Pulmonary Sarcomatoid Carcinoma Research Articles

Sarcomatoid carcinoma of the lung: a rare histological subtype of non-small cell lung cancer with a poor prognosis even at earlier tumour stages.

Pulmonary sarcomatoid carcinoma (PSC) is a rare histological subtype of non-small cell lung cancer and comprises a diagnostically and therapeutically challenging group of tumours. We explored the clinicopathological features and prognostic factors of this tumour. We conducted a retrospective study of all patients who were treated for PSC in the Department of Thoracic Surgery between May 2005 and December 2014. Primary outcomes of interest were patient survival and prognostic factors. A total of 58 patients were treated for sarcomatoid carcinoma within the described period and 46 patients underwent surgical resection with curative intent. The mean follow-up period was 30months. Of the operated patients, 21.7% had pathological stage I disease, and 78.3% had more advanced disease. There were 25 carcinosarcomas, 10 pleomorphic carcinomas, 7 spindle cell carcinomas, 3 giant cell carcinomas and 1 pulmonary blastoma. Overall 5-year survival of the operated patients was 28.7%. A total of 28 patients experienced recurrence and died cancer-related. Our analysis revealed that tumour size, gender, histological entity, lymphatic vessel invasion (L1) and vascular invasion (V1) did not influence survival. There was a trend for decreased survival in older patients (>65years). Surgical treatment can achieve satisfactory results with low perioperative mortality, but the overall prognosis even with multimodality concepts and in earlier tumour stages is worse compared to other types of non-small cell lung cancer.

Pathologic Findings and Long-Term Results After Surgical Treatment for Pulmonary Sarcomatoid Tumors: A Multicenter Analysis

Pulmonary sarcomatoid carcinoma (PSC) is a very rare subtype of non-small cell lung cancer (NSCLC). The aim of this study was to clarify the pathologic characteristics and long-term survival after surgical treatment in patients with PSC. From January 2003 to December 2013, we retrospectively reviewed the clinical findings, surgical notes, and pathologic and follow-up data from 148 consecutive patients who underwent curative resection for PSC in 5 institutions. The Kaplan-Meier method, log-rank test, and Cox regression analysis were used. Mean age and male to female ratio were 66.6 ± 9.9 years and 120:28, respectively. Surgical resection (pneumonectomy in 8 patients, bilobectomy in 132 patients, and sublobar resection in 8 patients) was complete in 142 cases (96%). At pathologic evaluation, 36 patients (24%) had stage I, 69 patients (47%) had stage II, 33 patients (22%) had stage III, and 10 patients (7%) had stage IV disease. A "biphasic tumor" (PSC with an NSCLC component) was observed in 77 patients (52%). We detected a high rate of vascular emboli in the surgical specimens (overall, 68%; 57% in pathologic stage I tumors), whereas lymphatic emboli were found in 30% of cases (5% of pathologic stage I tumors). Overall median and 5-year long-term survival (LTS) was 19 months and 12.6% (LTS, 16.3% in pathologic stage I), respectively. Distant recurrences frequently occurred after surgical treatment (81%), even in pathologic stage I tumors that underwent R0 resection (62%). Multivariable survival analysis identified R+ resection (hazard ratio [HR],12.3; 95% confidence interval [CI], 3.67-41.28; p < 0.0001), advanced pathologic stage (HR, 5.75; 95% CI, 2.55-12.98; p< 0.0001), and the presence of vascular emboli (HR, 1.67; 95% CI, 1.05-2.67; p= 0.0327) as independent negative prognostic factors. PSCs have very aggressive behavior and high metastatic potential even in early stages. R+ resection, pathologic TNM status, and the presence of vascular emboli are independent prognostic factors.

“Sarcomatoid” carcinomas of the lung: a clinicopathological study of 86 cases with a new perspective on tumor classification

