primary liver tumor
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Chemotherapy ◽  
2022 ◽  
Author(s):  
Claudia Angela Maria Fulgenzi ◽  
Antonio D'Alessio ◽  
Thomas Talbot ◽  
Alessandra Gennari ◽  
Mark R. Openshaw ◽  
...  

Background: Hepatocellular carcinoma (HCC) is the most common primary liver tumor, and it rates fourth as a cause of cancer-related death. The presence of underlying liver disease and poor chemosensitivity pose major treatment challenges in the management of HCC. However, in the last few years the therapeutic scenario has substantially changed, and immunotherapy in the form of immune checkpoint inhibitors (ICPIs) has become an essential therapeutic strategy in this field. Summary: After controversial results of monotherapy, ICPIs have been mainly investigated in association with anti-angiogenic agents or as dual checkpoint inhibition. The combination of atezolizumab plus bevacizumab has become the new therapeutic standard for unresectable HCC. Currently, a number of ICPIs-based combinations are being studied in phase III clinical trials as front-line therapy for advanced HCC, with growing interest in integration of early-stage disease management in the form of adjuvant or neoadjuvant therapies. With most of the trials investigating ICPIs as first line treatment, the second line scenario relies mainly on tyrosine kinase inhibitors, which however, have not been formally trialed after ICPIs. Key messages: In this review we summarize the main therapeutic advances in the systemic management of HCC focusing on the most relevant ongoing trials. We also discuss the main issues arising from a such rapidly evolving field including therapeutic sequencing and patient stratification.


2021 ◽  
Vol 11 ◽  
Author(s):  
Zhe Fan ◽  
Chengjun Zhuang ◽  
Shuang Wang ◽  
Yewei Zhang

Hepatocellular carcinoma (HCC) is the most common primary liver tumor. It is ranked the sixth most common neoplasm and the third most common cause of cancer mortality. At present, the most common treatment for HCC is surgery, but the 5-year recurrence rates are still high. Patients with early stage HCC with few nodules can be treated with resection or radiofrequency ablation (RFA); while for multinodular HCC, transarterial chemoembolization (TACE) has been the first-line treatment. In recent years, based on medical engineering cooperation, nanotechnology has been increasingly applied to the treatment of cancer. Photodynamic therapy and photothermal therapy are effective for cancer. This paper summarizes the latest progress of photodynamic therapy and photothermal therapy for HCC, with the aim of providing new ideas for the treatment of HCC.


2021 ◽  
Vol 11 ◽  
Author(s):  
Meng Gao ◽  
Chengjie Mei ◽  
Yonghua Guo ◽  
Peng Xia ◽  
Hao Zhang ◽  
...  

Intrahepatic cholangiocarcinoma (ICC) is one of the most commonly diagnosed malignancies worldwide, and the second most common primary liver tumor. The lack of effective diagnostic and treatment methods results in poor patient prognosis and high mortality rate. Atypical protein kinase C-ι (aPKC-ι) is highly expressed in primary and metastatic ICC tissues, and regulates epithelial mesenchymal transition (EMT) through the aPKC-ι/P-Sp1/Snail signaling pathway. Recent studies have correlated aberrant glucose metabolism with EMT. Given the vital role of FBP1 in regulating glucose metabolism in cancer cells, we hypothesized that aPKC-ι downregulates FBP1 in ICC cells through the Snai1 pathway, and enhances glycolysis and metastasis. We confirmed the ability of aPKC-ι promotes glycolysis, invasion and metastasis of cancer cells, and further demonstrated that FBP1 inhibits the malignant properties of ICC cells by antagonizing aPKC-ι. Our findings provide novel insights into the molecular mechanisms of ICC progression and metastasis, as well as a theoretical basis for exploring new treatment strategies.


Cancers ◽  
2021 ◽  
Vol 13 (23) ◽  
pp. 6049
Author(s):  
Salvatore Gruttadauria ◽  
Floriana Barbera ◽  
Duilio Pagano ◽  
Rosa Liotta ◽  
Roberto Miraglia ◽  
...  

Intrahepatic cholangiocarcinoma (iCCA) is a rare and aggressive primary liver tumor, characterized by a range of different clinical manifestations and by increasing incidence and mortality rates even after curative treatment with radical resection. In recent years, growing attention has been devoted to this disease and some evidence supports liver transplantation (LT) as an appropriate treatment for intrahepatic cholangiocarcinoma; evolving work has also provided a framework for better understanding the genetic basis of this cancer. The aim of this study was to provide a clinical description of our series of patients complemented with Next-Generation Sequencing genomic profiling. From 1999 to 2021, 12 patients who underwent LT with either iCCA or a combined hepatocellular and cholangiocellular carcinoma (HCC-iCCA) were included in this study. Mutations were observed in gene activating signaling pathways known to be involved with iCCA tumorigenesis (KRAS/MAPK, P53, PI3K-Akt/mTOR, cAMP, WNT, epigenetic regulation and chromatin remodeling). Among several others, a strong association was observed between the Notch pathway and tumor size (point-biserial rhopb = 0.93). Our results are suggestive of the benefit potentially derived from molecular analysis to improve our diagnostic capabilities and to devise new treatment protocols, and eventually ameliorate long-term survival of patients affected by iCCA or HCC-iCCA.


