scholarly journals A Review on the Carcinogenic Roles of DSCAM-AS1

2021 ◽  
Vol 9 ◽  
Author(s):  
Soudeh Ghafouri-Fard ◽  
Tayyebeh Khoshbakht ◽  
Mohammad Taheri ◽  
Kaveh Ebrahimzadeh
Keyword(s):  
Breast Cancer ◽  
Colorectal Cancer ◽  
Antisense Rna ◽  
Breast Tumor ◽  
Cancer Colorectal ◽  
Small Cell ◽  
Small Cell Lung ◽  
Breast Tumor Cells ◽  
Non Coding Rnas

Long non-coding RNAs (lncRNAs) are a group of transcripts with fundamental roles in the carcinogenesis. DSCAM Antisense RNA 1 (DSCAM−AS1) is an example of this group of transcripts which has been firstly identified in an attempt to find differentially expressed transcripts between breast tumor cells and benign breast samples. The pathogenic roles of DSCAM-AS1 have been vastly assessed in breast cancer, yet its roles are not restricted to this type of cancer. Independent studies in non-small cell lung cancer, colorectal cancer, osteosarcoma, hepatocellular carcinoma, melanoma and cervical cancer have validated participation of DSCAM-AS1 in the carcinogenic processes. miR-577, miR-122-5p, miR-204-5p, miR-136, miR−137, miR−382, miR−183, miR−99, miR-3173-5p, miR-874-3p, miR-874-3p, miR-150-5p, miR-2467-3p, miR-216b, miR-384, miR-186-5p, miR-338-3p, miR-877-5p and miR-101 are among miRNAs which interact with DSCAM-AS1. Moreover, this lncRNA has interactions with Wnt/β-catenin pathway. The current study aims at summarization of the results of studies which focused on the assessment of oncogenic role of DSCAM-AS1.

scholarly journals Phase II studies of Elsamitrucin in breast cancer, colorectal cancer, non-small cell lung cancer and ovarian cancer

1994 ◽  
Vol 5 (4) ◽  
pp. 375-376 ◽  
Author(s):  
J. Verweij ◽  
J. Wanders ◽  
A.L. Nielsen ◽  
N. Pavlidis ◽  
F. Calabresi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Colorectal Cancer ◽  
Lung Cancer ◽  
Ovarian Cancer ◽  
Small Cell Lung Cancer ◽  
Phase Ii ◽  
Cancer Colorectal ◽  
Small Cell ◽  
Small Cell Lung ◽  
Phase Ii Studies

scholarly journals A PILOT CLINICAL TRIAL TO MONITOR RESPONSE TO CHEMOTHERAPY USING THE CA-62 MARKER OF EPITHELIAL CARCINOMAS

2019 ◽  
Vol 18 (5) ◽  
pp. 18-28
Author(s):  
G. G. Khakimova ◽  
Zh. R. Cherkasova ◽  
S. A. Tsurkan ◽  
G. A. Fedchikov ◽  
N. V. Suganov ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Gastric Cancer ◽  
Lung Cancer ◽  
Ovarian Cancer ◽  
Cancer Colorectal ◽  
Performance Status ◽  
Small Cell ◽  
Small Cell Lung ◽  
Neuroendocrine Cancer ◽  
Response To Chemotherapy

The objective of the study was to assess the feasibility of using CA -62 marker of epithelial carcinomas for monitoring treatment response and detecting cancer progression or recurrence during chemotherapy.Material and Methods. A 12-month double-blind clinical trial was conducted by two independent groups: clinical oncologists and biochemists, and involved 89 patients with different cancers confirmed by histopathological findings. The other inclusion criteria were: the presence of at least one measurable lesion according to the RECIST criteria, ECOG performance status 0-2 and satisfactory laboratory parameters. The expression of CA -62 cancer marker was measured by immunochemiluminescent assay used for the detection of epithelial carcinomas.Results. The elevated level of CA -62 marker was observed in 76 patients before starting the treatment. After completion chemotherapy, the level of this marker decreased to the normal reference ranges (<4600 U/ml) in 53 % of patients and remained increased in 24 % of patients. Of 24 % of patients with the initial low level of CA -62 marker (1000–4000 U/ml) before treatment, 12 % had no changes in the level of this marker during chemotherapy; however, 5 % of these patients had disease progression and 7 % had stable disease after starting the treatment. In 12 % of patients with an initial low CA -62 level, it increased during chemotherapy, indicating disease progression.Conclusion. The changes in the level of CA -62 marker during chemotherapy in patients with gastric cancer, small-cell lung cancer, colorectal cancer, neuroendocrine cancer and ovarian cancer showed a high correlation (76–100 % depending on the tumor site) with the performance status of the patients according to RECIST criteria. The CA -62 marker was shown to be feasible for monitoring gastric cancer, small-cell lung cancer, colorectal cancer, neuroendocrine cancer and ovarian cancer as well as for assessing the response to chemotherapy.

scholarly journals NORAD accelerates chemo-resistance of non-small-cell lung cancer via targeting at miR-129-1-3p/SOX4 axis

2020 ◽  
Vol 40 (1) ◽  
Author(s):  
Qiang Huang ◽  
Shijiang Xing ◽  
Aiping Peng ◽  
Zhiwu Yu
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung ◽  
Downstream Target ◽  
Non Coding Rna ◽  
Non Coding Rnas ◽  
Nsclc Patients

Abstract Substantial researches indicated that long non-coding RNAs (lncRNAs) exerted profound effects on chemo-resistance in cancer treatment. Nonetheless, the role of NORAD in non-small-cell lung cancer (NSCLC) remains unclear. In the present study, we chose NSCLC cell lines H446 and A549 to explore the function of non-coding RNA activated damage (NORAD) in response to cisplatin (DDP) resistance of NSCLC. Experimental data manifested that NORAD was up-regulated in DDP-resistant NSCLC tissues and cells. NSCLC patients with high NORAD expression suffered a poor prognosis. NORAD knockdown resensitized H446/DDP and A549/DDP to DDP. Besides, NORAD acted as a molecular sponge of miR-129-1-3p. MiR-129-1-3p showed a low level of expression in DDP-resistant NSCLC tissues. Moreover, miR-129-1-3p overexpression impaired DDP resistance in H446/DDP and A549/DDP cells. SOX4 was the downstream target of miR-129-1-3p. Especially, SOX4 overexpression offset the effects of NORAD silence on H446/DDP and A549/DDP cells resistance to DDP. NORAD knockdown resensitized H446/DDP and A549/DDP to DDP in NSCLC via targeting miR-129-1-3p/SOX4 axis, offering a brand-new target for NSCLC chemo-resistance.

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