Pulmonary sarcomatoid carcinoma includes a heterogenous group of tumors difficult to diagnose and treat. We report the clinicopathological features of 86 such tumors, including 74 pleomorphic and 12 spindle cell carcinomas, and propose a novel approach to the classification of these neoplasms in an attempt to better guide patient management. The patients were 47 men and 39 women aged 36 to 87 years (mean, 63 years) who primarily presented with shortness of breath, cough, and chest pain. Eighty-six percent of patients had a smoking history. Histologically, the pleomorphic carcinomas consisted of spindle and/or giant cells with varying proportions of conventional non-small cell carcinoma in the form of adenocarcinoma (n=29), squamous cell carcinoma (n=10), or large cell carcinoma (n=18); 17 cases contained a mix of spindle and giant cells only. The 12 spindle cell carcinomas consisted of spindle cells only. Based on the combined histopathologic and immunohistochemical features of these tumors, we were able to reanalyze the spectrum of these lesions and reclassify them accordingly. Statistical analysis revealed an overall survival at 3, 5, and 10 years of 42.9%, 34.6%, and 23.5%, respectively, and a median survival of 15 months. Log-rank test showed that in multivariate analysis, only pathological T stage was a factor associated with prognosis. The current classification of pulmonary sarcomatoid carcinomas precludes optimal triaging of these tumors with the risk of denying patients access to novel treatment. Our proposal for a reclassification of these tumors would more accurately guide patient management and facilitate targeted therapies.

Postoperative care and literature review of 1 case that massive pulmonary sarcomatoid carcinoma invaded the upper lobe bronchus of right lung and heart great vessels

Postoperative care and literature review of 1 case that massive pulmonary sarcomatoid carcinoma invaded the upper lobe bronchus of right lung and heart great vessels

Spindle cell and pleomorphic (“sarcomatoid”) carcinomas of the lung: an immunohistochemical analysis of 86 cases

Spindle cell and pleomorphic carcinomas are currently grouped among sarcomatoid carcinomas of the lung. Because of their unusual occurrence, these tumors have not been properly assessed by immunohistochemistry. We performed a comprehensive immunohistochemical analysis of 86 of these tumors. Seventy-four pleomorphic carcinomas (57 with differentiated elements) and 12 spindle cell carcinomas were subjected to immunohistochemistry with CAM5.2, cytokeratin (CK) 7, thyroid transcription factor 1, napsin A, CK5/6, p40, desmocollin 3, Sox2, calretinin, and D2-40. The percentage of positive tumor cells as well as the staining intensity were evaluated and scored. The spindle/giant elements were positive for CAM5.2 (93%), CK7 (79%), thyroid transcription factor 1 (41%), napsin A (20%), calretinin (20%), Sox2 (13%), CK5/6 (9%), p40 (8%), D2-40 (6%), and desmocollin 3 (3%). Of 29 cases in which immunohistochemistry was performed on spindle/giant cell and corresponding differentiated elements, 21 (72%) showed a consistent staining pattern in both components, whereas in 8 cases (28%), the immunophenotype in the spindle/giant cells was less lineage-specific than in the differentiated component. Therefore, we consider that 42% of neoplasms otherwise classified as sarcomatoid carcinoma can be reclassified as adenocarcinoma and 14% as squamous cell carcinoma, while the remaining 44% failed to show a more specific immunophenotype. The use of a comprehensive immunohistochemical panel allows reclassification of the majority of sarcomatoid carcinomas as poorly differentiated variants of adenocarcinoma or squamous cell carcinoma. Such reclassification will facilitate clinical management and allow molecular testing and pursuit of targeted treatment strategies. Application of immunohistochemistry should become the standard in the workup of pulmonary sarcomatoid carcinomas.

Molecular characterization of pulmonary sarcomatoid carcinoma: analysis of 33 cases

AbstractSeveral targetable genetic alterations have been found in lung cancer, predominantly in adenocarcinomas, which have led to important therapeutic advancements with the advent of targeted therapy. In contrast, the molecular features and presence of targetable genetic abnormalities in pulmonary sarcomatoid carcinomas are largely unknown. Thirty-three cases of pulmonary sarcomatoid carcinoma were tested for approximately 2800 mutations in 50 oncogenes and tumor-suppressor genes, including EGFR, KRAS, NRAS, TP53, BRAF, ERBB2, JAK3, AKT1, ATM, MET, KIT, and PIK3CA. ALK immunostaining was performed, and ALK FISH was performed on cases with any degree of staining. Twenty-four of the 33 cases (72%) had at least one genetic abnormality: 19 cases (58%) had TP53 mutations; 10 cases (30%) had KRAS mutations; AKT1, JAK3, BRAF, NRAS, and PIK3CA mutations were observed in 1 case each (3%). Six of the 19 cases (32%) with a mutation in TP53 had simultaneous mutations in KRAS (18%). The cases with alterations in JAK3, BRAF, and NRAS also had mutations in TP53. The case showing a mutation in PIK3CA had a mutation in KRAS. No EGFR mutations were observed. One case had ALK gene rearrangement. ALK rearrangement was observed in a single case of sarcomatoid carcinoma (3%), which has currently available targeted therapy. Four tumors had mutations in genes with experimental molecular-based therapy, including BRAF, NRAS, PIK3CA, and AKT1. Testing for targetable mutations should be considered for patients with pulmonary sarcomatoid carcinoma, as a subset may benefit from currently approved drugs or clinical trials of novel therapeutic options available for other types of lung cancer.

