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Sarcomatoid squamous cell carcinoma (SSCC) is a malignant tumor with epithelial and spindle cell components. It is common in visceral organs and rarely presents as a cutaneous tumor. We present a case of a 55-year-old Black male with multiple recurrences of SSCC. Prompt diagnosis and complete excision is prudent to prevent recurrence or further spread to adjacent structures.

Abstract Objectives Differentiating malignant pleural mesothelioma from benign reactive mesothelial processes can be quite challenging. Ancillary tests such as BRCA1-associated protein 1 (BAP1) immunohistochemistry and p16 fluorescence in situ hybridization (FISH) are helpful tools to aid in this distinction. Immunohistochemistry for methylthioadenosine phosphorylase (MTAP) has recently been proposed as an effective surrogate marker for p16 FISH and is an attractive alternative test due to shorter turnaround time. There are little data regarding the specificity of MTAP loss for mesothelioma or whether it may be useful to distinguish mesothelioma from the most common entity in the differential diagnosis, sarcomatoid carcinoma. Methods We studied well-characterized cases of sarcomatoid carcinoma (n = 34) and sarcomatoid mesothelioma (n = 62), which were stained for MTAP (clone 2G4) and BAP1 (clone C-4). Results Loss of MTAP expression was observed in 17 (50%) of 34 pulmonary sarcomatoid carcinomas; BAP1 expression was retained in all of the cases in which it was performed (n = 31). MTAP expression was lost in 38 (61%) of 62 sarcomatoid mesotheliomas; BAP1 was lost in 6 (10%) of 62. In the six cases with BAP1 loss, five also had loss of MTAP, while MTAP expression was retained in one. Conclusions Loss of MTAP expression by immunohistochemistry is common in pulmonary sarcomatoid carcinoma, as it is present in half of cases. This rate is similar to what is observed in sarcomatoid mesothelioma (61%). Therefore, this stain is not useful to distinguish between these two malignancies. MTAP loss is more common than BAP1 loss in the setting of sarcomatoid mesothelioma (61% vs 10%, respectively).

Background Sarcomatoid hepatocellular carcinoma (SHC) is a rare malignant hepatic tumor. Recurrent interventional therapies such as transcatheter arterial chemo-embolization (TACE), radiofrequency ablation (RFA), and percutaneous ethanol injection have been reported previously utilized in a majority of SHC cases. To date, the exact pathogenic mechanisms underlying sarcomatoid transformation of hepatocellular carcinoma (HCC) remain unknown. Case presentation In this study, we report a 68-year-old female SHC patient admitted to our hospital due to discrete abdominal distention for more than 20 days. Abdominal computed tomography (CT) with tri-phase enhancement revealed portal vein tumor thrombi (PVTT) and a left hepatic lobe lesion measuring 110.0 mm × 160.0 mm. The patient subsequently underwent liver resection, after which pathological examination revealed proliferation of spindle-shaped SHC cells. A sarcomatoid, T4 stage carcinoma was eventually diagnosed. Forty-seven days after the operation, tri-phase enhanced CT detected extensive lesions in the liver, spleen, peritoneum, omentum majus, and mesentery, indicating SHC recurrence and metastases. Combination chemotherapy with pirarubicin and cisplatin was initiated for 1 cycle, but terminated due to resultant severe myelosuppression and medication intolerance. The patient was lost to therapy after 3 months of follow-up. Conclusions This case is unique because of hepatitis C virus infection. We should consider the possibility of this disease in patients with atypical clinical presentation.

