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The aim of the present study was to investigate the D-loop gene mutation and microsatellite instability in the mitochondrial DNA (mtDNA) and the correlation with the clinical and pathological parameters in laryngeal cancer.
The tumor tissues and paratumor tissues in 60 cases of laryngeal cancer were selected, and DNA was extracted from these tissues. The D-loop region in mtDNA was amplified by PCR with the gene sequence of the amplified product being detected. The gene sequence of the detected region was compared with the revised Cambridge Reference Sequence (rCRS) and the related database by using the Mitomaster software. The correlation between the D-loop gene mutation and the clinical and pathological parameters was investigated.
A total of 174 mutations across 38 sites were detected in 51 (85%) of samples. Most of the mutations were concentrated in the high various (HV) I region, and the main types of mutations were the substitution of a single base or insertion and deletion of a single base. There was also microsatellite instability in the D310 region. The statistical results showed that there was no correlation between the age, gender, tumor diameter, and TNM stage, and the number of the D-loop mutations in mtDNA (P > 0.05).
There existed high-frequency mutation of the D-loop gene in mtDNA in laryngeal cancer, which might play an important role in the pathogenesis of laryngeal cancer.
There existed high-frequency mutation of the D-loop gene in mtDNA in laryngeal cancer, which might play an important role in the pathogenesis of laryngeal cancer.Estimated to comprise approximately 10% of lung cancer cases, multiple pulmonary lesions pose a diagnostic and therapeutic challenge in thoracic oncology. Distinction between multiple primary lung cancer (MPLC) and intrapulmonary metastasis (IPM) directly affects tumor staging and clinical management. In equivocal cases in which the lesions are histopathologically indistinguishable, targeted sequencing can provide key additional evidence for differential diagnosis. Herein, we describe an unusual patient who presented with seven lung lesions that consisted of primary tumors and metastatic lesions, each showing distinct clonality status based on histomolecular findings. Specifically, the 45-year-old female never-smoker underwent a surgery that removed one invasive lepidic predominant adenocarcinoma and five microinvasive adenocarcinomas. Next-generation sequencing revealed three of the lesions to carry a clonal driver mutation EGFR p.L858R, supporting an IMP diagnosis. EGFR p.L858R was not detected in two other surgical specimens, which instead harbored respective oncogenic BRAF p.G469A and an uncommon EGFR p.G779F. These results led to diagnosis of the two lesions as primary tumors of lineages different from that of the metastases. The patient had achieved a recurrence-free survival of 21 months as of the latest follow-up. In this rare case that presented with evidence of both MPLC and IPM, targeted sequencing proved valuable in facilitating the diagnostic workup.
Nucleolar and spindle-associated protein 1 (NUSAP1) is a significant mitotic regulator and has been found to be implicated in carcinogenesis of several cancers. The aim of this study was to explore the functional role and underlying mechanisms of NUSAP1 in osteosarcoma.
Western blot assay and Real-time fluorescent quantitative polymerase chain reaction (RT-qPCR) were employed to assess the expressions of NUSAP1, cell division cycle 20 homologue (CDC20) and cyclin A2 (CCNA2) in osteosarcoma cells. Cell proliferation was evaluated by Cell Counting Kit-8 (CCK-8) assay and 5-ethynyl-2'-deoxyuridine (EdU) assay, and flow cytometry was applied for exploring cell cycle. In addition, an osteosarcoma tumor-bearing mouse model was established by injection of transfected osteosarcoma cells. Tumor volume and protein expressions of Ki67 and PCNA were examined. Bioinformatics analysis and immunoprecipitation were used to identify the combination of NUSAP1 with CDC20 and CCNA2.
The mRNA and protein expression of NUSAP1 were extremely upregulated in osteosarcoma cells. Overexpression of NUSAP1 promoted whereas NUSAP1 silencing suppressed cell proliferation and cell cycle progression in transfected osteosarcoma cells. In osteosarcoma mouse model, NUSAP1 expression affected tumor volume and levels of Ki67 and PCNA. Moreover, CDC20 or CCNA2 silencing inhibited NUSAP1-induced cell proliferation and cell cycle in osteosarcoma cells.
Our data demonstrated that upregulated NUSAP1 may exacerbate the development of osteosarcoma by accelerating the proliferation and cell cycle process of osteosarcoma cells by binding to CDC20 and CCNA2, suggesting NUSAP1 as a possible therapeutic target for treatment of osteosarcoma.
Our data demonstrated that upregulated NUSAP1 may exacerbate the development of osteosarcoma by accelerating the proliferation and cell cycle process of osteosarcoma cells by binding to CDC20 and CCNA2, suggesting NUSAP1 as a possible therapeutic target for treatment of osteosarcoma.
Breast cancer (BC) is the most common type of cancer among women worldwide, and about 30% of males will have recurrent disease.
In order to treat recurrent BC, we designed a type of silica nanodelivery system loaded with epirubicin and curcumin (composite nanoparticles, CNPs). LBH589 in vivo To promote CNPs clinical application, the stability, the blood, immune and cell compatibility, skin stimulation experiments, anti-tumor activity in vivo and in vitro were studied.
In our study, the CNPs had a particle size of 73.9 nm and a uniform size and morphology; moreover, they maintained physical and chemical stability in the blood protein environment. Additionally, results showed that nanoparticles had good blood and immune compatibility, and they did not affect intracellular superoxide dismutase (SOD) and intracellular catalase (CAT). Skin stimulation experiments showed that CNPs did not cause any obvious irritative damage to the intact skin of rabbits. In the cytotoxicity study, CNPs showed strongest antitumor activity. The results of cell cycle and apoptosis studies showed that CNPs could mainly induce apoptosis of S and G2/M phase cells. In vivo, CNPs showed strongest aggregation in the tumor after 6 h of tail vein administration, and a large amount of CNPs continued to accumulate in the blood after 12 h of administration, indicating that CNPs had long circulation ability. The in vivo antitumor activities showed that CNPs had the strongest antitumor activity and tumor targeting ability, and hematoxylin-eosin staining of internal organs showed no obvious difference between treatment groups and negative control.
CNPs have an ideal biosafety and therapeutic effect for recurrent BC, and they have potential clinical application value.
CNPs have an ideal biosafety and therapeutic effect for recurrent BC, and they have potential clinical application value.
Read More: https://www.selleckchem.com/products/LBH-589.html
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