2021 ◽  
Vol 11 ◽  
Author(s):  
Qifeng Wang ◽  
Fen Li ◽  
Qingming Jiang ◽  
Yifeng Sun ◽  
Qiong Liao ◽  
...  

BackgroundLiver metastases (LM) are the most common tumors encountered in the liver and continue to be a significant cause of morbidity and mortality. Identification of the primary tumor of any LM is crucial for the implementation of effective and tailored treatment approaches, which still represents a difficult problem in clinical practice.MethodsThe resection or biopsy specimens and associated clinicopathologic data were archived from seven independent centers between January 2017 and December 2020. The primary tumor sites of liver tumors were verified through evaluation of available medical records, pathological and imaging information. The performance of a 90-gene expression assay for the determination of the site of tumor origin was assessed.ResultA total of 130 LM covering 15 tumor types and 16 primary liver tumor specimens that met all quality control criteria were analyzed by the 90-gene expression assay. Among 130 LM cases, tumors were most frequently located in the colorectum, ovary and breast. Overall, the analysis of the 90-gene signature showed 93.1% and 100% agreement rates with the reference diagnosis in LM and primary liver tumor, respectively. For the common primary tumor types, the concordance rate was 100%, 95.7%, 100%, 93.8%, 87.5% for classifying the LM from the ovary, colorectum, breast, neuroendocrine, and pancreas, respectively.ConclusionThe overall accuracy of 93.8% demonstrates encouraging performance of the 90-gene expression assay in identifying the primary sites of liver tumors. Future incorporation of the 90-gene expression assay in clinical diagnosis will aid oncologists in applying precise treatments, leading to improved care and outcomes for LM patients.


2021 ◽  
Vol 16 (9) ◽  
pp. 2337-2342
Author(s):  
Charles Runyan ◽  
Mittun Patel ◽  
Mostafa Youssfi ◽  
Steve Taylor ◽  
Deepa Biyyam

2021 ◽  
Vol 28 (2) ◽  
pp. 1
Author(s):  
Sandra Strainienė ◽  
Kipras Jauniškis ◽  
Ilona Savlan ◽  
Justinas Pamedys ◽  
Ieva Stundienė ◽  
...  

Background. Hepatic angiosarcoma is an uncommon, malignant, primary liver tumor, comprising 2% of liver cancers and accounting for < 1% of all sarcomas. Patients usually present with nonspecific symptoms, such as fatigue, weight loss, right upper quadrant pain, anemia, which leads to late diagnosis of an advanced stage tumor. The median life expectancy after the diagnosis of hepatic angiosarcoma is about 6 months, with only 3% of patients surviving more than 2 years. Liver failure and hemoperitoneum are the leading causes of death in patients with liver angiosarcoma. In rarer cases, it might cause paraneoplastic syndromes such as disseminated intravascular coagulopathy. The treatment of angiosarcomas is complicated as there are no established and effective treatment guidelines due to the tumor’s low frequency and aggressive nature.Case summary. We present the case of a 68-year old woman who was admitted to the hospital due to fatigueand severe anemia (hemoglobin 65 g/l). Laboratory results also revealed high-grade thrombocytopenia(8 × 109/l). The abdominal ultrasound and computed tomography scan showed multiple lesions throughout with hepatic angiosarcoma. The treatment with first-line chemotherapy (doxorubicin) was initiated despiteongoing paraneoplastic syndrome – disseminative intravascular coagulopathy. However, the disease was terminal, and the patient died 2 months since diagnosed.Conclusions. Hepatic angiosarcoma is a rare and terminal tumor. Therefore, knowledge about its manifestations and effective treatment methods is lacking. Disseminative intravascular coagulopathy is a unique clinical characteristic of angiosarcoma seen in a subset of patients.


