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BackgroundCarcinosarcoma is a rare esophageal tumor, accounting for approximately 0.27-2.8% of malignant esophageal tumors. This study aims to investigate the clinical pathological characteristics, surgical treatment outcomes, and analysis of prognostic factors in esophageal carcinosarcoma (ECS).MethodsClinical data from sixteen patients diagnosed with esophageal sarcomatoid carcinoma who underwent surgical interventions were retrospectively analyzed. Clinical and pathological features, treatment modalities, and postoperative outcomes were systematically examined.ResultsOut of the 1261 patients who underwent surgical treatment for esophageal cancer, 16 cases were pathologically confirmed as carcinosarcoma. Among them, two underwent neoadjuvant chemotherapy, six received postoperative chemotherapy. Carcinosarcomas predominantly occurred in the middle (43.75%) and lower (50%) segments of the esophagus. Among the 16 cases, 10 presented as polypoid, 4 as ulcerative, and 2 as medullary types. Microscopic examination revealed coexistence and transitional transitions between sarcomatous and carcinoma components. Pathological staging showed 5 cases in stage T1, 2 in stage T2, and 9 in stage T3, with lymph node metastasis observed in 8 cases (50%). TNM staging revealed 2 cases in stage I, 9 in stage II, and 5 in stage III. The overall 1, 3, and 5-year survival rates were 86.67%, 62.5%, and 57.14%, respectively. Univariate analysis indicated that pathological N staging influenced survival rates, while multivariate analysis demonstrated that pathological N staging was an independent prognostic factor.ConclusionsCarcinosarcoma is a rare esophageal tumor, accounting for approximately 0.27-2.8% of malignant esophageal tumors. Histologically, the biphasic pattern is a crucial diagnostic feature, although the carcinomatous component may not always be evident, especially in limited biopsies, leading to potential misclassification as pure sarcoma or squamous cell carcinoma. Despite its large volume and cellular atypia, carcinosarcoma carries a favorable prognosis. Complete surgical resection of the tumor and regional lymph node dissection is the preferred treatment approach for esophageal carcinosarcoma.

To investigate the effect of Lentinan (LNT) on lung adenocarcinoma (LUAD) cell stemness and its mechanism. In this study, we founded that LNT significantly reduce the cell proliferation, activity, migration, invasion, and stemness of LUAD cells, and promote their apoptosis compared with the control group in vitro. Moreover, LNT significantly inhibited the volume and weight of tumors of nude mice in vivo. At the same time, LNT can significantly up-regulate miR-216a-5p levels and reduce the protein expression of phospho-JAK2 (Y1007/1008) and phospho-STAT3 (Tyr705), thereby inhibiting the JAK2/STAT3 signaling pathway. Interfering with miR-216a-5p expression and activating the JAK2/STAT3 signaling pathway can significantly reverse LNT inhibitory effects on LUAD. Collectively, LNT can inhibit the JAK2/STAT3 signaling pathway by up-regulating miR-216a-5p, reducing stemness, and promoting LUAD cells apoptosis, then slow down LUAD occurrence and development, providing concepts and experimental foundation treating patients with LUAD.

Pyroptosis, a lytic pro-inflammatory type of programmed cell death, has been widely studied in diverse inflammatory disease models. Membrane perforation and cell swelling induced by cleaved gasdermin family members is the main characteristic of pyroptosis. Emerging evidence has revealed a complicated relationship between pyroptosis and cancer. On the one hand, as inflammatory cell death, pyroptosis provides a comfortable environment for tumor proliferation. On the other hand, excessive activation of pyroptosis can inhibit the development of tumor cells. In this review, we first summarized the latest progress about the molecular mechanism of pyroptosis. Then, members from gasdermin family, the central molecules of pyroptosis which formed pores on the cell membrane, were highlighted. In the second part of this review, we summarized drugs that induced pyroptosis in different tumors and their concrete mechanisms based on recent literature reports. In the final section, we discussed several hotspots in pyroptosis and cancer therapy, which will point out the direction of sequent research. In brief, inducing pyroptosis in cancer cells is a promising strategy for cancer therapy.