Sarcomatoid malignant mesothelioma (SMM) tends to occur in the pleura and is morphologically similar to lung sarcomatoid carcinoma (LSC) and organizing pleuritis (OP). Because SMM often does not express mesothelial markers, it is very difficult to distinguish from LSC and OP. GATA-binding protein 3 (GATA3) is a specific immunohistochemical (IHC) marker of breast and urothelial carcinoma. We routinely find that GATA is expressed in MM; however, GATA3 expression in SMM and its reference value for distinguishing SMM from LSC and OP remain unclear. Here, we used IHC methods to detect the expression of GATA3 and classic mesothelial markers in 17 SMM, 12 LSC, and 7 OP cases. We detected the following expression rates in SMM versus LSC cases: GATA3 (70.6% vs. 16.7%, p = 0.008), calretinin (52.9% vs. 8.3%, p = 0.019), Wilms tumor (WT)-1 (64.7% vs. 0%, p = 0.000), D2-40 (47.1% vs. 16.7%, p = 0.126), CK5/6 (35.3% vs. 25.0%, p = 0.694), and pan-cytokeratin (CKpan) (88.2% vs. 100.0%, p = 0.498). The specificities of calretinin, WT-1, and GATA3 in distinguishing SMM from LSC were 91.7%, 100%, and 83.3%, respectively, and combinations of any two of these three markers exhibited 100% specificity for SMM. Notably, the sensitivity of calretinin+/WT1+ staining for SMM was only 23.5%, which increased to 64.7% after including GATA3. Furthermore, all OP cases showed partial or diffuse expression of CKpan, WT-1, and D2-40 but no GATA3 and calretinin expression. In conclusion, GATA3 is an IHC marker with excellent sensitivity and specificity for SMM, and the combined consideration of GATA3, calretinin, and WT-1 was best for distinguishing SMM from LSC. Moreover, CKpan, WT-1, and D2-40 had no value for distinguishing SMM from OP, and GATA3 and calretinin were the most specific markers for distinguishing these two lesions.

Basal cell carcinosarcoma (BCCS) is a rare malignant biphasic tumor of the skin, composed of epithelial and mesenchymal components, and may be underdiagnosed. We sought to summarize the current understanding of BCCS including its reported history, clinical presentation, diagnosis, and treatment. We also reappraise and present our recommendations of histological interpretation for its diagnosis and treatment. A systematic review of PubMed and EMBASE, from inception of databases to December 1, 2022, identified all reported cases of basal cell carcinosarcoma. A total of 34 reports containing 54 patients with basal cell carcinosarcoma were included. The neoplasm was most commonly associated in areas of sun-exposed skin and primarily affected the elderly. Diagnosis was made on histology specimens using H&E. To address underdiagnosis, additional immunohistochemical markers have been proposed due to unreliable phenotypic appearance in this poorly differentiated neoplasm. Treatment consists of excision of the tumor, typically with Mohs surgery, and is curative in most cases. There are limited treatment options for metastatic disease. There were limitations to this study as various immunohistochemical stains used on suspected BCCS without providing an explanation as to why certain markers were included and others were excluded. Continued efforts in characterizing this complex neoplasm are critical in establishing reliable and accurate diagnostic tests and accompanying treatment options, especially in cases of metastatic disease.

Background: We present an interesting case involving a tumour comprising both basal cell tumour cells and sarcomatoid tumour cells. An 86-year-old woman presented with an erythematous lesion on her left cheek. Clinical and dermoscopic findings suggested BCC. Complete excision and histopathological examination revealed a BCC with a separate proliferation of atypical spindle and epithelioid cells. Immunohistochemical staining supported the diagnosis, with basaloid cells positive for CK5/6 and Ber-EP4 and sarcomatoid cells positive for CD10 and vimentin. Results: Histology and immunohistochemistry confirmed a basal cell carcinoma with sarcomatoid differentiation. The close proximity of sarcomatoid cells to the BCC component suggests a potential role of epithelial–mesenchymal interactions in tumour development. Further investigations into the exact origin of this tumour are required. Conclusion: Basal cell carcinoma with sarcomatoid differentiation is rare. This case highlights the importance of thorough histological and immunohistochemical evaluation. Further studies are necessary to better understand the pathogenesis of such collision tumours.

Hepatic sarcomatoid carcinoma (HSC) is characterized by its aggressive behavior and poor prognosis. As of now, no universally endorsed standard therapeutic approaches for HSC have been established. Herein, we describe the case of a 60-year-old individual diagnosed with HSC, subsequently presenting with multiple metastases postoperatively. Owing to the pronounced expression of programmed cell death protein 1 (PD-1), the individual was subjected to monotherapy utilizing sintilimab for a duration spanning 12 months. Following this regimen, a synergistic treatment approach comprising both anlotinib and sintilimab was instituted, culminating in an ensuing 11 months of efficacious therapeutic response. Throughout the course of treatment, the patient's quality of life remained satisfactory. This particular therapeutic strategy not merely reinforces the efficacy of PD-1 inhibitors in the realm of HSC management, but more pivotally, suggests that tyrosine kinase inhibitors (TKIs) might counteract resistance to PD-1 antagonists, thus offering a potentially augmented treatment paradigm for HSC.