Cancers ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 1830
Author(s):  
Yekaterina Krutsenko ◽  
Aatur D. Singhi ◽  
Satdarshan P. Monga

Hepatocellular cancer (HCC), the most common primary liver tumor, has been gradually growing in incidence globally. The whole-genome and whole-exome sequencing of HCC has led to an improved understanding of the molecular drivers of this tumor type. Activation of the Wnt signaling pathway, mostly due to stabilizing missense mutations in its downstream effector β-catenin (encoded by CTNNB1) or loss-of-function mutations in AXIN1 (the gene which encodes for Axin-1, an essential protein for β-catenin degradation), are seen in a major subset of HCC. Because of the important role of β-catenin in liver pathobiology, its role in HCC has been extensively investigated. In fact, CTNNB1 mutations have been shown to have a trunk role. β-Catenin has been shown to play an important role in regulating tumor cell proliferation and survival and in tumor angiogenesis, due to a host of target genes regulated by the β-catenin transactivation of its transcriptional factor TCF. Proof-of-concept preclinical studies have shown β-catenin to be a highly relevant therapeutic target in CTNNB1-mutated HCCs. More recently, studies have revealed a unique role of β-catenin activation in regulating both tumor metabolism as well as the tumor immune microenvironment. Both these roles have notable implications for the development of novel therapies for HCC. Thus, β-catenin has a pertinent role in driving HCC development and maintenance of this tumor-type, and could be a highly relevant therapeutic target in a subset of HCC cases.


2021 ◽  
Vol 11 ◽  
Author(s):  
Hong-Yu Zhang ◽  
Hong-Xia Liang ◽  
Shu-Huan Wu ◽  
He-Qing Jiang ◽  
Qin Wang ◽  
...  

BackgroundHepatocellular carcinoma (HCC) is the most common primary liver tumor, and the main reason is the unclear pathogenesis of HCC, which leads to a high fatality rate of HCC. Therefore, it is of great clinical significance to explore the molecular mechanism of HCC and find a targeted therapeutic approach from the molecular level.Materials and MethodsMicroRNA-15a-5p (miR-15a-5p) expression level was measured by bioinformatics and qRT-PCR. Luciferase assay and RIP assays were used to verify the relationship between programmed cell death protein 1 (PD1) PD 1 with miR-15a-5p. Exosomes were identified using TEM, Zetasizer Nano ZS, and western blot. Edu, Transwell, and scratch assay were performed to explore the role of miR-15a-5p or exo-miR-15a-5p on HepG2 cells progression.ResultsMicroRNA-15a-5p (miR-15a-5p) was decreased in HCC tissues and cell lines, which indicated a poor prognosis. Overexpression of miR-15a-5p inhibited viability, proliferation, migration and invasion of HepG2 cells. Then, we isolated exosomes from cancer cells, and found that miR-15a-5p was packaged into exosomes from cancer cells. Furthermore, exo-miR-15a-5p was secreted into CD8+ T cells, then directly inhibited PD1 expression via targeted binding. Then, we co-cultured CD8+ T cells transfected with PD1 with HepG2 transfected with miR-15a-5p, PD1 remitted the inhibitory role of miR-15a-5p on HCC progression.ConclusionTogether, present study revealed exo-miR-15a-5p from cancer cells inhibited PD1 expression in CD8+ T cells, which suppressed the development of HCC.


2021 ◽  
Vol 12 ◽  
Author(s):  
Zhuolin Li ◽  
Yao Lin ◽  
Bizhen Cheng ◽  
Qiaoxin Zhang ◽  
Yingmu Cai

BackgroundHepatocellular carcinoma (HCC) is a type of primary liver tumor with poor prognosis and high mortality, and its molecular mechanism remains incompletely understood. This study aimed to use bioinformatics technology to identify differentially expressed genes (DEGs) in HCC pathogenesis, hoping to identify novel biomarkers or potential therapeutic targets for HCC research.MethodsThe bioinformatics analysis of our research mostly involved the following two datasets: Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA). First, we screened DEGs based on the R packages (limma and edgeR). Using the DAVID database, the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses of DEGs were carried out. Next, the protein-protein interaction (PPI) network of the DEGs was built in the STRING database. Then, hub genes were screened through the cytoHubba plug-in, followed by verification using the GEPIA and Oncomine databases. We demonstrated differences in levels of the protein in hub genes using the Human Protein Atlas (HPA) database. Finally, the hub genes prognostic values were analyzed by the GEPIA database. Additionally, using the Comparative Toxicogenomics Database (CTD), we constructed the drug-gene interaction network.ResultsWe ended up with 763 DEGs, including 247 upregulated and 516 downregulated DEGs, that were mainly enriched in the epoxygenase P450 pathway, oxidation-reduction process, and metabolism-related pathways. Through the constructed PPI network, it can be concluded that the P53 signaling pathway and the cell cycle are the most obvious in module analysis. From the PPI, we filtered out eight hub genes, and these genes were significantly upregulated in HCC samples, findings consistent with the expression validation results. Additionally, survival analysis showed that high level gene expression of CDC20, CDK1, MAD2L1, BUB1, BUB1B, CCNB1, and CCNA2 were connected with the poor overall survival of HCC patients. Toxicogenomics analysis showed that only topotecan, oxaliplatin, and azathioprine could reduce the gene expression levels of all seven hub genes.ConclusionThe present study screened out the key genes and pathways that were related to HCC pathogenesis, which could provide new insight for the future molecularly targeted therapy and prognosis evaluation of HCC.


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