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1 se consequences (development of cirrhosis or liver cancer).
2 rug administration in a preclinical model of liver cancer.
3 ironmental factors, such as aflatoxin, cause liver cancer.
4 on, triglyceride accumulation, fibrosis, and liver cancer.
5 d discuss the future of these strategies for liver cancer.
6 fected persons to cirrhosis of the liver and liver cancer.
7 and a diminished chemotherapeutic effect on liver cancer.
8 ability, manifesting as premature ageing and liver cancer.
9 atitis (NASH) and lead to liver cirrhosis or liver cancer.
10 managing and/or preventing this challenging liver cancer.
11 antibody-drug conjugates (ADCs) for treating liver cancer.
12 rowth in human and mouse models of colon and liver cancer.
13 oma (iCCA) is the second most common primary liver cancer.
14 gene is dysregulated in approximately 30% of liver cancer.
15 the development of a NASH-like phenotype and liver cancer.
16 ibution of IR to the mutational landscape of liver cancer.
17 deaths (620 000-670 000) from cirrhosis and liver cancer.
18 and lead to new treatments for patients with liver cancer.
19 , one of the leading causes of cirrhosis and liver cancer.
20 B virus (HBV) infection, a leading causes of liver cancer.
21 as a potential therapeutic agent for primary liver cancer.
22 linical murine model of steatosis-associated liver cancer.
23 t of NKG2D in a model of inflammation-driven liver cancer.
24 has been associated with the development of liver cancer.
25 the ER-resident calnexin (Cnx) in breast and liver cancer.
26 tly biological modules, which related to the liver cancer.
27 with non-Hodgkin lymphoma, lung cancer, and liver cancer.
28 insights for immunotherapeutic strategies in liver cancer.
29 flammation and impair immune surveillance in liver cancer.
30 h pancreatic adenocarcinoma and another with liver cancer.
31 P4) augmented Y5R activation and function in liver cancer.
32 million people who are at risk of developing liver cancer.
33 ent in human malignancies, including primary liver cancer.
34 might be developed for treatment of primary liver cancer.
35 0.82% with liver disease, including primary liver cancer.
36 ammation and metabolic pathways important in liver cancer.
37 on) and cause hepatitis, liver cirrhosis and liver cancer.
38 e developed as therapeutics for this form of liver cancer.
39 CUGBP1 is a key event in the development of liver cancer.
40 ay, were found to be tightly associated with liver cancer.
41 g technology to deliver therapeutic genes to liver cancer.
42 can result in progressive liver disease and liver cancer.
43 a common risk factor for the development of liver cancer.
44 ts millions worldwide, causing cirrhosis and liver cancer.
45 of patients with liver metastases or primary liver cancer.
46 CUGBP1 is reduced in patients with pediatric liver cancer.
47 he steatosis had a potential to develop into liver cancer.
48 pathway might be developed as treatments for liver cancer.
49 the converged pathways in NMJ formation and liver cancer.
50 ly associated with good clinical outcomes in liver cancer.
51 has been shown to accelerate progression of liver cancer.
52 surgery, still the main curative option for liver cancer.
53 n treating advanced renal-cell carcinoma and liver cancer.
54 mber of patients with primary and metastatic liver cancer.
55 d 1.1% with liver disease, including primary liver cancer.
56 y, is associated with increased incidence of liver cancer.
57 holic steatohepatitis (NASH), cirrhosis, and liver cancer.
58 hepatocytes might be effective in preventing liver cancer.
59 pathologic conditions such as cirrhosis and liver cancer.
60 strategy to restore immune permissiveness in liver cancer.
61 ty to induce liver necrosis and, eventually, liver cancer.
62 ated in clinical trials for the treatment of liver cancer.
63 ed drug only being locally-used for treating liver cancer.
64 1.05-1.12), and reduced risks of ovarian and liver cancer.
65 tine patient evaluation and surveillance for liver cancer.
66 2 patients further reveals heterogeneity in liver cancer.
67 lishing this kinase as a tumor suppressor in liver cancer.