Abstract 2320: CD70 immune checkpoint ligand is associated with the epithelial-to-mesenchymal transition in non-small cell lung cancer

Abstract Non-small-cell lung cancers (NSCLC) account for 85% of lung cancers and are mostly diagnosed at advanced stage. Drugs interrupting immune checkpoints, such as anti-CTLA-4, anti-PD-1, anti-PD-L1, have proven to unleash anti-tumor immunity and mediate durable cancer regressions in a portion of patients with NSCLC. Epithelial-to-mesenchymal transition (EMT) is a developmental process that enables reprogramming of polarized epithelial cells towards a mesenchymal phenotype with migratory and invasive properties. EMT has been involved in escape from oncogenic-induced senescence, resistance to chemotherapy and development of metastatic disease. Moreover, EMT promotes cancer cell plasticity and favors their adaptability to selective pressures. Here we made use of in silico approaches and further in vivo validation to evaluate the potential role of EMT as a major escape mechanism to tumor immunosurveillance in NSCLC. We performed an initial in silico analysis to assess the expression of immune checkpoint ligands (ICPLs) in 129 NSCLC cell lines (CCLE), in relation to their EMT status defined by a 72-gene EMT signature that was previously reported in NSCLC. Unsupervised hierarchical clustering analysis revealed that the expression of selected ICPLs was associated with the mesenchymal or epithelial phenotype. In particular, CD70, a member of the tumor necrosis factor superfamily, was significantly associated with the mesenchymal status (p &amp;lt; 0.001). We identified an E-box sequence (CANNTG) in CD70 gene promoter thus suggesting the possible regulation of CD70 by ZEB1 and/or SNAI. We extended the in silico analysis to a set of 488 adenocarcinomas (ADC) and 501 squamous cell carcinomas (SCC) from the TCGA and confirmed that CD70 expression was associated with a mesenchymal status (q-value &amp;lt;0.001). In a set of E-like (H441 and H1650) and M-like (H23 and HCC44) NSCLC cell lines we validated the association between an increased level of CD70 by flow cytometry and the mesenchymal status. Expression of CD70 by immunohistochemistry was observed in 5/51 lung ADC (10%), 6/45 (13%) lung SCC, 16/26 (63%) pulmonary sarcomatoid carcinomas and 2/10 (20%) small cell lung carcinomas. Interestingly, in pulmonary sarcomatoid carcinomas, CD70 expression was closely associated with the mesenchymal component. Our results suggest an association between the expression of CD70 and the mesenchymal phenotype, thus shedding light on the potential role of CD70 in immune escape of a subset of NSCLC. Citation Format: Sandra Ortiz-Cuaran, Aurélie Swalduz, Maria A. Albaret, Christine Menetrier-Caux, Véronique Haddad, Arnaud Paré, Geneviève De Souza, Anne P. Morel, Maurice Pérol, Christophe Caux, Sylvie Lantuejoul, Alain Puisieux, Pierre Saintigny. CD70 immune checkpoint ligand is associated with the epithelial-to-mesenchymal transition in non-small cell lung cancer. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 2320.

MET DNA Alterations in NSCLC—Reply

We thank Mengoli and colleagues for their interest in our article ([1][1]) and their comprehensive review of MET Δ14-positive pulmonary sarcomatoid carcinomas (PSC) been reported in the literature. We agree with their observation that MET Δ14 seems to be associated with the presence of

Lung Sarcomatoid Carcinoma Metastasis to Skin: A Case Report and Review of the Literature

ABSTRACTSarcomatoid carcinoma is a biphasic neoplasm composed of highly complex, intimately admixed malignant epithelial and mesenchymal elements. We herein report a rare case of cutaneous metastasis of pulmonary sarcomatoid carcinoma that contains liposarcomatous, rhabdosarcomatous and chondrosarcomatous heterologous differentiation, and review relevant literatures to lead to a better understanding of this rare but highly aggressive tumor.

Primary Sarcomatoid Carcinoma of the Lung: Radiometabolic ((18)F-FDG PET/CT) Findings and Correlation with Clinico-Pathological and Survival Results.

