Case Report: Transformation From Non-Small Cell Lung Cancer to Small Cell Lung Cancer During Anti-PD-1 Therapy: A Report of Two Cases

Shen, Qian; Qu, Jingjing; Sheng, Lingyan; Gao, Qiqi; Zhou, Jianying

doi:10.3389/fonc.2021.619371

Cited by 11 publications

(10 citation statements)

References 22 publications

(28 reference statements)

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“…In addition, HTs of adenocarcinoma to SqCC and vice versa have been reported after treatment with PD-1 inhibitors such as nivolumab, pembrolizumab, and sintilimab. 34 – 38 In contrast, HTs after programmed cell death ligand 1 (PD-L1) inhibitor administration has been reported rarely, likely due to differences in the timing of its introduction into clinical practice and its infrequent use as a single agent for advanced NSCLC. 39 HTs to SCLC were detected in only one case after treatment with nivolumab followed by atezolizumab.…”

Section: Ht Induced By Agents Other Than Egfr-tkismentioning

confidence: 99%

Histologic transformation in lung cancer: when one door shuts, another opens

2022

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Histologic transformation (HT) is a major cause of drug resistance to therapy in patients with lung cancer. HTs to small-cell lung cancer (SCLC) have been reported frequently in patients with epidermal growth factor receptor ( EGFR)-mutated lung cancer. Although HTs have an impact on the clinical outcomes in patients owing to a high refractoriness to treatments, there is limited data on the prevalence, causes, mechanisms, treatment efficacy, and future treatment strategies. In this review, we assess the literature regarding HTs comprehensively, including those describing EGFR-tyrosine kinase inhibitors, other molecular targeted drugs, and immune checkpoint inhibitors. Furthermore, we discuss the mechanisms of HTs and the lineage plasticity to SCLC and squamous cell carcinoma in lung cancer. In addition, we summarize the treatment efficacy and future perspectives of HTs in patients with lung cancer, and propose better management strategies for this group of patients.

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Section: Ht Induced By Agents Other Than Egfr-tkismentioning

confidence: 99%

Histologic transformation in lung cancer: when one door shuts, another opens

2022

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“…Our cases emphasize the importance of repeated biopsy in the treatment process and propose a possible source of transformed cells. In addition, we provide a review of the literature and summarize the clinical characteristics of rare SCLC transformation cases with PD-1 inhibitors (12,(15)(16)(17)(18)(19)(20)(21)(22)(23).…”

Section: Introductionmentioning

confidence: 99%

“…However, transformation to SCLC is considered drug resistance, and the underlying mechanisms remain unclear ( 11 , 12 ). The transformation of NSCLC to SCLC after targeted therapy or treatment with ICIs alone or in combination with other drugs as anti-tumor therapy has been reported ( 13 – 15 ). Here, we report a case of TKI resistance due to SCLC transformation and another case of tumor transformation from squamous cell carcinoma to SCLC during treatment with pembrolizumab.…”

Section: Introductionmentioning

confidence: 99%

Histomorphological transformation from non-small cell lung carcinoma to small cell lung carcinoma after targeted therapy or immunotherapy: A report of two cases

Líu

Zhang²,

Wang³

et al. 2022

Front. Oncol.

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Molecular targeting and immunotherapy provide durable responses for advanced lung cancer clinical therapy in many patients. However, the mechanisms of occurrence of progressive disease and resistance to targeted therapy and immunotherapy have not been elucidated. Herein, we report two cases of small cell transformation of non-small cell lung cancer (NSCLC) after targeted therapy or immunotherapy. The first case was a 63-year-old female patient presenting with cough and expectoration. Left lung invasive adenocarcinoma was diagnosed after left lung tumor biopsy. After epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) targeted therapy for almost 2 years, disease progression and symptom aggravation were observed. Pathological and immunohistochemical staining results after biopsy revealed small cell lung cancer (SCLC). The second case was a 75-year-old male patient diagnosed with stage IV squamous cell carcinoma of the lung, who received carboplatin/paclitaxel adjuvant chemotherapy and pembrolizumab treatment with partial response. Disease progression and metastasis occurred within 15 cycles of immunotherapy. Computed tomography revealed a lower left lung tumor. Cytological examination of lung lavage fluid and biopsy under thoracoscope revealed SCLC. In conclusion, histological transformation to SCLC is a potential mechanism of NSCLC resistance to targeted therapy or immunotherapy. During treatment, clinicians should monitor serum tumor markers or genome sequencing, particularly in patients with disease progression, as this may be beneficial for early detection of SCLC transformation. Repeated biopsy can be performed if necessary, and the therapeutic regimen can be adjusted in a timely manner according to the results of molecular pathological tests for personalization and whole-process management.