68 r while they were beta-catenin and CTNNB1 in liver cancer.
69 Fibrolamellar carcinoma (FLC) is a rare liver cancer.
70 ses would facilitate precision treatment for liver cancers.
71 rich resource facilitating drug discovery in liver cancers.
72 etic lethalities to prevalent alterations in liver cancers.
73 er time and constituted <10% of all reported liver cancers.
74 erapy with respect to metastatic and primary liver cancers.
75 angiocarcinoma (n = 36), the two most common liver cancers.
76 atabase (HMDD) and are related to breast and liver cancers.
78 ; 421628 due to kidney cancer; 487518 due to liver cancer; 13927 due to testicular cancer; and 829396
82 kinase substrate, were further confirmed in liver cancer and adjacent normal tissue collected from i
83 ctions of diethylnitrosamine (DEN) to induce liver cancer and alpha-galactosylceramide to activate na
85 ociated with an increased risk of developing liver cancer and cirrhosis in chronic hepatitis B (CHB)
86 rtance of PROM1(+) cells in the evolution of liver cancer and DDR1 as a potential driver of this proc
87 One patient discontinued treatment due to liver cancer and died 22 days after treatment discontinu
88 for FBP1 as a metabolic tumour suppressor in liver cancer and establish a critical crosstalk between
89 we have combined preclinical mouse models of liver cancer and genetic studies of a human liver biopsy
91 deacetylase 4 (HDAC4) is highly expressed in liver cancer and known to regulate oncogenesis through c
92 g high potency to reverse gene expression in liver cancer and validate that all four compounds are ef
94 roach to examine the personalized biology of liver cancers and the influence of host tissues is with
95 ce of druggable mutations in the majority of liver cancers and the significant heterogeneity of the d
96 the global incidence and mortality rates of liver cancer, and evaluated the association between inci
97 inogenesis in malignancies such as colon and liver cancer, and has recently been implicated in the pa
99 In almost all countries, incidence rates of liver cancer are 100-200% higher in males than in female
103 ver tumorigenesis and clarify the classes of liver cancer based on molecular features and how they af
104 rogeneity and corresponding tumor biology of liver cancer based only on bulk genomic and transcriptom
105 gression and maintenance in a mouse model of liver cancer, based on oncogenic transformation and adop
106 HCC and 156 whole exome of Barcelona Clinic Liver Cancer (BCLC) 0/A were analyzed by whole-exome seq
107 f hepatitis B, the stage of Barcelona Clinic Liver Cancer (BCLC) B and C, and the presence of cirrhos
108 t patients clustered within Barcelona Clinic Liver Cancer (BCLC) C or D criteria (n = 1,168 [74%]) an
110 FP) level (>100 ng/mL), and Barcelona Clinic Liver Cancer (BCLC) stage B or C as independent features
112 id models in furthering the understanding of liver cancer biology and in developing personalized-medi
114 d oxidative stress are major determinants of liver cancer but in a complex, context-dependent manner.
115 NNB1, encoding beta-catenin) can co-occur in liver cancer, but how these oncogenes cooperate in tumor
116 may make a major contribution to HCV-induced liver cancer by shifting Ras signaling away from prosene
117 understanding of the cell types originating liver cancer can aid in exploring molecular mechanisms o
118 were early-stage tumors by Barcelona Clinic Liver Cancer, Cancer of the Liver Italian Program, and t
119 plasma samples of 191 post-menopausal female liver cancer cases (HCC n=83, ICC n=56) and 426 controls
121 nsports citrate across cell membranes, halts liver cancer cell growth by altering both energy product
122 profile the uptake and excretion fluxes of a liver cancer cell line (HepG2) and use genome-scale meta
124 plied this new approach in hematological and liver cancer cell lines and confirm the feasibility of t
125 alian target of rapamycin signaling in human liver cancer cell lines and in both an in vitro and in v
129 , we developed a protocol to establish human liver cancer cell models at a success rate of around 50%
130 n blocked metabolic adaptation and inhibited liver cancer cell proliferation and HCC growth in mice.
