Identification of Prognostic Biomarkers for Suppressing Tumorigenesis and Metastasis of Hepatocellular Carcinoma through Transcriptome Analysis

Mishra, Divya; Mishra, Ashish; Nand, Sachchida; Vamanu, Emanuel; Singh, Mohan

doi:10.3390/diagnostics13050965

Cited by 8 publications

(2 citation statements)

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“…The isochromosome I (12)p or a deletion in 12pa germ cell chromosomal marker -was observed in 25% of patients with poorly differentiated carcinoma and predominant lymph nodal disease [32][33][34]. Chromosomal instability (aneuploidy) was found in 70% of patients with metastatic adenocarcinoma or undifferentiated carcinoma [35,36].…”

Section: Molecular Abnormalitiesmentioning

confidence: 99%

Structural carcinoma overall process: a systematic review

Arabestanino,

Naghibi Irvani,

et al. 2024

Cell. Mol. Biomed. Rep.

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Abnormalities of several oncogenes and tumor suppressor genes have been identified in carcinomas during the last decade and of pathological warfare and physiological traits, and multiple genetic changes have been demonstrated in individual carcinomas. We conducted a systematic review of studies enrolling adolescents and adults with Carcinoma, every type in which a cancer intervention was randomized, or all study designs in which there was a primary or secondary outcome. We searched Ovid MEDLINE, EMBASE, and Evidence-Based Medicine Reviews from 1990 to June 2015. Two reviewers evaluated study eligibility and abstracted data. In total, 67 studies were included and consisted of 62 randomized trials, reviews, and 5 studies. None of the studies (0/81) provided a definition. Only one randomized trial provided a definition. We were unable to identify any definitions used in studies of adolescents and adults with Carcinoma. Given that a proportion of this population may receive intensive treatment, there is an urgent need for consensus-based definitions of use across trials and review systematic and meta-analysis. Article info

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Section: Molecular Abnormalitiesmentioning

confidence: 99%

Structural carcinoma overall process: a systematic review

Arabestanino,

Naghibi Irvani,

et al. 2024

Cell. Mol. Biomed. Rep.

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“…Eg5 could be a new valid biomarker to be added in the panel of protein markers and to be analyzed by immunohistochemistry after tumor tissue biopsy: high rates of Eg5 expression could modify the therapeutic approach, with the possibility to add an Eg5 inhibitor to the standard therapy. In addition, future researches could detect possible association between Eg5 expression levels and tumor stage or identify Eg5 as a potential metastatic marker: transcriptome analysis could be a valid approach for this type of identification [ 81 ].…”

Section: Eg5 In Tumor Onset and Progressionmentioning

confidence: 99%

Eg5 and Diseases: From the Well‐Known Role in Cancer to the Less‐Known Activity in Noncancerous Pathological Conditions

Ricci,

Carradori,

Cataldi

et al. 2024

Biochemistry Research International

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Eg5 is a protein encoded by KIF11 gene and is primarily involved in correct mitotic cell division. It is also involved in nonmitotic processes such as polypeptide synthesis, protein transport, and angiogenesis. The scientific literature sheds light on the ubiquitous functions of KIF11 and its involvement in the onset and progression of different pathologies. This review focuses attention on two main points: (1) the correlation between Eg5 and cancer and (2) the involvement of Eg5 in noncancerous conditions. Regarding the first point, several tumors revealed an overexpression of this kinesin, thus pushing to look for new Eg5 inhibitors for clinical practice. In addition, the evaluation of Eg5 expression represents a crucial step, as its overexpression could predict a poor prognosis for cancer patients. Referring to the second point, in specific pathological conditions, the reduced activity of Eg5 can be one of the causes of pathological onset. This is the case of Alzheimer’s disease (AD), in which Aβ and Tau work as Eg5 inhibitors, or in acquired immune deficiency syndrome (AIDS), in which Tat‐mediated Eg5 determines the loss of CD4+ T‐lymphocytes. Reduced Eg5 activity, due to mutations of KIF11 gene, is also responsible for pathological conditions such as microcephaly with or without chorioretinopathy, lymphedema, or intellectual disability (MCLRI) and familial exudative vitreous retinopathy (FEVR). In conclusion, this review highlights the double impact that overexpression or loss of function of Eg5 could have in the onset and progression of different pathological situations. This emphasizes, on one hand, a possible role of Eg5 as a potential biomarker and new target in cancer and, on the other hand, the promotion of Eg5 expression/activity as a new therapeutic strategy in different noncancerous diseases.

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