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“…Lung cancer is a major cause of mortality worldwide, and non-small cell lung cancer (NSCLC) accounts for approximately 85% of all lung cancer cases [ 1 ]. Although surgery, radiation, and platinum-based chemotherapy, all of which induce apoptotic cell death, have proven the ability to improve survival rates in NSCLC, NSCLC is typically characterized by resistance to radiotherapy and chemotherapy and is often detected at a very late stage for surgical intervention.…”

Section: Introductionmentioning

confidence: 99%

Pennogenin-3-O-α-L-Rhamnopyranosyl-(1→2)-[α-L-Rhamnopyranosyl-(1→3)]-β-D-Glucopyranoside (Spiroconazol A) Isolated from Dioscorea bulbifera L. var. sativa Induces Autophagic Cell Death by p38 MAPK Activation in NSCLC Cells

Chung

Lee

et al. 2022

Pharmaceuticals

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In our previous study, we reported the isolation of pennogenin-3-O-α-L-rhamnopyranosyl-(1→2)-[α-L-rhamnopyranosyl-(1→3)]-β-D-glucopyranoside (spiroconazol A), a steroidal saponin, from the flowers of Dioscorea bulbifera L. var. sativa. In the present study, we aimed to investigate the effects of spiroconazol A on autophagy and its underlying mechanisms in A549 and NCI-H358 human non-small cell lung cancer (NSCLC) cells. Spiroconazol A inhibited the proliferation of NSCLC cells in a concentration- and time-dependent manner. To determine the type of programmed cell death induced by spiroconazol A, we performed a characterization of apoptosis in spiroconazol A-treated A549 cells. Our results showed that spiroconazol A significantly suppressed A549 cell viability but did not influence cell apoptosis because phosphatidylserine and caspase activation were not detected. Furthermore, spiroconazol A treatment upregulated the expression of LC3-II and autophagy-related Beclin-1 protein, suggesting that spiroconazol A induces autophagy in A549 cells. Moreover, spiroconazol A activated the phosphorylation of p38 mitogen-activated protein kinase (MAPK) but did not affect the phosphorylation of Janus kinase or ERK1/2. Notably, SB203580, a p38 MAPK inhibitor, had a significant inhibitory effect on spiroconazol A-induced autophagic cell death in A549 cells. Our results indicated that spiroconazol A-induced autophagy is dependent on p38 MAPK signaling and has potential as a therapeutic target in NSCLC.

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Case Report: Transformation From Non-Small Cell Lung Cancer to Small Cell Lung Cancer During Anti-PD-1 Therapy: A Report of Two Cases

Cited by 11 publications

References 22 publications

Histologic transformation in lung cancer: when one door shuts, another opens

Histologic transformation in lung cancer: when one door shuts, another opens

Histomorphological transformation from non-small cell lung carcinoma to small cell lung carcinoma after targeted therapy or immunotherapy: A report of two cases

Pennogenin-3-O-α-L-Rhamnopyranosyl-(1→2)-[α-L-Rhamnopyranosyl-(1→3)]-β-D-Glucopyranoside (Spiroconazol A) Isolated from Dioscorea bulbifera L. var. sativa Induces Autophagic Cell Death by p38 MAPK Activation in NSCLC Cells

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