132 nhibition of adiponectin secretion increases liver cancer cell proliferation, since adiponectin prote
133 ion in AATD liver-impacting genes related to liver cancer, cell cycle, and fibrosis, as well as key r
135 e, CRISPR-mediated knockout of FN3K in human liver cancer cells altered the abundance of redox metabo
136 ingly, CCDC3, as a secreted protein, targets liver cancer cells and increases long chain polyunsatura
137 our growth and lung metastasis of breast and liver cancer cells are inhibited by anti-Cnx antibodies.
139 arrying miR122 and PTX were delivered to the liver cancer cells efficiently due to their rubber-like
140 charged with doxorubicin, selectively kills liver cancer cells in culture, as the selectivity of the
145 quired in human hepatoma cell line 7 (Huh-7) liver cancer cells to maintain BOK at low levels, and BO
146 f both the PI3K/Akt and MAPK/ERK pathways in liver cancer cells, and Nqo1 ablation blocked metabolic
147 The expression of FAM83H is elevated in liver cancer cells, and nuclear expression of FAM83H pre
148 porters which cause high drug effluxion from liver cancer cells, leading to chemoresistance and a dim
149 critical determinants of the growth of human liver cancer cells, providing a strong rationale to eluc
159 a six-letter DNA library to selectively bind liver cancer cells; and 2) in a six-letter self-assembli
161 gged form of MAN2A1-FER in NIH3T3 and HEP3B (liver cancer) cells; Golgi were isolated for analysis.
163 o case studies that use data from breast and liver cancer cohorts and features uni- and multivariate
164 duction pathway mutations in gastric cancer, liver cancer, colorectal cancer, and pancreatic cancer w
166 colorectal, pancreatic, uterine corpus, and liver cancers constituted considerable proportions of th
167 Downregulation of AMOTL2 is found in human liver cancers, correlating with the concomitant activati
171 ions and 1.5 million (1.4-1.6) cirrhosis and liver cancer deaths, corresponding to an 81% (78-82) red
175 feration, since adiponectin protects against liver cancer development through the activation of AMP-a
183 e asymmetrically localized RhoGAP Deleted in liver cancer (DLC1) in the cytoplasm at the cell front.
184 llion) and hepatitis C virus (10.4 million), liver cancer due to hepatitis B virus (9.4 million), rhe
186 lar carcinoma (HCC), the most common form of liver cancer, for which there is no effective treatment.
187 s correlate with tandem duplications, and-in liver cancer-frequently activate the telomerase gene TER
195 and KMT2B (also known as MLL4) gene loci in liver cancer, HPV and BKV in bladder cancer, and EBV in
196 understanding of the detailed mechanisms of liver cancer immunogenicity and the specific role of TGF
200 aminating corn and other commodities, causes liver cancer in humans and can pose severe economic loss
201 accurate DNA replication and suppression of liver cancer in mice and humans and provides a clinicall
