10 research outputs found
Surgical resection of multiple liver metastasis of functional malignant pheochromocytoma: A case report and literature review
No full textClinical study on the sensitivity test guided hepato-arterial/portal-vein chemotherapy in patients with unresectable hepatocellar carcinoma
Get PDFPurpose: Approximately 20 % of tumors have the opportunity to be resected in patients with hepatocellar carcinoma (HCC) and their prognoses were acceptable. For the unrespectable HCC, however, the outcomes were rather poor because the specialty of the tumor blood supply and the tumor was insensitive to the chemotherapy drug. The objective of this study was to find sensitive drugs for individual patients and determine the safety and antitumor activity of hepatic intra-arterial and portal vein infusion chemotherapy. Methods: A total of 120 patients with the mean patient age of 56 years and with unresectable HCC were randomly divided into experimental group and control group. The experiment group was infused through an intra-arterial and portal vein catheter 3 different drugs were chosen by the results of drug sensitive test, whereas the control group was treated for TACE. The changes in tumor-size and AFP, two-step operation rate, survival rate, and complications were observed in these patients. Results: The tumor size reduced in 28(47.6 %) cases, stabilized in 14(23.3 %) cases, and progressed in 18(30 %) cases in experimental group as measured by CT or MRI after six chemotherapy cycles, whereas the corresponding data was 17(28.5 %) cases, 7(11.5 %) cases and 36(60 %) cases in the control group (P < 0.05). The AFP was declined in 51 cases in experimental group and in 30 cases in control group (P < 0.05). In the experimental group, the median follow-up time was 21 months; the overall survival rates (OS) of 6 months, 12 months, and 18 months were 86 %, 72 %, and 65 %, respectively. In the control group, the median follow-up time was 16 months; the OS rates of 6 months and 12 months were 58 % and 40 %, respectively. Six patients in the experimental group and 3 patients in the control group had two-step operation. There was no severe incidence of complications in both groups. In the experimental group, 2 (3 %) patients had wound infection, 8 cases had the chemotherapy relative diarrhea, and 18 (30 %) cases had grade Ⅰ or Ⅱ bone marrow suppression. In the control group, the chemotherapy relative diarrhea were 15 (25 %) cases and grade Ⅰ or Ⅱ bone marrow suppression were 33 (55 %) cases. Conclusion: The artery and portal vein pump transfusion chemotherapy guided by drug sensitive test was efficient for HCC treatment. The patients can get longer OS and lower complication incidence.--------------------------------------------------------Cite this article as: Wu D, Wei S, Luo C, Wu X, Feng Y, Zhang F, Nie L, Xia X. Clinical study on the sensitivity test guided hepato-arterial/portal -vein chemotherapy in patients with unresectable hepatocellar carci-noma. Int J Cancer Ther Oncol 2014; 2(2):02029. DOI: 10.14319/ijcto.0202.
ORC6, Negatively Regulated by miR-1-3p, Promotes Proliferation, Migration, and Invasion of Hepatocellular Carcinoma Cells
No full textBackgroundIn recent years, microRNA-1-3p (miR-1-3p) has been linked to the progression of multiple cancers, whereas little is known about its role in hepatocellular carcinoma (HCC). Herein, we investigated the function of miR-1-3p in HCC, and its regulatory function on origin recognition complex subunit 6 (ORC6).MethodsQuantitative real-time polymerase chain reaction (qRT-PCR) was performed for detecting the expression levels of miR-1-3p and ORC6 mRNA in HCC samples and cell lines. ORC6 expression at the protein level was quantified by Western blot. After gain-of-function and loss-of-function models were established, cell counting kit-8 (CCK-8) assays, Transwell assays, flow cytometry, and 5-Ethynyl-2′-deoxyuridine (EdU) assay were performed for examining cell proliferation, migration, invasion, cell cycle, and apoptosis. The targeting relationship between miR-1-3p and ORC6 was confirmed with bioinformatic analysis and dual-luciferase reporter assays.ResultsThe expression of miR-1-3p was reduced in HCC samples and cell lines. Overexpression of miR-1-3p suppressed the proliferation, migration, and invasion, and induced cell-cycle arrest and apoptosis of HCC cells, whereas the opposite effects were induced by miR-1-3p inhibition. ORC6 is identified as a novel target of miR-1-3p, the expression of which is negatively correlated with miR-1-3p expression in HCC tissues. ORC6 overexpression facilitated the proliferation, migration, invasion, and cell cycle progression, and reduced apoptosis of HCC cells, whereas the opposite effects were induced by ORC6 knockdown. What is more, ORC6 overexpression counteracted the biological functions of miR-1-3p in HCC cells.ConclusionMiR-1-3p targets ORC6 to suppress the proliferation, migration, invasion, and cell cycle progression, and promote apoptosis of HCC cells
The spin-dependent electronic transport properties of M(dcdmp) 2 (M = Cu, Au, Co, Ni) molecular devices based on zigzag graphene nanoribbon electrodes
No full textCombined DLL3-targeted bispecific antibody with PD-1 inhibition is efficient to suppress small cell lung cancer growth