Pulmonary sarcomatoid carcinoma (PSC) is a very rare and uninvestigated subtype of non-small cell lung cancer (NSCLC). The aims of this study were to define the radiometabolic features (by (18)F-FDG PET/CT) in a bi-centric cohort of 49 PSC patients and to explore their relation with clinico-pathological characteristics and long-term survival results after surgical treatment. There were 40 males and 9 females aged 65.2±10.47years. Overall long-term survival was 26.7% at 5years. Mean and median values of SUVmax were 15.21 and 15, respectively (SD ±5.5). Performing an age-, gender- and staging-matched analysis comparing PSC Stage-I only with a cohort of Stage-I NSCLC (n=93), we observed significantly higher SUVmax values in PSC group (15.11 vs 7.66, p=0.001). No differences in terms of SUVmax were found with regard to tumour dimensions, histology (pure vs mixed, pleomorphic vs others), pathological stage and pattern of recurrence. P-stage, surgical radicality, vascular/lymphatic invasion but not SUVmax affected long-term survival in PSC.

Characteristics and Prognostic Analysis of 69 Patients With Pulmonary Sarcomatoid Carcinoma.

Pulmonary sarcomatoid carcinoma (PSC) is a rare malignancy. A total of 69 patients with PSC treated at a single institution in southern China with long-term follow-up were evaluated in this study. We analyzed the clinical characteristics, immunohistochemical profiles, epidermal growth factor receptor mutation status, K-RAS mutation status, treatments, and prognosis. PSC mainly occurred in young male patients with a history of smoking. Most patients received multimodality treatments and the majority had early-stage disease. The median survival time was 19.1 months, and the 5-year survival rate was 17.4%. The patients without distant metastasis, with normal or higher body mass index (≥18.5), with normal hemoglobin, with smaller tumor size (≤4 cm), and those who received complete resection had significantly better overall survival (P<0.05). The patients with pleomorphic carcinoma had much worse prognosis. In a Cox regression model, M stage, pathology, and having received a complete resection were independent prognostic factors (P<0.05). PSC is a unique lung malignancy with poor prognosis. Patients receiving complete resection had better prognosis, likely a reflection of early-stage disease. Neither neoadjuvant nor adjuvant chemotherapy improved patient survival for those with early-stage disease. The retrospective design and small sample size limited the generalizability. Future multicenter collaborations may be necessary to determine the optimal treatment.

Pulmonary sarcomatoid carcinoma (PSC): A 40 year experience at a comprehensive cancer center.

e20044Background: PSC is rare and standard therapy is not well defined. We evaluated experience at our center to identify factors influencing the outcome. Methods: Retrospective review of PSC patie...

Pulmonary Sarcomatoid Carcinoma with ALK rearrangement: Frequency, Clinical-Pathological Characteristics, and Response to ALK inhibitor.

e20055Background: Pulmonary sarcomatoid carcinoma (PSC) is a poor-differentiated subtype of non-small cell lung cancer (NSCLC) distinguished from other subtypes of NSCLC with higher aggressive cour...

Deep Sequencing Analysis Reveals That KRAS Mutation Is a Marker of Poor Prognosis in Patients with Pulmonary Sarcomatoid Carcinoma

IntroductionPulmonary sarcomatoid carcinoma (PSC) is a rare and aggressive subset of non–small cell lung cancer with limited treatment options. The molecular characterization of PSC has been strongly hampered by the relative rarity of these tumors. However, understanding the molecular and genetic bases of PSCs is critical to pave the way to new treatment options. In this work, we aimed to explore the complexity of the genetic asset of PSC and investigate its prognostic impact on survival in a large cohort of patients with PSC. MethodsNext-generation sequencing analysis of a panel of 26 genes with potential clinical relevance was performed on surgical specimens of 49 PSCs. The prognostic impact of genetic profiles on patient survival and the association between the genetic alterations and clinicopathological features were tested. ResultsFifty-five somatic mutations were detected in 13 genes. Thirty-nine PSCs (80%) showed at least one mutation. Survival probability decreased in patients with mutated PSC compared with in those with PSC without mutations (p = 0.02). In particular, mutations in Kirsten rat sarcoma viral oncogene homolog gene (KRAS), alone or in combination with tumor protein p53 gene (TP53) mutations, were associated with decreased survival probability and with the occurrence of local metastases at recurrence. Finally, comparison of our results with data in The Cancer Genome Atlas showed that PSCs have a mutational profile similar to that of smokers' lung adenocarcinoma. ConclusionsOverall, our analysis provides further information on the mutational profiles of PSCs and demonstrates for the first time a role of KRAS mutations in driving the aggressiveness of this type of cancer.

