Abstract Background Ciliated muconodular papillary tumor (CMPT) is an incredibly rare pulmonary tumor. Currently, little is known about CMPT, and it has not yet been classified by the World Health Organization. The clinical manifestation of CMPT is nonspecific and the diagnosis is only based on pathology. CMPT has been documented in limited reports as a benign tumor, thus the treatment is typically with surgical excision if a solid tumor is identifiable. The prognosis of CMPT is very positive, as no recurrence has been reported in the limited literature available. However, CMPT accompanied with adenocarcinoma in situ has not been reported previously in the literature. Case presentation In this report, we presented a case of a 53-year-old male smoker with CMPT associated with adenocarcinoma in situ. This diagnosis was confirmed by pathological examination, including immunohistostaining. No solid resectable lesion was identified on CT scan; therefore, no surgery was performed. The patient’s adenocarcinoma in situ was disseminated in both lungs, thus chemotherapeutic treatment with cisplatin and pemetrexed was given. The patient will be continually followed up closely on a wait-and-watch basis. Conclusions In summary, our report reveals a unique case of CMPT in conjunction with adenocarcinoma in situ, potentially revealing an association between CMPT and malignancy which has not been previously reported. More similar case studies will be beneficial to determine the authentic relationship between CMPT and adenocarcinoma in situ.
Background/Aim: This study was designed to investigate the effect of IL-39 on T24 bladder cancer (BC) cell line survival and growth. Materials and Methods: In order to assess the direct effect of IL-39 on survival, proliferation, and apoptosis of T24 BC cells, we utilized a clonogenic survival assay, a cell proliferation assay, and caspase-3 activity kits. Potential proliferative and apoptotic molecular mechanisms were evaluated by RT-PCR. Results: Treatment of T24 BC cells with IL-39 resulted in a significant reduction in the percentage of colonies. The anti-tumor effect of IL-39 on T24 bladder cancer cells correlated strongly with a decrease in cyclin E, in combination with an increase in the mRNA levels of Fas. Conclusion: IL-39 impedes the growth and survival of T24 BC cells by inhibiting growth and promoting apoptosis. This ability to modulate gene transcription in neoplastic cells shows promise and warrants further research in immunotherapy.
Cervical cancer is the most common cancer of the female reproductive system. Late-stage cervical cancer treatment has been largely unsuccessful, and urgent anti-cancer therapy is needed. Mangosteen, a tropical fruit, has been studied and found to be rich in xanthones, known anti-cancer compounds. This study was designed to investigate the effect of mangosteen extract (ME) on SiHa cervical cancer cells and to explore the underlying molecular mechanisms.Clonogenic survival assay, Quick Cell Proliferation Assay, terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) staining, and caspase-3 activity kits were used to investigate the in vitro role of ME treatment in SiHa cervical cancer cell growth. We further investigated the possible molecular mechanisms using RT-PCR. Statistical analysis was done with unpaired two-tailed Student's t-test and significance at p-value <0.05; each experiment was repeated three times.Our study found that the growth and proliferation of SiHa cervical cancer cells was inhibited by ME. ME also induced apoptosis in SiHa cervical cancer cells. The anti-proliferative effect of ME on cervical cancer cells was associated with statistically significant (p<0.05) down-regulation of the pro-proliferative molecules cyclin B, cyclin D and cyclin E. The pro-apoptotic effect of ME was associated with statistically significant (p<0.05) down-regulation of the anti-apoptotic molecules flice-like inhibitory protein (FLIP) and survivin.ME impedes the growth and survival of SiHa cervical cancer cells by down-regulating cyclin B, cyclin D, cyclin E as well as FLIP and survivin. ME may be a promising strategy for targeted cancer immunotherapy development.
Collagen triple helix repeat containing-1 (CTHRC1) promotes tumor progression by regulating the immunosuppression of the tumor microenvironment. However, the function of CTHRC1 in gastric cancer (GC) and its relationship with tumor-infiltrating immune cells remains unclear.Data were downloaded from The Cancer Genome Atlas (TCGA) database. The difference in expression of CTHRC1 in GC and adjacent non-tumor tissues was analyzed by R software and verified by the online database Oncomine. A Kaplan-Meier survival analysis was selected for evaluating the impact of CTHRC1 expression on the survival of GC and verified by the Kaplan-Meier plotter. The relationship between CTHRC1 expression and clinicopathological parameters was assessed by univariate and multivariate Cox regression. The correlation with tumor-infiltrating immune cells was analyzed by Tumor Immune Estimation Resource (TIMER). A gene set enrichment analysis (GSEA) was used to screen the signaling pathways between low and high CTHRC1 expression datasets.The expression of CTHRC1 in GC tissue was higher than that in adjacent non-tumor tissues. The Kaplan-Meier curve showed that patients with higher CTHRC1 expression had a worse prognosis. The univariate and multivariate Cox analyses showed that high expression of CTHRC1 was an important independent predictor of poor overall survival in GC. The TIMER database analysis revealed that CTHRC1 was associated with five tumor immunosuppressive cells in GC. The GSEA indicated that 10 signaling pathways were enriched in samples with a high CTHRC1 expression phenotype.CTHRC1 might be a new prognostic biomarker for CG and might be a potential target for treatment of GC.
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