[This corrects the article DOI: 10.3389/fimmu.2022.956982.].[This corrects the article DOI: 10.3389/fimmu.2022.956982.].

: Immunotherapy based on anti PD-1/PD-L1 inhibitors has proven to be more effective than sunitinib in the first-line setting of advanced renal cell carcinoma (RCC). RCC patients with sarcomatoid histology (sRCC) have a poor prognosis and limited therapeutic options. We performed a systematic review and a meta-analysis of randomized-controlled trials (RCTs) of first-line anti PD-1/PDL-1 agents vs. sunitinib, presenting efficacy data in the sub-group of sRCC patients. The systematic research was conducted on Google Scholar, Cochrane Library, PubMed and Embase and updated until 31th January, 2020. Abstracts from ESMO and ASCO (2010–2019) were also reviewed. Full texts and abstracts reporting about RCTs testing first-line anti-PD-1/ PD-L1 agents vs. sunitinib in RCC were included if sRCC sub-group analyses of either PFS (progression-free survival), OS (overall survival) or radiological response rate were available. Pooled data from 3814 RCC patients in the ITT (intention-to-treat) population and from 512 sRCC patients were included in the quantitative synthesis. In the sRCC sub-group vs. the ITT population, pooled estimates of the PFS-HRs were 0.57 (95%: 0.45–0.74) vs. 0.79 (95% CI: 0.70–0.89), respectively, with a statistically meaningful interaction favoring the sRCC sub-group (pooled ratio of the PFS-HRs = 0.64; 95% CI: 0.50–0.82; p < 0.001). Pooled estimates of the difference in CR-R (complete response-rate) achieved with anti-PD-1/PDL-1 agents vs. sunitinib were + 0.10 (95% CI: 0.04–0.16) vs. + 0.04 (95% CI: 0.00–0.07) in the sRCC vs. the non-sRCC sub groups, with a statistically meaningful difference of + 0.06 (95% CI: 0.02–0.10; p = 0.007) favoring the sRCC sub-group. Sarcomatoid histology may be associated with improved efficacy of anti PD-1/PDL-1 agents vs. sunitinib in terms of PFS and CR-R.

Background In contemporary surgically treated patients with localized high-grade (G3 or G4) clear-cell renal cell carcinoma (ccRCC), it is not known whether presence of sarcomatoid dedifferentiation is an independent predictor and/or an effect modifier, when cancer-specific mortality (CSM) represents an endpoint. Methods Within the Surveillance, Epidemiology, and End Results database, all surgically treated localized high-grade ccRCC patients treated between 2010 and 2020 were identified. Univariable and multivariable Cox-regression models were used. Results In 18,853 surgically treated localized high-grade (G3 or G4) ccRCC patients, 5-year CSM-free survival was 87% (62% vs. 88% with vs. without sarcomatoid dedifferentiation, p  < 0.001). Presence of sarcomatoid dedifferentiation was an independent predictor of higher CSM (hazard ratio [HR] 1.8, p  < 0.001). In univariable survival analyses predicting CSM, presence versus absence of sarcomatoid dedifferentiation in G3 versus G4 yielded the following hazard ratios: HR 1.0 in absent sarcomatoid dedifferentiation in G3; HR 2.7 ( p  < 0.001) in absent sarcomatoid dedifferentiation in G4; HR 3.9 ( p  < 0.001) in present sarcomatoid dedifferentiation in G3; HR 5.1 ( p  < 0.001) in present sarcomatoid dedifferentiation in G4. Finally, in multivariable Cox-regression analyses, the interaction terms defining present versus absent sarcomatoid dedifferentiation in G3 versus G4 represented independent predictors of higher CSM. Conclusions In contemporary surgically treated patients with localized high-grade ccRCC, sarcomatoid dedifferentiation is not only an independent multivariable predictor of higher CSM, but also interacts with tumor grade and results in even better ability to predict CSM.