lung biopsy did not reveal any significant findings. This suggests that due to its high malignancy and the diversity of its metastatic sites, the diagnosis and differential diagnosis of SMARCA4-UT are extremely difficult—a challenge which oncologists should be keenly aware of.

The high TMB in this case indicates high tumor immunogenicity, which is highly consistent with our mIF findings showing abundant immune cell infiltration and high expression of PD-1 and related immune checkpoints. This high immunogenicity provides a key biological explanation for the favorable clinical response to combined chemo-immunotherapy in this patient.

This study is the first to systematically analyze the expression profile of six key immune, stromal, and epithelial markers in a SMARCA4-UT subcutaneous metastatic lesion using mIF staining. This analysis revealed a distinct expression pattern: the high expression of CD56, PD-1, and pan-CK, along with the low expression of CD8, CD68, and CD20. CD56, a member of the immunoglobulin superfamily, is a classic marker of natural killer (NK) cells and neuroendocrine cells and is also expressed in certain types of malignant tumors, such as neuroendocrine carcinoma and undifferentiated tumors (10,11). We found high CD56 expression in the SMARCA4-UT subcutaneous metastatic lesion, which is a notable finding that has not been reported in previous studies on SMARCA4-UT. The discrepant CD56 expression results between pathological immunohistochemistry and mIF staining may be attributed to multiple factors, including the highly heterogeneous nature of SMARCA4-UT with focal/regional CD56 expression in tumor tissues, differences in detection sensitivity, and variations in antibody selection and antigen retrieval conditions. The high expression of CD56 in tumor cells has two possible implications. First, it may indicate that the SMARCA4-UT cells have partial neuroendocrine differentiation characteristics. Although SMARCA4-UT is defined as an undifferentiated tumor according to the World Health Organization (3), the expression of neuroendocrine markers such as CD56 suggests that it may have a slight tendency to differentiation. This may provide a greater understanding of the histological heterogeneity of SMARCA4-UT. Second, CD56 may promote the subcutaneous metastasis of SMARCA4-UT. Research suggests that CD56 expression in tumor cells is closely related to tumor invasion and metastasis: CD56 can mediate cell-cell adhesion and interaction with the extracellular matrix, thereby enhancing the migration and colonization ability of tumor cells in distant tissues (12). In our case, the high CD56 expression in the subcutaneous metastatic lesion suggests that it may promote the adhesion, infiltration, and growth of SMARCA4-UT cells in the subcutaneous tissue, which is consistent with the patient’s clinical manifestation of a hard, fixed subcutaneous mass. In addition, CD56⁺ tumor cells can secrete a variety of cytokines and chemokines to regulate the TME, which may further promote tumor metastasis by inhibiting the antitumor immune response (13). The high CD56 expression in this case also suggests that CD56 may be a potential prognostic marker and therapeutic target for SMARCA4-UT with subcutaneous metastasis, but this remains to be verified by further functional experiments and large-sample studies.

The expression of high PD-1 and low CD8/CD20 further confirms the presence of an “immune desert” TME characteristic of SMARCA4-UT. CD8⁺ T cells are the core effector cells of adaptive antitumor immunity, and their infiltration and normal function are the basis for effective antitumor immune response and sensitivity to immunotherapy (14). CD20 is a marker of B lymphocytes, which participate in antitumor immunity by secreting antibodies, presenting antigens, and regulating T-cell function (15). The low expression of CD8 and CD20 in the subcutaneous metastatic lesion indicates that both adaptive cellular immunity and humoral immunity are severely impaired in the TME of SMARCA4-UT subcutaneous metastasis, which creates favorable conditions for tumor cell escape from immune surveillance and distant metastasis.

Notably, the high expression of PD-1 in the context of low CD8/CD20 expression forms the unique immune escape pattern of SMARCA4-UT. PD-1 is mainly expressed on the surface of activated T cells, B cells, NK cells, and other immune cells, and its binding to PD-L1/PD-L2 mediates immune cell exhaustion and immune escape (16). The combination of high PD-1 expression and low CD8/CD20 expression in our case suggests that the limited immune cells in the TME were in an activated or exhausted state, and that the antitumor immune response was further suppressed. This is different from the classic immune escape mode of most solid tumors (high PD-L1 expression on tumor cells mediating T-cell exhaustion) (17), indicating that the immune escape mechanism of SMARCA4-UT is more complex. It is possible that, in addition to the PD-1 pathway, other immune checkpoint pathways (such as LAG-3 and TIM-3) or immune-suppressive cells (such as regulatory T cells) may also be involved in the immune escape of SMARCA4-UT, but this needs to be further verified through the detection of additional immune markers.

CD68 is a specific marker of macrophages, which are important components of the innate immune system and play a dual role in tumor progression: M1-type macrophages exert antitumor effects by secreting proinflammatory cytokines, while M2-type macrophages promote tumor growth and metastasis by mediating immune suppression and TME remodeling (18). In our case, there was low CD68 expression in the subcutaneous metastatic lesion of SMARCA4-UT, indicating that the total number of macrophages in the TME was small and that the innate immune response was impaired. This, when considered in conjunction with the low expression of CD8 and CD20 (impaired adaptive immunity), suggests that both the innate and adaptive immune responses in the TME of SMARCA4-UT subcutaneous metastasis are in a state of comprehensive impairment, which likely explains the high degree of invasiveness and metastatic potential of SMARCA4-UT.

