|
Liver Cirrhosis, Experimental
|
0.300 |
Biomarker
|
disease |
CTD_human |
Systems level analysis and identification of pathways and networks associated with liver fibrosis.
|
25380136 |
2014 |
|
Leukemia, Myelocytic, Acute
|
0.090 |
GeneticVariation
|
disease |
BEFREE |
Early induction intensification with cladribine, cytarabine, and mitoxantrone (CLAM) in AML patients treated with the DAC induction regimen: a prospective, non-randomized, phase II study of the Polish Adult Leukemia Group (PALG).
|
31661339 |
2020 |
|
Leukemia, Myelocytic, Acute
|
0.090 |
Biomarker
|
disease |
BEFREE |
The clinical activity of decitabine (5-aza-2-deoxycytidine, DAC), a hypomethylating agent, has been demonstrated in acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) patients.
|
30793488 |
2019 |
|
Leukemia, Myelocytic, Acute
|
0.090 |
Biomarker
|
disease |
BEFREE |
Decitabine (5-Aza-2'-deoxycytidine, DAC), an anti-leukemic drug, is effective in treating acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS).
|
30210693 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.090 |
Biomarker
|
disease |
BEFREE |
The hypomethylating agents azacitidine (Vidaza®, AZA) and decitabine (Dacogen®, DAC) have been approved for the treatment of AML patients, but their mechanisms of action are poorly understood.
|
28404876 |
2017 |
|
Leukemia, Myelocytic, Acute
|
0.090 |
Biomarker
|
disease |
BEFREE |
DAC (5-aza-2-deoxycytidine) is an antitumor drug useful to lung cancer, myelodysplastic disorders, myelodysplasia and acute myeloid leukemia.
|
25611377 |
2015 |
|
Leukemia, Myelocytic, Acute
|
0.090 |
Biomarker
|
disease |
BEFREE |
Undergoing allo-HSCT significantly improved the LFS and OS for the entire group of patients with AML in CR1, along with the DAC induction subgroup and for the group with unfavorable cytogenetics aged 41-60.
|
26149802 |
2015 |
|
Leukemia, Myelocytic, Acute
|
0.090 |
Biomarker
|
disease |
BEFREE |
Preclinical data indicate that DAC is much more effective against human AML than ARA-C.
|
23660386 |
2013 |
|
Leukemia, Myelocytic, Acute
|
0.090 |
Biomarker
|
disease |
BEFREE |
This study, the first to investigate the relationship between TERT methylation and telomerase activity in leukemia cells, demonstrated a differential methylation pattern and response to DAC in three AML cell lines.
|
22517724 |
2012 |
|
Leukemia, Myelocytic, Acute
|
0.090 |
Biomarker
|
disease |
BEFREE |
The promoter of p73 was hypermethylated in AML cell lines in vitro and in primary AML cells ex vivo but not in DAC-resistant epithelial cells.
|
16193303 |
2005 |
|
Neoplasms
|
0.080 |
PosttranslationalModification
|
group |
BEFREE |
Together, these experiments provide preclinical evidence that the FDA-approved DNA methylation inhibitor DAC may be repurposed to treat patients with osteosarcoma based on its efficacy to decrease proliferation, to induce osteoblast differentiation, and to reduce metastasis to visceral organs.<b>Significance:</b> These findings describe the effects of DNA methyltransferase inhibition on ERα and its potential role as a tumor suppressor in osteosarcoma.<i>See related commentary by Roberts, p. 1034</i><i>See related article by El Ayachi and colleagues; Cancer Res 79(5);982-93</i>.
|
30593524 |
2019 |
|
Neoplasms
|
0.080 |
AlteredExpression
|
group |
BEFREE |
In the tumor cell-xenograft mouse model and ELISPOT assays, DAC increased the expression of MAGE-A3 and T cell mediated tumor clearance in ESCC as well.
|
30797153 |
2019 |
|
Neoplasms
|
0.080 |
AlteredExpression
|
group |
BEFREE |
DAC can restore expression of NALP1 to suppress tumor growth in colon cancer.
|
25611377 |
2015 |
|
Neoplasms
|
0.080 |
Biomarker
|
group |
BEFREE |
Cytotoxic T cells specifically recognizing MAGE-A family and NY-ESO-1 clustered at the tumor site in mice pre-treated with DAC and resulted in tumor growth suppression, while it was not observed in mice without DAC pre-treatment.