No full textBackground Small cell lung cancer (SCLC) accounts for 15% of lung cancers, and the primary treatment of this malignancy is chemotherapy and radiotherapy. Delta-like 3 (DLL3) is an attractive target for SCLC immunotherapy since its expression is highly restricted to SCLC with a neglectable appearance on normal adult tissues. In the current study, we aimed to explore the efficacy of DLL3-targeted SCLC immunotherapy via the engagement of T cell.Methods As a proof of concept, we constructed DLL3-targeted bispecific antibody and chimeric antigen receptor (CAR)-modified T cells. In vitro and in vivo tumor-suppression activity of these treatments alone or in combination with a Program Death-1 (PD-1) inhibitory antibody was evaluated.Results In vitro studies showed that both DLL3 bispecific antibody and CAR-T efficiently killed DLL3-positive cancer cells, including the native SCLC cell lines H446, H196, H82, and the artificial A431 cells that were forcefully overexpressing DLL3. In vivo studies in xenograft mouse models demonstrated that both bispecific antibody and CAR-T suppressed the tumor growth, and combination therapy with PD-1 inhibitory antibody dramatically improved the efficacy of the DLL3 bispecific antibody, but not the CAR-T cells.Conclusions Our results demonstrated that DLL3-targeted bispecific antibody plus PD-1 inhibition was effective in controlling SCLC growth
NNT-AS1 in CAFs-derived exosomes promotes progression and glucose metabolism through miR-889-3p/HIF-1α in pancreatic adenocarcinoma
No full textAbstract It is metabolic and signaling crosstalk between stromal cells and tumors in the tumor microenvironment, which influences several aspects of tumor formation and drug resistance, including metabolic reprogramming. Despite considerable findings linking lncRNAs in HIF-1-related regulatory networks to cancer cell, little emphasis has been given to the role in communication between cancer-associated fibroblasts (CAFs) and tumor cells. Previously, we observed that NNT-AS1 was substantially expressed in CAFs cells and CAFs exosomes, and subsequently investigated the influence of CAFs exosomal NNT-AS1 on glucose metabolism, proliferation, and metastasis of pancreatic ductal adenocarcinoma (PDAC) cells. Transmission electron microscopy was used to examine exosomes secreted by PDAC patient-derived CAFs. qRT-PCR was used to evaluate the expression of NNT-AS1, miR-889-3p, and HIF-1. The role of CAFs-derived exosomal NNT-AS1 in PDAC cell progression and metabolism have been identified. Dual luciferase reporter assays examined the binding between NNT-AS1, miR-889-3p, and HIF-1. After PDAC cells co-culture exosomes secreted by CAFs, we found that they alter glucose metabolism, proliferation, and metastasis. In PDAC cells, CAF-derived exosomal lncRNA NNT-AS1 acted as a molecular sponge for miR-889-3p. Furthermore, HIF-1 could be targeted by miR-889-3p and was controlled by NNT-AS1. This study explores the mechanism by which NNT-AS1 influences the interaction of CAFs on glycolytic remodeling, proliferation, and metastasis of tumor cells through regulating miR-889-3p/HIF-1α, which also helps discover new clinical treatment targets for PDAC
Increased expression of long non-coding RNA CCAT2 predicts poorer prognosis in patients with hepatocellular carcinoma
No full textA novel circ_0099999/miR-330-5p/FSCN1 ceRNA crosstalk in pancreatic cancer
No full textPancreatic cancer is a lethal malignancy in both sexes throughout the world. Circular RNAs (circRNAs) have been implicated in the development of pancreatic cancer by operating as competing endogenous RNAs (ceRNAs). Here, we explored circ_0099999-mediated ceRNA activity in regulating pancreatic tumorigenesis. Ribonuclease R (RNase R) and subcellular localization assays were utilized to characterize circ_0099999. The levels of circ_0099999, microRNA (miR)-330-5p, and fascin actin-bundling protein 1 (FSCN1) were gauged by quantitative real-time PCR (qRT-PCR) and western blot. Cell proliferation, colony formation, apoptosis, migration, and invasion were evaluated by the Cell Counting Kit-8 (CCK-8), colony formation, flow cytometry, and transwell assays, respectively. The levels of glucose consumption and lactate production were determined using the assay kits. A direct relationship between miR-330-5p and circ_0099999 or FSCN1 was validated by dual-luciferase reporter assay. Tumour xenograft assays were used to analyse the role of circ_0099999 in vivo. Circ_0099999 was highly up-regulated in pancreatic cancer tissues and cells. Knockdown of circ_0099999 impeded cell proliferation, migration, invasion, glycolysis, and promoted apoptosis in vitro, as well as diminished tumour growth in vivo. Circ_0099999 targeted miR-330-5p, and miR-330-5p was a downstream mediator of circ_0099999 function. FSCN1 was a direct and functional target of miR-330-5p. Furthermore, circ_0099999 operated as a ceRNA for miR-330-5p to modulate FSCN1 expression. Our findings established a novel causal mechanism, circ_0099999/miR-330-5p/FSCN1 ceRNA crosstalk, in regulating pancreatic carcinogenesis and provided that inhibition of circ_0099999 might have therapeutic benefits in pancreatic cancer.</p
Liver protection of CACA technical guidelines for holistic integrative management of cancer
No full textAbstract Background Antitumor drugs (such as chemotherapy, targeted therapy, immunotherapy, etc.) and local treatments like surgery and radiotherapy are widely used in cancer treatment, but they often carry the risk of liver injury, which seriously affects the prognosis and quality of life of patients. Therefore, liver protection is of crucial importance in cancer treatment. Methods Relevant experts organized by the Oncology Hepatology Committee of China Anti-Cancer Association Association formulated this guideline based on the latest research achievements and clinical practice experience at home and abroad, aiming to provide comprehensive and systematic guidance for clinicians on liver protection. Results This guideline elaborates on the importance of liver protection during cancer treatment, comprehensively introduces the pathophysiological mechanisms, diagnosis, treatment, and preventive measures of antitumor treatment-related liver injury. Conclusion This guideline is helpful for clinicians to formulate individualized treatment plans, improve the treatment outcome and quality of life of cancer patients, and provides an important reference for the clinical practice of liver protection in cancer treatment
