Introduction
Pulmonary sarcomatoid carcinoma (PSC) is a rare and
aggressive subtype of non-small cell lung cancer (NSCLC),
accounting for <1% of all lung cancer cases (1). It is characterized by the presence of
carcinomatous and sarcomatoid components, leading to biological
behaviors marked by high levels of malignancy, invasiveness and
treatment resistance (2). A total
of ~70% of patients with PSC are diagnosed in the middle to
advanced stages (3). Despite
surgical intervention, the risk of recurrence and metastasis
remains high and patients with advanced PSC have short survival
times, resulting in an unfavorable prognosis.
Current treatment strategies for PSC are primarily
based on those for NSCLC, with radiotherapy as the core modality
for local palliative or curative treatment. However, conventional
radiotherapy approaches yield poor efficacy or are associated with
rapid resistance in PSC (4). This
is especially true in patients with locally advanced tumors and a
large tumor burden, in whom achieving rapid downstaging and
creating opportunities for systemic treatment remain challenging.
Currently, high-quality, large-scale clinical studies to guide the
updating of treatment guidelines are lacking. Therefore, the
clinical management of PSC presents a notable challenge, and the
exploration of novel, comprehensive treatment strategies capable of
overcoming therapeutic resistance is key.
In the present case report, a case is described of
locally advanced PSC treated with tomotherapy-based spatially
fractionated radiotherapy (SFRT) combined with Endostar
antiangiogenic therapy for local treatment, followed by sequential
chemo-immunotherapy. Although this approach achieved favorable
local control, the patient succumbed to an opportunistic infection.
The present case report aims to provide a preliminary demonstration
of the clinical implementation process, acute adverse reactions and
short-term efficacy of this innovative combination therapy and
offer a novel therapeutic perspective for this challenging disease.
The present case report also provides preliminary evidence and
practical experience for future large-scale clinical trials on PSC
treatment.
Case report
The patient was a 64-year-old Chinese man who had
undergone transcatheter aortic valve replacement in 2023 and had
been diagnosed with type 2 diabetes for >1 year, managed with
metformin tablets. The patient reported a history of smoking, with
a smoking index of 900 (30 cigarettes daily over 30 years) and
social drinking.
In June 2025, the patient was admitted to Quzhou
People's Hospital, (Quzhou, China), presented with a 2-day history
of worsening chest tightness and fatigue, accompanied by mild
coughing with thin, white sputum. The patient denied the presence
of other symptoms such as chest pain, hemoptysis or syncope. Upon
presentation, the patient had a body temperature of 38.1°C
(100.6°F) and a blood pressure of 74/50 mmHg, with an
electrocardiogram showing atrial flutter with a 2:1 conduction
ratio. A CT scan was performed, revealing a mass (9.7×13.3 cm) in
the right upper lobe, with obstruction of the right main bronchus
and upper lobe (Fig. 1A). The
patient was diagnosed with a space-occupying lesion in the right
lung (lung cancer suspected) and admitted for emergency
treatment.
Physical examination on admission indicated Eastern
Cooperative Oncology Group Performance Status (5) score of 3 and decreased breath sounds
in the right lung. Laboratory test results (performed June 2025)
included squamous cell carcinoma antigen (3.95 ng/ml; normal
reference range, 0–1.5 ng/ml), CEA (136.82 ng/ml; normal reference
range, 0–5.0 ng/ml) and CA 19–9 (70.79 U/ml; normal reference
range, 0–37.0 U/ml). Positron emission tomography (PET)-CT
(performed June 2025) revealed a space-occupying lesion in the
right upper lobe with markedly increased fluorodeoxyglucose uptake
[maximum standardized uptake value (SUVmax)=13.19], suggestive of
lung cancer, and slightly elevated fluorodeoxyglucose uptake
(SUVmax=3.28) in the mediastinal 2R and 4R lymph nodes (Fig. 2). Bronchoscopic examination
(performed June 2025) and treatment revealed a neoplasm covered
with necrotic material in the right main bronchus, which largely
obstructed the lumen. An intraluminal tumor was resected using a
snare (Fig. 3A). Follow-up
contrast-enhanced chest CT performed following bronchoscopic
treatment showed that the right main bronchus and middle and lower
lobe bronchi were patent (Fig. 1B).
