Kyedhill4590

Hepatocellular carcinoma (HCC) is often diagnosed at an advanced stage where only systemic treatment can be offered. The emergence of immune checkpoint inhibitors (ICIs) provides hope for the treatment of HCC. In this study, we performed a meta-analysis to provide evidence for the efficacy and safety of ICIs in the treatment of HCC.

The following databases and websites were searched Embase, PubMed, Cochrane Library and ClinicalTrials.gov. The primary endpoints were response rate (RR), disease control rate (DCR), progression-free survival (PFS) and overall survival (OS).

Finally, twelve studies were included in this meta-analysis. When the corresponding outcome indicators and their 95% confidence intervals (CIs) were pooled directly, the overall RR, DCR, PFS and OS were 0.17 (0.15-0.19, I

= 56.2%, P=0.009), 0.58 (0.55-0.61, I

= 75.9%, P<0.001), 3.27 months (2.99-3.55, I

= 73.0%, P=0.001), 11.73 months (10.79-12.67, I

= 90.3%, P<0.001). Compared to the control group, treatment with ICIs significantly improved RR, PFS and OS, the OR and HRs were 3.11 (2.17-4.44, P<0.001), 0.852 (0.745-0.974, P=0.019) and 0.790 (0.685-0.911, P=0.001), respectively. However, no significant improvement in DCR was found in ICIs treatment in this meta-analysis.

HCC patients would benefit from ICIs treatment, however, more studies are needed in the future to provide more useful evidence for the treatment of HCC by programmed death-1 (PD-1) or programmed death ligand 1 (PD-L1) inhibitors.

HCC patients would benefit from ICIs treatment, however, more studies are needed in the future to provide more useful evidence for the treatment of HCC by programmed death-1 (PD-1) or programmed death ligand 1 (PD-L1) inhibitors.Background Colorectal cancer, the fourth leading cause of cancer mortality, is prone to metastasis, especially to the liver. AZD1390 ATR inhibitor The pre-metastatic microenvironment comprising various resident stromal cells and immune cells is essential for metastasis. However, how the dynamic evolution of immune components facilitates pre-metastatic niche formation remains unclear. Methods Utilizing RNA-seq data from our orthotopic colorectal cancer mouse model, we applied single sample gene set enrichment analysis and Cell type Identification By Estimating Relative Subsets Of RNA Transcripts to investigate the tumor microenvironment landscape of pre-metastatic liver, and define the exact role of myeloid-derived suppressor cells (MDSCs) acting in the regulation of infiltrating immune cells and gene pathways activation. Flow cytometry analysis was conducted to quantify the MDSCs levels in human and mice samples. Results In the current work, based on the high-throughput transcriptome data, we depicted the immune cell infiltration on in the targeted liver.

This study aims to retrospectively evaluate and compare the clinical efficacy in patients with stage IB2 and IIA cervical cancer, who treated with neoadjuvant chemotherapy combined with brachytherapy or not before radical hysterectomy.

The data of patients who have diagnosed with stage IB2 and IIA cervical cancer between January 2010 and December 2013 were retrieved through the Hospital Information System (HIS) of Gansu Provincial Maternal and Child Health Hospital. Patients were divided into two groups neoadjuvant chemotherapy combined with brachytherapy followed by radical hysterectomy group (NACT+BT Group) and direct radical hysterectomy group (RH Group). The rate of adjuvant radiotherapy, progression-free survival (PFS), and overall survival (OS) were compared between the two groups.

A total of 183 patients were included in this study with 82 in the NACT+BT group and 101 in the RH group. The median follow up duration was 44.9 months for the NACT+BT group and 38.1 months for the RH group. The 5-year PFS for NACT+BT Group was 93.8%, which was significantly higher compared to the RH group (77.2%,

= 0.0202). The rate of postoperative adjuvant pelvic radiotherapy was significantly lower in the NACT+BT group compared to the RH group (30.49% vs 79.21%;

0.05). COX multivariate analysis showed that NACT+BT increased PFS by 29% compared with RH treatment, and Positive margin decreased PFS and OS by by 4.7 and 6.87 times, respectively.

Neoadjuvant chemotherapy combined with brachytherapy followed by radical hysterectomy (NACT+BT) can extend PFS, reduce postoperative pathological risk, and postoperative adjuvant pelvic radiotherapy compared to the direct radical hysterectomy (RH).

Neoadjuvant chemotherapy combined with brachytherapy followed by radical hysterectomy (NACT+BT) can extend PFS, reduce postoperative pathological risk, and postoperative adjuvant pelvic radiotherapy compared to the direct radical hysterectomy (RH).The expression of Centromere Protein U (CENP-U) is closely related to tumor malignancy. Till now, the role of CENP-U in the malignant progression of breast cancer remains unclear. In this study, we found that CENP-U protein was highly expressed in the primary invasive breast cancer tissues compared to the paired adjacent histologically normal tissues and ductal carcinoma in situ (DCIS) tissues. After CENP-U was knocked down, the proliferation and colony-forming abilities of breast cancer cells were significantly suppressed, whereas the portion of apoptotic cells was increased. Meanwhile, the PI3K/AKT/NF-κB pathway was significantly inhibited. In vivo studies showed that, the inhibition of CENP-U repressed the tumor growth in orthotopic breast cancer models. Therefore, our study demonstrated that the CENP-U might act as an oncogene and promote breast cancer progression via activation of the PI3K/AKT/NF-κB pathway, which suggests a promising direction for targeting therapy in breast cancer.Cancer is one of the leading causes of mortality worldwide. PPAR modulators may hold great potential for the management of cancer patients. Indeed, PPARs are critical sensors and regulators of lipid, and they are able to promote eNOS activation, regulate immunity and inflammation response, and affect proliferation and differentiation of cancer cells. Cancer, a name given to a group of diseases, is characterized by multiple distinctive biological behaviors, including angiogenesis, abnormal cell proliferation, aerobic glycolysis, inflammation, etc. In the last decade, emerging evidence has shown that PPAR-α, a nuclear hormone receptor, can modulate carcinogenesis via exerting effects on one or several characteristic pathological behaviors of cancer. Therefore, the multi-functional PPAR modulators have substantial promise in various types of cancer therapies. This review aims to consolidate the functions of PPAR-α, as well as discuss the current and potential applications of PPAR-α agonists and antagonists in tackling cancer.