The low expression of CD68 also suggests that macrophages may not be the main mediator of immune suppression in SMARCA4-UT subcutaneous metastasis, which is different from many solid tumors in which tumor-associated macrophages are the main immune-suppressive cells (19). This finding further clarifies the nature of the TME heterogeneity in SMARCA4-UT. Moreover, it indicates that targeted therapy for macrophages (such as CSF-1R inhibitors) may not be effective for all patients with SMARCA4-UT and that the selection of targeted drugs should be based on the specific TME characteristics of patients.

Pan-CK is an epithelial cell marker, and its high expression in the subcutaneous metastatic lesion supports the notion that the metastatic tumor cells retain epithelial characteristics. SMARCA4-UT is an undifferentiated tumor, but the high pan-CK expression suggests that the tumor cells partly maintain epithelial differentiation features, which may be related to its subcutaneous metastatic potential. Epithelial-mesenchymal transition (EMT) is a key mechanism for tumor metastasis, and complete EMT leads to the loss of epithelial characteristics (20). The high pan-CK expression in this case suggests that the SMARCA4-UT cells may not undergo complete EMT, which may be a unique metastatic characteristic of SMARCA4-UT subcutaneous metastasis, and further investigation of this mechanism is warranted.

For our patient with SMARCA4-UT and subcutaneous metastasis, therapy combining PD-1 inhibitor (tislelizumab) and chemotherapy (albumin-bound paclitaxel + carboplatin) achieved stable disease, which is consistent with previous small-sample studies reporting that chemotherapy combined with immunotherapy has better efficacy than monotherapy for SMARCA4-UT (21,22). Indeed, it has been speculated that immune checkpoint inhibitors will become the standard treatment strategy for patients with SMARCA4-UT (23,24).

This therapeutic effect can be explained by the following: Chemotherapy can kill tumor cells, release tumor-associated antigens to ab trigger antitumor immune response, and reverse the immune-suppressive TME; meanwhile, PD-1 inhibitors can block the PD-1 pathway, restore the function of exhausted CD8⁺ T cells (even with low infiltration density), and enhance antitumor immunity. The mIF staining results of our study provide a potential explanation for the treatment response: the high PD-1 expression on immune cells suggests that PD-1 inhibitors can exert a therapeutic effect even when CD8⁺ T-cell infiltration is low, and chemotherapy may further increase CD8⁺ T-cell infiltration and enhance the efficacy of immunotherapy.

This study involved certain limitations that should be addressed. To begin, the conclusions were drawn from a single case, and thus verification in large-sample, multicenter cohort studies is needed. Additionally, only six markers were analyzed, and the expression of other immune/stromal markers (e.g., LAG-3, TIM-3, and CD4) and their correlation with treatment efficacy remain to be examined. Finally, no functional experiments were performed to clarify the causal relationship between marker expression and metastatic potential/immune response.

The mIF-based TME profile in this study is derived from a single rare case of subcutaneous metastasis of a SMARCA4-deficient undifferentiated thoracic tumor. These findings only represent the immune characteristics of this specific lesion and cannot be generalized to all similar metastatic lesions. Further large-scale cohort studies are still needed for verification. In the future, we will expand the sample size to determine the correlation between the marker expression profile (detected by mIF) and clinical outcomes (progression-free survival and overall survival) of patients with SMARCA4-UT and subcutaneous metastasis. Furthermore, we will conduct functional experiments to clarify the role of high CD56 and low CD8 expression in SMARCA4-UT subcutaneous metastasis and, based on the marker profile, develop individualized combined treatment strategies (e.g., PD-1 inhibitor + chemotherapy + TME-targeted therapy) to improve the therapeutic effect among patients with SMARCA4-UT. Indeed, the development of combinatorial therapeutic strategies for SMARCA4-UT represents a critical direction for future clinical translation (25-30).

Conclusions

SMARCA4-UT is a rare, highly aggressive tumor with insidious onset and high variability in metastatic sites, and accurate diagnosis relies on comprehensive examinations, including biopsies of multiple sites, SMARCA4 immunostaining, and genetic testing of cancer. The subcutaneous metastatic lesion of SMARCA4-UT has a distinct marker expression profile (high CD56, PD-1, and pan-CK expression with low CD8, CD68, and CD20 expression), which reflects its unique TME characteristics (i.e., immune suppression and impaired an antitumor immune response) and is closely related to its metastatic potential and immunotherapeutic response. Chemotherapy combined with immunotherapy may provide good efficacy in treating SMARCA4-UT with subcutaneous metastasis, and the mIF-based marker expression profile may provide a basis for optimizing individualized treatment strategies for this rare disease. However, these findings only represent the immune characteristics of this specific lesion of the patient and cannot be generalized to all similar metastatic lesions. As it relates to the patient discussed in this report, he believes that the treatment plan is scientific and effective. It precisely targets his condition to relieve symptoms and control disease progression. Moreover, all procedures during treatment have been standardized, and medical guidance has been thorough, minimizing discomfort as much as possible.

Acknowledgments

We would like to thank the pathology department for providing the pathological images.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://tlcr.amegroups.com/article/view/10.21037/tlcr-2026-0218/rc

Peer Review File: Available at https://tlcr.amegroups.com/article/view/10.21037/tlcr-2026-0218/prf

Funding: This work was supported by the Tianjin Key Medical Discipline Construction Project (No. TJYXZDXK-3-003A) and the Cangzhou Central Hospital Level Project (No. YJ2024019).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://tlcr.amegroups.com/article/view/10.21037/tlcr-2026-0218/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 Declaration of Helsinki and its subsequent amendments. Approval for this study was provided by the ethics committee of Tianjin Medical University Cancer Institute and Hospital (No. E20250575). Written informed consent was obtained from patient’s family for 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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