Hematoxylin-Eosin staining was performed by pathologists after
tumor tissue sections according to standard procedures (Fig. 3B). The results demonstrated a
malignant tumor with extensive necrosis, showing scattered areas of
atypical squamous epithelium locally (based on tissue from
endoscopic resection of the right main bronchus). Meanwhile,
immunohistochemical staining was performed by pathologists using
the EnVision system (6), and the
immunohistochemistry results were as follows: Insulinoma-associated
protein 1 (−), CD34 (vascular +), leukocyte common antigen (−),
S-100 (−), vimentin (+), SWI/SNF related BAF chromatin remodeling
complex subunit B1 (SMARCB1; +), SMARCA4/Brg1 (+), cytokeratin 5/6
(partial +), P40 (focal +), Ki-67 (+; 80%), napsin A (−), thyroid
transcription factor-1 [TTF-1 (focal +)], cytokeratin 7 (partial
+), cytokeratin (partial +), anaplastic lymphoma kinase (−) and
programmed cell death-ligand 1 (PD-L1) tumor proportion score=0
(Fig. 3C-R). All antibodies used
for immunohistochemistry were ready-to-use antibody reagents.
Insulinoma-associated protein 1 antibody reagent (cat. no.
GT246802), CD45 antibody reagent (cat. no. GM070104), S100 antibody
reagent (cat. no. GZ031104), vimentin antibody reagent (cat. no.
GM072504), integrase interactor-1 antibody reagent (cat. no.
GT225704), SMARCA4/Brg1 antibody reagent (cat. no. GT233302), Ki-67
antibody reagent (cat. no. GT209404), were from Shanghai Gene Tech.
CD34 antibody reagent (cat. no. BFM-0456-6), cytokeratin 5/6
antibody reagent (cat. no. BFM-0482-6), P40 antibody reagent (cat.
no. BFM-0062-6), napsin A antibody reagent (cat. no. BFM-0499-6),
TTF-1 antibody reagent (cat. no. BFM-0379-6), cytokeratin 7
antibody reagent (cat. no. BFM-0604-6), cytokeratin antibody
reagent (cat. no. BFM-0016-6), were from Hangzhou Baiyin Biotech.
Anaplastic lymphoma kinase antibody reagent (cat. no. GA785) was
from Agilent Tech, and PD-L1 (cat. no. 8.17.0069.02) antibody
reagent was from Xiamen AmoyDx. High-throughput sequencing of tumor
tissue was performed at Hangzhou Buping Medical Laboratory
(www.bphealth.com). Genetic testing showed
positive findings for tumor protein 53, phosphatase and tension
homolog deleted on chromosome 10, AT-rich interaction domain 1A and
cyclin-dependent kinase inhibitor 2A mutations, the tumor was
microsatellite stable and negative for PD-L1 (tumor proportion
score <1%). This result indicated that there were currently no
approved or recommended targeted drugs for the patient.
The results of immunohistochemistry were key for
differential diagnosis. The positive expression of epithelial
marker cytokeratin was the core basis for diagnosis (7) (Fig.
3C); meanwhile, the sarcomatoid component often expresses
vimentin (Fig. 3D), which is a
marker of mesenchymal origin (8).
The high Ki-67 index (Fig. 3E)
reflects malignant biological behavior (9). These three indicators supported the
pathological diagnosis of sarcomatoid carcinoma. TTF-1 1 was
positive (Fig. 3F), suggesting that
the tumor originated from the lung or thyroid. However, PET-CT
indicated that only the lung had tumor lesions, which ruled out the
possibility of tumor metastasis from other sites to the lung.
Therefore, the final diagnosis was PSC. The pathological result was
formally reported after discussion and review by professional
pathologists.
The patient was diagnosed with NSCLC of the right
lung (sarcomatoid carcinoma; cT4N2M0 stage IIIB;
PD-L1−). Considering the high tumor burden and
unfavorable performance status score of 3 of the patient,
tomotherapy-based SFRT was initiated in June 2025 (Fig. 4A). According to internationally
recognized expert recommendations (10), an individualized SFRT plan was
formulated for the patient. Target volume delineation was based on
PET-CT, with the right lung tumor defined as the gross tumor volume
(GTV). Within the GTV, voxels of 1 cm in diameter spaced 3 cm apart
(GTV1-6) were designated as the lattice. The hypofractionated
radiotherapy dose (GTV: 30 Gy/10 F and GTV1-6: 60 Gy/10 F) was
used. Endostar was administered via intravenous infusion at 30 mg
on days 1–7. After 10 fractions, follow-up chest CT indicated that
the right upper lung mass (9.3×12.8 cm) had shrunk slightly
(Fig. 1C), and the performance
status of the patient score had recovered to 1. The limits of the
organ at risk remained within the tolerable range and the dose was
raised as high as possible for local control. In July 2025, five
additional fractions were added to the original radiotherapy plan,
adjusting the total dose to GTV: 45 Gy/15 F, with the lattice
region receiving 90 Gy/15 F (Fig.