|
25301731 |
2014 |
|
Neoplasms
|
0.080 |
AlteredExpression
|
group |
BEFREE |
The high expression levels of MAGE-A1, MAGE-A3, and NY-ESO-1 were sustained in sarcoma lines and primary tumor lines over 30 days after the cessation of DAC.
|
24584817 |
2014 |
|
Neoplasms
|
0.080 |
Biomarker
|
group |
BEFREE |
The p-GSK3β (Ser9) protein level in Caki-2 cells was significantly down-regulated, while the DNA fragmentation rate increased after treatment with 5 μM DAC at 96 h. Our data show that sFRP2 functions as a tumor suppressor gene in RCC and that its restoration may offer a new therapeutic approach for the treatment of RCC.
|
23975733 |
2013 |
|
Neoplasms
|
0.080 |
AlteredExpression
|
group |
BEFREE |
Putative methylation markers were selected from DAC-upregulated genes through a literature search and an upfront methylation-specific PCR on 20 primary neuroblastoma tumors, as well as through MBD- seq in combination with publicly available neuroblastoma tumor gene expression data.
|
23034519 |
2012 |
|
Neoplasms
|
0.080 |
AlteredExpression
|
group |
BEFREE |
Ovarian cancer cells (Hey and SKOv3) were treated with demethylating agents (5-aza-20-deoxycytidine [DAC] or 5-azacitidine [AZA]) or with HDAC inhibitors (suberoylanilide hydroxamicacid [SAHA] or trichostatin A [TSA]) to determine their impact on cellular proliferation, cell cycle regulation, apoptosis, autophagy, and re-expression of 2 growth inhibitory imprinted tumor suppressor genes: guanosine triphosphate-binding Di-RAS-like 3 (ARHI) and paternally expressed 3 (PEG3).
|
21491416 |
2011 |
|
MYELODYSPLASTIC SYNDROME
|
0.060 |
Biomarker
|
group |
BEFREE |
The clinical activity of decitabine (5-aza-2-deoxycytidine, DAC), a hypomethylating agent, has been demonstrated in acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) patients.
|
30793488 |
2019 |
|
MYELODYSPLASTIC SYNDROME
|
0.060 |
Biomarker
|
group |
BEFREE |
Decitabine (5-Aza-2'-deoxycytidine, DAC), an anti-leukemic drug, is effective in treating acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS).
|
30210693 |
2018 |
|
MYELODYSPLASTIC SYNDROME
|
0.060 |
Biomarker
|
group |
BEFREE |
DAC (5-aza-2-deoxycytidine) is an antitumor drug useful to lung cancer, myelodysplastic disorders, myelodysplasia and acute myeloid leukemia.
|
25611377 |
2015 |
|
MYELODYSPLASTIC SYNDROME
|
0.060 |
Biomarker
|
group |
BEFREE |
Low-dose demethylating agents such as 5-aza-2'-deoxycytidine (decitabine, DAC) and 5-azacytidine (azacitidine, Vidaza) have been explored for the treatment of myelodysplasia, acute myeloid leukemia, and hemoglobinopathies since the early 1980s, aiming to revert a methylator phenotype.
|
16292549 |
2005 |
|
MYELODYSPLASTIC SYNDROME
|
0.060 |
Biomarker
|
group |
BEFREE |
During the last 10 years, three European phase II studies were performed to investigate the treatment of elderly patients with myelodysplastic syndrome (MDS) with low-dose 5-aza-2'-deoxycytidine (decitabine, DAC).
|
16211386 |
2005 |
|
MYELODYSPLASTIC SYNDROME
|
0.060 |
GeneticVariation
|
group |
BEFREE |
Encouraging response rates of about 50% in myelodysplasia with 5-azacytidine and 5-aza-2'-deoxycytidine (decitabine or DAC) have resulted in a number of phase III studies being initiated in this disorder.
|
16210092 |
2005 |
|
Malignant Neoplasms
|
0.030 |
Biomarker
|
group |
BEFREE |
Functional assays, such as flow cytometry, cytotoxicity assays and ELISA, were performed to determine the demethylation agent, decitabine (5-aza-2'-deoxycytidine, DAC)-treated cancer cell improved antigen specific T cells response.
|
30797153 |
2019 |