Mutations at the splice sites of exon 14 of MET gene: a new target for sarcomatoid carcinomas?

The pulmonary sarcomatoid carcinoma (SC) represents less than 1% of non-small cell lung cancer (NSCLC). Its prognosis is worse than that of other histological subtypes, by its particular aggressiveness and resistance to conventional therapies (1,2). Therefore, alternative therapies are sought, via immunotherapy or targeting molecular abnormalities. Liu et al . performed in Asian patients whole exome sequencing of 10 samples from SC followed by targeted sequencing of a set of five key genes on a validation cohort with 26 samples (3). The first analysis of the 10 samples showed two samples with mutations at the splice sites of exon 14 of MET . Subsequent targeted mutation screening of all 36 tumors confirmed these 2 mutations and identified 6 additional tumors with DNA alterations leading to exon 14 skipping.

Computed Tomographic and Pathological Features of Primary Pulmonary Sarcomatoid Carcinoma.

To investigate the computed tomographic (CT) and pathological features of primary pulmonary sarcomatoid carcinoma (PSC). The clinical data and CT images of 20 patients with pathologically confirmed PSC were retrospectively analyzed. Solitary pulmonary mass was identified in 18 patients and multiple pulmonary masses in 2 patients, amounting to 22 masses. There were 17 peripheral masses and 5 central masses, including 11 masses larger than 5 cm. The smooth margin was identified in 9 masses, deep lobulation and/or spinous protuberance in 11 masses, and ill-defined margin in 2 masses. Pleural indentation was identified in 2 masses and pleural thickening with wide basement was identified in 14 masses. On plain CT, cavity was observed in 5 masses, hypo-density in 7 masses, and homogeneous density in 10 masses. On contrast-enhanced CT scanning, irregular ring/patchy enhancement were shown in 15 masses and slightly homogenous enhancement in 2 masses. Of all patients, 6 patients had unilateral or bilateral hilar and/or mediastinal lymphadenopathy. There were 16 pleomorphic carcinomas and 4 spindle cell carcinomas. Immunohistochemically, anti-pan cytokeratin antibody was positive in 13 patients, cytokeratin was positive in 8 patients, Vimentin was positive in 15 patients, epithelial membrane antigen was positive in 1 patient, and thyroid transcription factor-1 was positive in 8 patients. PSC has some specific CT features; however, the final confirmation of PSC still depends on pathological and immunohistochemical examinations.

Synergistic Activation upon MET and ALK Coamplification Sustains Targeted Therapy in Sarcomatoid Carcinoma, a Deadly Subtype of Lung Cancer

IntroductionGenetic alterations suitable for targeted therapy are poorly known issues in pulmonary sarcomatoid carcinoma (PSC), an uncommon and life-threatening family of non–small cell lung cancers. MethodsNinety-eight PSCs were assessed for MNNG HOS Transforming gene (MET) and anaplastic lymphoma receptor tyrosine kinase gene (ALK) status by fluorescence in situ hybridization (FISH) and for relevant protein expression by immunohistochemical analysis, also taking advantage of phosphorylated (p-) antibodies. Moreover, levels of ALK and MET mRNA were also determined by real-time polymerase chain reaction and Western blot analysis for downstream activation pathways involving p-MET, p–protein kinase B, p–mitogen-activated protein kinase, p-SRC proto-oncogene tyrosine-protein kinase, and p–focal adhesion kinase (p-FAK). ResultsMET amplification was detected by FISH in 25 of 98 PSCs (25.6%) and ALK amplification (but not the relevant rearrangement) was found in 16 of 98 (16.3%), with all ALK-amplified tumors also showing MET amplification (p < 0.0001). Nine PSCs, however, showed MET amplification without any ALK gene alteration. ALK protein expression was always lacking, whereas MET and p-MET were confined to the relevant amplified tumors only. Increased levels of ALK and MET mRNA were detectable in tumors with no direct relationship between mRNA content, protein expression, or alterations detected by FISH. Western blot assays showed complete activation of downstream signal pathways up to p-SRC proto-oncogene tyrosine-protein kinase, and p–focal adhesion kinase recruitment in MET and ALK–coamplified tumors only, whereas isolated MET amplification, MET and ALK borderline amplification (5%–10% of tumor cells with ≥15 copies of the relevant gene), or negative tumors showing eusomy or chromosome polysomy were confined to p–mitogen-activated protein kinase, p–protein kinase B, and/or p-MET activation. Multivariate survival analysis pushed a higher percentage of MET altered cells or a higher value of MET copy gain per cell to marginally emerge for overall survival (p = 0.140) and disease-free survival (p = 0.060), respectively. ConclusionsALK and MET seemed to act as synergistic, nonrandom coactivators of downstream signal when coamplified in a subset of patients with PSC, thus likely suggesting a combined mechanism of oncogene addiction. These alterations could be a suitable target for therapy based on specific inhibitors.