4B). The peak-to-valley dose ratio of the SFRT plan was 2.9 and
the SFRT target volume/GTV ratio was 0.5%. The organs at risk were
tolerable and total dose values as follows: V5 of the right lung
was 31.7% (limit value: <60%), V20 was 9.7% (limit value:
<30%), V30 was 6.4% (limit value: <20%), the mean dose to the
right lung and heart was 925 cGy (limit value: <1,500 cGy) and
195 cGy (limit value: <800 cGy), respectively, and the maximum
doses to the esophagus and spinal cord were 4,443 cGy and 2204 cGy
(limit value: <4,500 cGy), respectively. Additionally, 100 mg
albumin-bound paclitaxel was administered twice weekly as
concurrent chemotherapy. Following the completion of this treatment
phase, the patient was discharged without incident.
Subsequently, in August and September 2025, two
sequential cycles of systemic therapy were administered using 210
mg of paclitaxel liposome and 1,000 mg of ivonescimab. Imaging
revealed continued tumor shrinkage to 7.8×10.0 cm (Fig. 1D), accompanied by decreased tumor
markers (Fig. 1F). The therapeutic
effect was evaluated as ‘partial response’ according to the RECIST
criteria (11); local control was
achieved.
In October 2025, the patient developed a fever,
cough and sputum production. Chest CT revealed multiple infiltrates
in the lungs (Fig. 1E). Pathogen
testing showed positive nucleic acid detection for Pneumocystis
jirovecii and aspergillus, suggesting pulmonary
infection; however, the possibility of immune-related pneumonia
could not be ruled out. A combination regimen of meropenem 1.0 g
intravenously every 8 h, compound sulfamethoxazole tablets 1.44 g
orally every 6 h, voriconazole tablets 200 mg orally twice daily
and methylprednisolone 80 mg intravenously once daily was
administered. After 10 days, the pulmonary inflammation decreased
and the antibiotic was de-escalated to piperacillin-tazobactam 4.5
g intravenously every 8 h, methylprednisolone was reduced to 40 mg
once daily, and compound sulfamethoxazole tablets and voriconazole
tablets were continued at the original dose. In November 2025, the
patient's pulmonary inflammatory lesions increased again and
nintedanib capsules 100 mg orally every 12 h were added.
Subsequently, sputum test showed aspergillus nucleic acid
positive, alveolar lavage fluid galactomannan test 8.38 µg/l
(positive), fungal glucan 677.29 pg/ml (positive) and
Pseudomonas aeruginosa positive. Despite aggressive
antimicrobial therapy, the condition of the patient continued to
deteriorate. In November 2025, the patient died of respiratory
failure (with an overall survival of 5.5 months). Detailed
antitumor and pneumonia treatments are presented in Table I.
 | Table I.Timeline of clinical events. |
Table I.
Timeline of clinical events.
