Strouderiksen2019

As prostate cancer (PrC) shows a

mutation rate as high as 30%, it becomes crucial to find the optimal selection criteria for genetic testing. The primary objective of this study was to evaluate the

mutation rate in families with PrC associated with breast and/or ovarian cancers; secondary aims were to compare the characteristics of families and BRCA-related PrC outcome among

and

carriers.

Following the Modena criteria for the

test, we evaluated the mutation rate in families with breast and/or ovarian cancer with a Gleason score ≥7 PrCs, by testing breast or ovarian cases and inferring the mutation in the prostate cases. The characteristics of families and BRCA-related PrC outcomes were measured using the chi-square (χ

) test and Kaplan-Meier methods, respectively.

Among 6,591 families, 580 (8.8%) with a Gleason score ≥ 7 PrCs were identified, of which 332 (57.2%) met the Modena selection criteria for BRCA testing. Selleckchem SB273005 Overall, 215 breast or ovarian cancer probands (64.8%) were tested, of which 41 resulted positive for

and one for

genes (19.5%). No statistically significant differences were found in BRCA-related PrC prognosis and in the characteristics of families among BRCA1, BRCA2 and non-tested patients. Ten of 23 (44%) mutations in the

gene fell in the prostate cancer cluster region (PCCR) at the 3´ terminal of the 7914 codon.

It appears the Modena criteria are very useful for BRCA testing selection in families with breast and/or ovarian cancer and PrC. A trend toward a worse prognosis has been found in

carriers.

It appears the Modena criteria are very useful for BRCA testing selection in families with breast and/or ovarian cancer and PrC. A trend toward a worse prognosis has been found in BRCA2 carriers.

Dysfunction in fibroblast growth factor receptor (FGFR) signaling has been reported in diverse cancer types, including non-small cell lung cancer (NSCLC). The frequency of

aberrations in Chinese NSCLC patients is therefore of great clinical significance.

A total of 10,966 NSCLC patients whose tumor specimen and/or circulating cell-free DNA (cfDNA) underwent hybridization capture-based next-generation sequencing were reviewed. Patients' clinical characteristics and treatment histories were also evaluated.

aberrations, including mutations, fusions, and gene amplifications, were detected in 1.9% (210/10,966) of the population.

abnormalities were more frequently observed in lung squamous cell carcinomas (6.8%, 65/954) than lung adenocarcinomas (1.3%, 128/9,596).

oncogenic mutations were identified in 19 patients (~0.17%), of which, 68% were male lung squamous cell carcinoma patients. Eleven out of the 19 patients (58%) had concurrent altered PI3K signaling, thus highlighting a potential combination therapeutic strategy of dual-targeting FGFR and PI3K signaling in such patients. Furthermore,

fusions retaining the intact kinase domain were identified in 12 patients (0.11%), including 9

, 1

, 1 novel

, and 1 novel fusion between the

and

5'-untranslated regions, which may have caused

overexpressions. Concomitant

mutations or amplifications were observed in 6 patients, and 4 patients received anti-EGFR inhibitors, in whom

fusions may have mediated resistance to anti-EGFR therapies.

amplification was detected in 24 patients, with the majority being

amplifications. Importantly,

oncogenic mutations, fusions, and gene amplifications were almost always mutually exclusive events.

We report the prevalence of

anomalies in a large NSCLC population, including mutations, gene amplifications, and novel

fusions.

We report the prevalence of FGFR anomalies in a large NSCLC population, including mutations, gene amplifications, and novel FGFR fusions.The epithelial-mesenchymal transition (EMT) is a highly complex phenotypic conversion during embryogenesis, and is important for metastasis, which contributes to tumor deterioration and poor prognoses of cancer patients. Lung carcinoma has a high tendency to develop the EMT. Circular RNAs (circRNAs) are involved in EMT-related cell invasion and metastasis in various types of cancers. Moreover, circRNAs have been found to be a link to EMT-related transcription factors and EMT-associated signaling pathways. This review mainly focuses on the influence of EMT-related circRNAs on lung carcinomas. More specifically, the roles of EMT-inducing and EMT-suppressive circRNAs in lung carcinomas are discussed. With circRNAs potentially becoming promising biomarkers and therapeutic targets for cancer managements, they will hopefully stimulate the interest of medical workers in the early diagnosis, personalized treatment, and positive prognoses in the era of precision oncology.

L1 cell adhesion molecule (L1CAM) exhibits oncogenic activity in tumors. However, the link between L1CAM and the tumor microenvironment remains poorly understood in patients with esophageal squamous cell carcinoma (ESCC). In this study, we investigated how L1CAM expression in ESCC affects the oncogenic characteristics of tumor cells and the tumor microenvironment.

Human ESCC samples were collected, and the mRNA and protein levels of L1CAM were examined by real-time PCR and immunohistochemistry. Overexpression and knockdown gene expression assays were used for mechanistic studies. The cell proliferation and cell cycle were measured with CCK-8 assays and flow cytometry. Cell migration and invasion ability were measured with Transwell assays. Multiplex bead-based assays were performed to identity the factors downstream of L1CAM. Xenograft studies were performed in nude mice to evaluate the effects of L1CAM on tumor growth and regulatory T cell (Treg) recruitment.

L1CAM expression was significantly elevateday offer a unique means to improve treatment of patients with ESCC.

The dysregulation of ribosome biogenesis is associated with the progression of numerous tumors, including hepatocellular carcinoma (HCC). Small nucleolar RNAs (snoRNAs) regulate ribosome biogenesis by guiding the modification of ribosomal RNAs (rRNAs). However, the underlying mechanism of this process in HCC remains elusive.

RNA immunoprecipitation and sequencing were used to analyze RNAs targeted by ribosome proteins. The biological functions of SNORA23 were examined in HCC cells and a xenograft mouse model. To elucidate the underlying mechanisms, the 2'-O-ribose methylation level of rRNAs was evaluated by qPCR, and the key proteins in the PI3K/Akt/mTOR pathway were detected using Western blot.

Twelve snoRNAs were found to co-exist in 4 cancer cell lines using RPS6 pull-down assays. SNORA23 was downregulated in HCC and correlated with the poor prognoses of HCC patients. SNORA23 inhibited the proliferation, migration, and invasion of HCC cells both

and

. We also found that SNORA23 regulated ribosome biogenesis by impairing 2'-O-ribose methylation of cytidine

of 28S rRNA.