liver neoplasms/phosphatase

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Expansion of CD133-expressing liver cancer stem cells in liver-specific phosphatase and tensin homolog deleted on chromosome 10-deleted mice.

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PTEN (phosphatase and tensin homolog deleted on chromosome 10) is a lipid phosphatase that regulates mitogenic signaling pathways, and deficiency of PTEN results in cell proliferation, survival, and malignancy. Murine liver-specific Pten deletion models develop liver malignancy by 12 months of age.

Diagnosis of primary liver cancer using lectin affinity chromatography of serum alkaline phosphatase.

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Serum alkaline phosphatase (sALP) can be separated into unbound liver type (L-ALP) and bound bone type (B-ALP) by means of WGA affinity chromatography. The L-ALP from the sera of normal adults and various liver diseases was found to show different chromatographic behaviours on DSA affinity column

Molecular cloning of rat phosphoprotein phosphatase 2A beta cDNA and increased expressions of phosphatase 2A alpha and 2A beta in rat liver tumors.

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A cDNA clone coding for an isotype of the catalytic subunit of rat phosphoprotein phosphatase 2A was isolated. The deduced amino acid sequence of the clone was different at 8 positions from that of rat phosphatase 2A alpha determined in a previous study. The deduced amino acid sequence of the clone

Alkaline phosphatase activity in human and rat liver tumors.

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Enzyme activity measurements of alkaline phosphatase in surgically removed human liver tumors showed elevated level of the enzyme in 6 focal nodular hyperplasias, reduction in 8 primary hepatocellular carcinomas, and no change in the 4 adenoma samples. The activity represented liver type of alkaline

Occurrence of an atypical alkaline phosphatase fraction ("biliary") in primary liver cancer.

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The appearance and clinical significance of an atypical fraction of serum alkaline phosphatase called "biliary" have been evaluated in patients with primary liver cancer (PLC) and control subjects. The "biliary" fraction was present in all 42 PLC patients and proved to be the most sensitive of the

Epidermal growth factor activates the Rho GTPase-activating protein (GAP) Deleted in Liver Cancer 1 via focal adhesion kinase and protein phosphatase 2A.

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Deleted in Liver Cancer 1 (DLC1) is a RHO GTPase-activating protein (GAP) that negatively regulates RHO. Through its GAP activity, it modulates the actin cytoskeleton network and focal adhesion dynamics, ultimately leading to suppression of cell invasion and metastasis. Despite its presence in

Lupeol targets liver tumor-initiating cells through phosphatase and tensin homolog modulation.

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Liver tumor-initiating cells (T-ICs) are capable of self-renewal and tumor initiation and are more chemoresistant to chemotherapeutic drugs. The current therapeutic strategies for targeting stem cell self-renewal pathways therefore represent rational approaches for cancer prevention and treatment.

Impact of liver tumour burden, alkaline phosphatase elevation, and target lesion size on treatment outcomes with 177Lu-Dotatate: an analysis of the NETTER-1 study.

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PURPOSE

To assess the impact of baseline liver tumour burden, alkaline phosphatase (ALP) elevation, and target lesion size on treatment outcomes with ¹⁷⁷Lu-Dotatate.

In the phase 3 NETTER-1 trial, patients with advanced, progressive midgut

Protein phosphatase 2 regulatory subunit B''Alpha silencing inhibits tumor cell proliferation in liver cancer.

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To explore the effects of protein phosphatase 2 regulatory subunit B''Alpha (PPP2R3A) on the proliferation and migration of liver cancer cells.Expression of PPP2R3A in tumor tissues of hepatocellular carcinoma (HCC) patients was detected by

Cdc25A protein phosphatase: a therapeutic target for liver cancer therapies.

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Cdc25A, a dual specificity protein phosphatase, is well-recognized as a critical regulator for cell cycle progression. We recently found that it also regulates mitogen-activated protein kinase (MAPK) signal transduction pathway. Inhibition of Cdc25A activity by a K vitamin analog Compound 5 (Cpd 5)

Intestinal alkaline phosphatase isoenzyme in patients with primary liver cancer during treatment with N10-propargyl 5, 8-dideazafolic acid (CB 3717).

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Serum aspartate transaminase (AST), alkaline phosphatase (ALP), and gamma-glutamyl transferase (gamma GT) activities and the serum ALP isoenzyme pattern have been measured in eleven patients undergoing treatment with CB3717. There were increases in the activity of all three enzymes. The ALP

The source of serum alkaline phosphatases in liver-tumour-bearing rats.

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Patients with hepatic tumours have increased serum activities of alkaline phosphatases. In order to clarify the origin of the increased enzyme activity, two experimental models of rat liver carcinogenesis were studied. In one model, the resistant hepatocyte model, the process was initiated by

Structure-function relationships of microcystins, liver tumor promoters, in interaction with protein phosphatase.

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Microcystins, isolated from toxic blue-green algae, are potent inhibitors of protein phosphatases 1 and 2A. Recently, we have reported that microcystin LR has a potent tumor-promoting activity on rat liver initiated with diethylnitrosamine. The structure of microcystins is unique in having an

Increased expression of GATA zinc finger domain containing 1 through gene amplification promotes liver cancer by directly inducing phosphatase of regenerating liver 3.

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We identified that GATA zinc finger domain containing 1 (GATAD1), a transcriptional factor, was significantly up-regulated in hepatocellular carcinoma (HCC) through gene amplification. We demonstrated the critical role, molecular mechanisms, and clinical implications of GATAD1 as a novel oncogenic

Suppression of miR-21 Expression Inhibits Cell Proliferation and Migration of Liver Cancer Cells by Targeting Phosphatase and Tensin Homolog (PTEN).

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BACKGROUND Liver cancer is considered one of the main causes of cancer related deaths across the globe. Moreover, the incidence of liver cancer in developed countries is likely to increase in future. The increase in the incidence of liver cancer, the limited availability of standard treatments, and

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