| Time point | Clinical events |
|---|
| June, 2025 (day
1) | The patient was
diagnosed with PSC, cT4N2M0 stage IIIB, with lung tumor size of
9.7×13.3 cm. |
| June to July, 2025
(days 12–22) | SFRT was administered
to the right lung tumor, one radiotherapy session per day, daily
dose: GTV 3 Gy and GTV1-6 6 Gy. Total course of 10 days (excluding
weekends): Total dose of the first stage radiotherapy: GTV 30
Gy/10F and GTV1-6 60 Gy/10F. |
| June to July, 2025
(days 12–18) | Endostar 30 mg was
administered once daily by intravenous infusion. |
| July, 2025 (day
22) | CT showed the lung
tumor reduced to 9.3×12.8 cm; performance status score had
recovered. |
|
| Albumin-bound
paclitaxel 100 mg was administered once by intravenous
infusion. |
| July to July, 2025
(days 24–28) | Five additional
fractions added to the original radiotherapy plan, adjusting the
total dose to GTV: 45 Gy/15F, with the lattice region receiving 90
Gy/15F. |
| July, 2025 (day
28) | Albumin-bound
paclitaxel 100 mg was administered once by intravenous
infusion. |
| August, 2025 (day
56) | CT indicated the lung
tumor had reduced to 9.0×11.8 cm. |
| August, 2025 (day
58) | Cycle 1 of paclitaxel
liposome 210 mg and ivonescimab 1,000 mg was administered by
intravenous infusion. |
| September, 2025 (day
80) | Cycle 2 of paclitaxel
liposome 210 mg and ivonescimab 1,000 mg was administered by
intravenous infusion. |
| October, 2025 (day
123) | CT showed multiple
infiltrates in the lungs; the tumor continued to reduce to 7.8×10.0
cm. Meropenem 1 g administered every 8 h and methylprednisolone 80
mg administered once daily. |
| October, 2025 (day
126) | Sputum test:
Pneumocystis jirovecii and aspergillus nucleic acid were
positive. Compound sulfamethoxazole tablets 1.44 g were taken
orally every 6 h and voriconazole tablets 200 mg were taken orally
twice daily. |
| October, 2025 (day
133) | Reduction in
pulmonary inflammatory lesions. Piperacillin-tazobactam 4.5 g was
administered every 8 h; methylprednisolone was reduced to 40 mg
once a day. Compound sulfamethoxazole tablets and voriconazole
tablets continued orally. |
| November, 2025 (day
145) | The tumor size
remained stable, but the pulmonary inflammatory lesions increased.
Nintedanib capsules 100 mg were taken orally every 12 h. |
| November, 2025 (day
150) | Sputum test showed
positive aspergillus nucleic acid. Alveolar lavage fluid
galactomannan test 8.38 ug/l (positive), fungal glucan 677.29 pg/ml
(positive) and Pseudomonas aeruginosa positive. |
| November, 2025 (day
154) | The inflammatory
lesions in the lungs continued to increase. The condition of the
patient deteriorated further and respiratory failure occurred. A
ventilator was used for assisted breathing. |
| November, 2025 (day
160) | The patient
died. |
Discussion
PSC often presents as a large, irregular mass that
closely adjoins key organs such as the spinal cord, heart and major
blood vessels (12), posing a
dilemma in conventional radiotherapy. Increasing the dose to
enhance local control elevates the risk of severe radiation injury,
whereas reducing the dose may lead to treatment failure, thereby
presenting difficulties in striking a balance between treatment
risks and benefits. Therefore, there is an urgent clinical need to
explore innovative radiotherapy techniques that can effectively
improve local tumor control rates while maintaining safety.
SFRT is an innovative radiotherapy technique that
uses advanced imaging guidance to achieve high-dose coverage of
tumors via an alternating ‘peak-and-valley’ (similar to a
three-dimensional lattice) dose distribution pattern (13). SFRT safely increases the local tumor
dose and more effectively eliminates tumors via complex
radiobiological effects such as vascular normalization, abscopal
effects and enhanced immunogenicity (14), making it particularly suitable for
large tumors (15).
Regarding biology, hypoxia is a key factor
contributing to radiotherapy resistance (16). Endostar is a recombinant human
endostatin that suppresses tumor angiogenesis. By exploiting the
‘vascular normalization’ window, it temporarily improves blood
perfusion and oxygenation within the tumor (17).
In the present case of PSC, the following was
observed: i) The tumor was invasive, presenting as a large mass
with necrosis. It was already locally advanced as initially
diagnosed and carried co-mutations in tumor suppressor genes, such
as tumor protein 53; ii) PD-L1 expression was negative, suggesting
a poor response to monotherapy with immune checkpoint inhibitors;
and iii) due to airway obstruction caused by the large tumor and
poor general condition, the patient was unable to tolerate
standard-dose chemoradiotherapy.
Therefore, the present case report proposes an
innovative integrated treatment approach for refractory PSC,
involving an induction regimen combining tomotherapy-based SFRT
with Endostar antiangiogenic therapy. This strategy aims to achieve
more effective tumor targeting by leveraging the dual synergistic
effects of physics (SFRT to overcome dose limitations) and biology
(Endostar to improve the microenvironment), while harnessing the
‘in situ vaccine’ effect to create favorable conditions for
the efficacy of subsequent immunotherapy (18). After the actual treatment, it was
observed this induction therapy achieved the effect of shrinking
the tumor and improving the performance status score of the
patient, thereby crea ting an opportunity for the subsequent
treatment.