202 MAN2A1-FER resulted in rapid development of liver cancer in mice with hepatic disruption of Pten.
203 estigated beta-defensin family expression in liver cancer in publicly available datasets and found th
208 ptible to N-diethylnitrosamine (DEN)-induced liver cancer, indicating that loss of these antioxidant
214 lar carcinoma (HCC), the most common type of liver cancer, is one of the leading causes of cancer-rel
215 enomic signature profile, based on Top1mt-KO liver cancers, is correlated with enhanced survival of h
216 In almost all countries, incidence rates of liver cancer (LC) are 100%-200% higher in males than in
218 SAA enzymes in HNF4alpha-positive epithelial liver cancer lines impairs SAA metabolism, increases res
220 al sensing were demonstrated by tests with a liver cancer mimicking hydrogel phantom, a solution samp
221 success rate of around 50% and generated the Liver Cancer Model Repository (LIMORE) with 81 cell mode
223 complete tumor suppression in an orthotopic liver cancer mouse model and ~1 month diabetes correctio
224 (n = 2,082) and an inverse association with liver cancer (n = 2,568), which disappeared after exclud
227 d into those proximal to genes implicated in liver cancer or to genes involved in stem cell developme
229 metastasis by orthotopic transplantation of liver cancer organoids propagated from primary tumors in
231 stablishes a quantitative tool for triage of liver cancer patients and also for cancer risk assessmen
235 n has reported that the incidence of primary liver cancer (PLC) has slowly declined over the last dec
237 culture system to the propagation of primary liver cancer (PLC) organoids from three of the most comm
238 osome aneuploidy are major traits of primary liver cancer (PLC), which represent the second most comm
239 sion oncoprotein associated with an atypical liver cancer potently blocks RIalpha LLPS and induces ab
241 Fibrolamellar carcinoma (FLC) is a unique liver cancer primarily affecting young adults and charac
253 enedione was associated with a 50% decreased liver cancer risk (OR=0.50,95%CI=0.30-0.82), while SHBG
256 globulin (SHBG) levels were associated with liver cancer risk, overall and by histology, by leveragi
258 occurrence of c-MET-expressing CECs in human liver cancer samples was confirmed at the single-cell le
259 tial use of these two orthogonal markers for liver cancer screening in patients with high-risk cirrho
261 lin D1 dependency positively correlated with liver cancer sensitivity to palbociclib, an FDA-approved
262 nd SNP array data across multiple regions of liver cancer specimens to map spatio-temporal interactio
263 d hepatocellular carcinoma, Barcelona Clinic Liver Cancer stage B or C disease, Child-Pugh class A li
264 sorafenib patients had more Barcelona Clinic Liver Cancer stage D ( P < .001), higher Model for End-S
266 /5 might be a good candidate for therapy for liver cancer stem cells together with liver cirrhosis.
270 response in the hepatitis B virally infected liver cancer TCGA cohort, and uncovered suggestive evide
271 with RAS(G12V) to promote the development of liver cancer that closely resembles human steatohepatiti
272 y baseline imaging features in patients with liver cancer that correlate with (90)Y distribution on p
273 e showed these mice develop much more severe liver cancer that is associated with elimination of the
274 patocellular carcinoma (FL-HCC) is a primary liver cancer that predominantly affects children and you
275 llular carcinoma (FL-HCC), a rare but lethal liver cancer that primarily affects adolescents and youn
276 coding beta-catenin, are common in colon and liver cancers, the most frequent mutation affecting Ser-
278 hat MDSCs are increased in non-CCA malignant liver cancers, these cells may represent suitable target
281 Here, we develop an in vivo mouse model of liver cancer to study oncogene cooperation in immunosurv
282 ned release of chemotherapeutic nanodrug for liver cancer treatment, or anchored delivery of pancreat
284 ine-approved image-guided therapy option for liver cancer using the radiopaque drug-carrier and micro
285 reveal a novel link between NR2E3, AHR, and liver cancer via LSD1-mediated H3K4me2 histone modificat
286 belt and along the Mississippi River, while liver cancer was high along the Texas-Mexico border, and
287 To determine the payload for ADCs against liver cancer, we screened three large drug libraries (>
288 landscape of pharmacogenomic interactions in liver cancers, we developed a protocol to establish huma
289 e doubling of circulating concentration) and liver cancer were calculated using multivariable-adjuste
290 ance of hospital death; people who died from liver cancer were less likely to die in hospital than pe
291 , chronic obstructive pulmonary disease, and liver cancer were the five leading causes of YLLs in 201
293 n, we present an oncogenic role of FAM83H in liver cancer, which is closely associated with the oncog
295 inoma (HCC) are clinically disparate primary liver cancers with etiological and biological heterogene
296 irus is a leading cause of liver disease and liver cancer, with approximately 3% of the world's popul
297 glioblastoma multiforme, ovarian cancer and liver cancer, with frequencies ranging from 12.9% to 85%
298 an expected DALYs per 100 000 population for liver cancer, with the observed to expected ratio rangin
299 rikingly better outcomes compared to typical liver cancers, with 5-year survival rates of 57% to 100%