Another CDK7 inhibitor, LDC4297, also potently interfered with the expression of mutated p53. Furthermore, endogenous CDK7 expression was positively correlated with the levels of mutated p53 in TNBC cells with p53 mutation. Downregulating mutated p53 expression significantly suppressed the proliferation of TNBC cells with p53 mutation. Our findings demonstrated that targeting CDK7 was an effective approach for the treatment of TNBC with p53 mutation.Our findings demonstrated that targeting CDK7 was an effective approach for the treatment of TNBC with p53 mutation. Understanding the safety and adverse event profiles of PD-1/PD-L1 inhibitors is important in guiding cancer immunotherapy. Consequently, we designed this meta-analysis to evaluate the safety of PD-1/PD-L1 inhibitors in clinical trials involving cancer patients. Four safety indicators comprising treatment-related adverse events, death, discontinuation of therapy and grades 3-5 adverse events were evaluated using the random effect model. The quality of enrolled trials was assessed using the Newcastle Ottawa Scale (NOS). Forty-four clinical trials were included in the final meta-analysis. Compared with chemotherapy, the risk of death due to the use of PD-1/PD-L1 inhibitors was much lower than that experienced in the control group (OR = 0.65, 95%CI [0.47, 0.91], I = 0%, Z = 2.52 (P = 0.01)). Similar observations were apparent regarding the other three indicators of safety and also when the use of PD-1/PD-L1 inhibitors alone is compared with the combined use of PD-1/PD-L1 and CTLA-4. When used together with chemotherapy, PD-1/PD-L1 inhibitors increased the incidence of the adverse events as compared to the use of chemotherapy alone. Increased risks for adverse events were also noticed with the use of PD-1/PD-L1 inhibitors over the use of a placebo. The use of PD-1/PD-L1 inhibitors alone is associated with a better safety profile compared to either the use of chemotherapy or the use of PD-1/PD-L1 inhibitors with other anticancer regimens.The use of PD-1/PD-L1 inhibitors alone is associated with a better safety profile compared to either the use of chemotherapy or the use of PD-1/PD-L1 inhibitors with other anticancer regimens. To compare the clinical value of contrast-enhanced ultrasonography (CEUS) versus computed tomography (CT) for distinguishing neoplastic and non-neoplasticgallbladder polyps. Given whether laparoscopic cholecystectomy is needed, differential diagnosis of neoplastic and non-neoplastic gallbladder polyps is more important than benign and malignant polyps. A total of 89 consecutive patients with polypoid lesionsof thegallbladder > 10mm in size without local invasion or distant metastasis during primary screening were enrolled in this prospective and comparative study. All patients who met the inclusion criteria underwent CEUS and CT examinations prior to surgical resection. The enhancement patterns and microvascular imaging types were analyzed on CEUS. The maximum diameter and CT value of the lesions were also recorded and subjected to a comparative analysis. The clinical value of the two diagnostic methods is compared. Of the 89 patients, there were 58 (65.2%) cases of non-neoplastic polyps and 31 (34.8or CT, respectively (P=0.406). CEUS and CT are useful for differential diagnosis of neoplastic and nonneoplastic polypoid lesions of the gallbladder. Diagnostic efficacy was comparable between CEUS and CT. Thus, CEUS is preferred over CT in the differential diagnosis of neoplastic and non-neoplastic gallbladderpolyps due to its comparable diagnostic efficacy and lack of radiation dose.CEUS and CT are useful for differential diagnosis of neoplastic and nonneoplastic polypoid lesions of the gallbladder. Diagnostic efficacy was comparable between CEUS and CT. Thus, CEUS is preferred over CT in the differential diagnosis of neoplastic and non-neoplastic gallbladder polyps due to its comparable diagnostic efficacy and lack of radiation dose.Circulating cell-free DNA (ccfDNA), released from normal and cancerous cells, is a promising biomarker for cancer detection as in neoplastic patients it is enriched in tumor-derived DNA (ctDNA). ctDNA contains cancer-specific mutations and epigenetic modifications, which can have diagnostic/prognostic value. However, in primary tumors, and in particular in localized prostate cancer (PCa), the fraction of ctDNA is very low and conventional strategies to study ccfDNA are unsuccessful. Here we demonstrate that prostate biopsy, by causing multiple injuries to the organ, leads to a significant increase in plasma concentration of ccfDNA (P less then 0.0024) in primary PCa patients. By calculating the minor allele fraction at patient-specific somatic mutations pre- and post-biopsy, we show that ctDNA is significantly enriched (from 3.9 to 164 fold) after biopsy, representing a transient "molecular window" to access and analyze ctDNA. Moreover, we show that newly released ccfDNA contains a larger fraction of di-, tri- and multi-nucleosome associated DNA fragments. This feature could be exploited to further enrich prostate-derived ccfDNA and to analyze epigenetic markers. Our data represent a proof-of-concept that liquid tumor profiling from peripheral blood performed just after the biopsy procedure can open a "valuable molecular metastatic window" giving access to the tumor genetic asset, thus providing an opportunity for early cancer detection and individual genomic profiling in the view of PCa precision medicine. The incidence of early stage multiple primary lung cancer (MPLC) has been increasing in recent years, while the ideal strategy for its diagnosis and treatment remains controversial. learn more The present study conducted genomic analysis to identify a new molecular classification method for accurately predicting the diagnosis and therapy for patients with early stage MPLC. A total of 240 tissue samples from 203 patients with multiple-non-small-cell lung cancers (NSCLCs) (n = 30), early stage single-NSCLC (Group A, n = 94), and advanced-stage NSCLC (Group B, n = 79) were subjected to targeted multigene panel sequencing. Thirty patients for whom next-generation sequencing was performed on >1 tumor were identified, yielding 45 tumor pairs. The frequencies of , and mutations exhibited significant differences between early and advanced-stage NSCLCs. The prevalence of the mutation in early stage NSCLC was remarkably higher than that in advanced-stage NSCLC ( = 0.047). The molecular method classified tumor pairs into 26 definite MPLC tumors and four intrapulmonary metastasis (IM) tumors.