Subsequent sequential treatment with ivonescimab
(simultaneously targeting programmed death-1 and vascular
endothelial growth factor) combined with chemotherapy showed a
certain extent of antitumor activity in PSC cases negative for
PD-L1 and without clinically notable mutations. This was reflected
in the decline of tumor markers and the continuous regression of
lesions on imaging. This antitumor effect may be related to
non-PD-L1-dependent mechanisms such as modulating T-cell function
and enhancing effector-cell infiltration (19).
However, the final outcome of this case may suggest
that this treatment approach still faces certain challenges. The
patient developed pulmonary inflammation following two cycles of
chemoradiotherapy. Considering the imaging characteristics of
multiple infiltrates in both lungs outside the field of
radiotherapy, radiation pneumonitis was temporarily ruled out, but
the possibility of immune-related pneumonitis could not be
completely excluded. The etiological results suggested that there
was a pulmonary infection, and a pneumonia treatment plan combined
with glucocorticoids and antibiotics was initiated. The pneumonia
was well controlled in the short term, but it eventually developed
into a fatal mixed-opportunistic infection, potentially associated
with the following: i) The advanced age of the patient and history
of diabetes and heart valve replacement surgery, which may have
compromised baseline immune function; ii) the use of immune
checkpoint inhibitors, leading to T-cell exhaustion or abnormal
activation, thereby disrupting the body's immune surveillance
against opportunistic pathogens; and iii) the tumor and
comprehensive treatment regimen themselves, which may have led to
systemic immune dysregulation.
The immune function of the patient was not
monitored, including the measurement of the CD4+ T-cell
count, and subsequent failure to use prophylactic antibiotics
during the treatment period. These were the limitations in the
present case. Although PSC itself carries an unfavorable prognosis,
the direct cause of mortality in the present patient was
respiratory failure due to severe pneumonia rather than the
progression of the tumor. As a result, it is suggested that
patients with lung cancer with underlying diseases who are
undergoing combined treatments such as radiotherapy, chemotherapy
and immunotherapy should be prophylactically administered
antibiotics (20) while monitoring
their immune function status, in order to prevent pneumocystis
pneumonia and aspergillosis.
In conclusion, for locally advanced,
PD-L1− PSC, a treatment regimen centered on SFRT
combined with antiangiogenic therapy may be an effective induction
treatment, thereby creating an opportunity for subsequent systemic
therapy. However, during chemotherapy, radiotherapy and
immunotherapy, vigilance must be maintained against opportunistic
infections. High-risk patients with underlying conditions and
undergoing combined treatments, in whom aggressive prophylaxis,
monitoring and early intervention are essential, require particular
attention. The present case provides a reference for personalized
treatment decisions; however, more clinical data are needed to
validate the efficacy and safety of this treatment model.
Acknowledgements
Not applicable.
Funding
Funding: No funding was received.
Availability of data and materials
The data generated in the present study may be
requested from the corresponding author. The high-throughput
sequencing datasets (SRX35321793) are available from the NCBI
Sequence Read Archive (https://www.ncbi.nlm.nih.gov/sra/PRJNA1531924).
Authors' contributions
ZQ was responsible for the study conception,
investigation, writing the original draft, and reviewing and
editing. FX was responsible for data analysis, writing the original
draft, and reviewing and editing. XM and PY were responsible for
investigation, resources and writing the original draft. XZ was
responsible for study conception, project administration, and
reviewing and editing. All authors read and approved the final
manuscript, and are responsible for all aspects of the work. ZQ and
XZ confirm the authenticity of all the raw data.
Ethics approval and consent to
participate
The present work was approved by the Ethics
Committee of Quzhou People's Hospital (Quzhou, China; approval no.
2026-050).
Patient consent for publication
As the patient is deceased, the patient's daughter
signed a written consent form for the use of the patient's clinical
data, medical images and clinical outcomes for publication.
Competing interests
The authors declare that they have no competing
interests.
Glossary
Abbreviations
Abbreviations:
|
CT
|
computed tomography
|
|
GTV
|
gross tumor volume
|
|
NSCLC
|
non-small cell lung cancer
|
|
PD-L1
|
programmed cell death-ligand 1
|
|
PSC
|
pulmonary sarcomatoid carcinoma
|
|
SFRT
|
spatially fractionated
radiotherapy
|
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