Carcinomes sarcomatoïdes pulmonaires

Pulmonary sarcomatoid carcinomas are a rare group of tumors accounting for about one percent of non-small cell lung carcinoma (NSCLC). In 2015, the World Health Organization classification united under this name all the carcinomas with sarcomatous-like component with spindle cell or giant cell appearance, or associated with a sarcomatous component sometimes heterologous. There are five subtypes: pleomorphic carcinoma, spindle cell carcinoma, giant cell carcinoma, carcinosarcoma and pulmonary blastoma. Clinical characteristics are not specific from the other subtypes of NSCLC. Epithelial to mesenchymal transition pathway may play a key role. Patients, usually tobacco smokers, are frequently symptomatic. Tumors are voluminous more often peripherical than central, with strong fixation on FDG TEP CT. Distant metastases are frequent with atypical visceral locations. These tumors have poorer prognosis than the other NSCLC subtypes because of great aggressivity, and frequent chemoresistance. Here we present pathological description and a review of literature with molecular features in order to better describe these tumors and perhaps introduce new therapeutics.

Pulmonary sarcomatoid carcinoma: An uncommon entity in a 40 years female

A middle-aged female presented with nonpleuritic chest pain with progressive dyspnea and unmeasured weight loss and anorexia for last 4 months. The patient had pallor, clubbing, but no peripheral lymphadenopathy. Clinically, vesicular breath sound was diminished over anterior, posterior, and lateral aspect of the right hemithorax with a dull note on percussion. Chest radiography showed homogenous opacity involving the right hemithorax with blunting of right costophrenic angle without contralateral shifting of the lower mediastinum. Contrast-enhanced computed tomography (CT) thorax revealed a large mixed density mass lesion occupying the entire right hemithorax with peripheral contrast enhancement. The lesion narrowed the right pulmonary artery and insinuated the adjacent mediastinum, but no evidence of pleural nodularity. CT guided fine-needle aspiration cytology from the mass was inconclusive. Tru-cut biopsy from the mass showed spindle-shaped cells, with nuclear pleomorphism and mitotic figures, arranged in interlacing fascicles. The histopathology was suggestive of spindle cell neoplasm. Immunohistochemistry (IHC) showed pancytokeratin (AE1/3), cytokeratin 7, vimentin, and epithelial membrane antigen positivity, whereas immunonegativity to thyroid transcription factor-1, WT-1, and calretinin. The radiological picture with IHC pattern favored the diagnosis of pulmonary sarcomatoid carcinoma.

Clinical analysis of 95 cases of pulmonary sarcomatoid carcinoma.

To collect data on the clinical characteristics, pathologic presentation, and prognosis of patients with pulmonary sarcomatoid carcinoma. From September 24, 2008 to June 3, 2014, 95 patients were hospitalized at the Shanghai Chest Hospital for the treatment of pulmonary sarcomatoid carcinoma. We retrospectively collected patient gender, age, smoking history, time of initial diagnosis, diagnostic methods, tumor location, pathohistological subtype, tumor size, TNM stage, immunohistochemical results, subsequent treatments, and patient survival. Of the 95 patients included in this study, 80 were male and 15 were female. Median patient age was 64 years (range: 43-80 years). There were 29 cases of pleomorphic carcinoma, one case of giant cell carcinoma, six cases of spindle cell carcinoma, and six cases of carcinosarcoma. The other 53 cases were not subtyped. The median survival was 11.54 months (range: 0.9-100.9 months). 1-, 2-, 3-, and 5-year survival was 32%, 30%, 25%, and 21%, respectively. Univariate analysis showed that tumor size, stage, T1+T2 vs T3+T4 stage, N stage, and M stage were prognostic factors for survival. Multivariate regression analysis showed that T stage and lymph node metastases were independent prognostic factors. Pulmonary sarcomatoid carcinoma is an uncommon, aggressive cancer. T1+T2 vs T3+T4 stage and lymph node metastases were independent prognostic factors. Our results underscore the importance of early detection and early diagnosis. Effective treatments for this disease are lacking.