Evaluation of biomarkers, genetic mutations, and epigenetic modifications in early diagnosis of pancreatic cancer

Rah, Bilal; Banday, Manzoor Ahmad; Bhat, G. M.; Shah, Omar Javed; Jeelani, Humira; Kawoosa, Fizalah; Yousuf, Tahira; Afroze, Dil

doi:10.3748/wjg.v27.i36.6093

Cited by 7 publications

(5 citation statements)

References 51 publications

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“…Another important gene of Smad family located on chromosome 18q is Smad4 ( Maru et al, 2004 ). Smad4 gene is remarkably absent in various cancers such as cervical, prostate, breast, pancreatic, and neuroblastoma due to greater frequency of loss of heterozygosity (LOH) of 18q ( Zhao et al, 2018 ; Rah et al, 2021 ). The inactivation of Smad4 occurs by various mechanisms which includes frameshift, loss of entire chromosome segment, nonsense and small deletion mutations ( Hata et al, 2018 ).…”

Section: Introductionmentioning

confidence: 99%

“…The inactivation of Smad4 occurs by various mechanisms which includes frameshift, loss of entire chromosome segment, nonsense and small deletion mutations ( Hata et al, 2018 ). Identified first as deleted in pancreatic carcinoma (DPC-4), Smad4 mutations mainly occurs in pancreatic cancer ( Rah et al, 2021 ). Presence of germ line mutations in MADH4 of juvenile polyposis families further supports that the Smad4 act as a tumor suppressor ( Harradine and Akhurst, 2006 ).…”

Section: Introductionmentioning

confidence: 99%

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Transforming Growth Factor-Beta (TGF-β) Signaling in Cancer-A Betrayal Within

et al. 2022

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A ubiquitously expressed cytokine, transforming growth factor-beta (TGF-β) plays a significant role in various ongoing cellular mechanisms. The gain or loss-of-function of TGF-β and its downstream mediators could lead to a plethora of diseases includes tumorigenesis. Specifically, at the early onset of malignancy TGF-β act as tumour suppressor and plays a key role in clearing malignant cells by reducing the cellular proliferation and differentiation thus triggers the process of apoptosis. Subsequently, TGF-β at an advanced stage of malignancy promotes tumorigenesis by augmenting cellular transformation, epithelial-mesenchymal-transition invasion, and metastasis. Besides playing the dual roles, depending upon the stage of malignancy, TGF-β also regulates cell fate through immune and stroma components. This oscillatory role of TGF-β to fight against cancer or act as a traitor to collaborate and crosstalk with other tumorigenic signaling pathways and its betrayal within the cell depends upon the cellular context. Therefore, the current review highlights and understands the dual role of TGF-β under different cellular conditions and its crosstalk with other signaling pathways in modulating cell fate.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Transforming Growth Factor-Beta (TGF-β) Signaling in Cancer-A Betrayal Within

et al. 2022

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“…As a result, 47 PRGs and 33 ICDGs were identi ed 14,16 . Gene mutations and copy number variations reportedly promote the progression of cancer [17][18][19] . Therefore, the gene mutation frequency and copy number variation frequency of PRGs and ICDGs in HNSCC were investigated in the present study.…”

Section: Comparison Of the Genome And Transcriptome Alterations In Hnsccmentioning

confidence: 99%

Identification of Subtypes Associated with Pyroptosis and Immune Cell Death, Prediction using Prognostic Models, and Analysis of Tumor Microenvironment in Head and Neck Squamous Cell Carcinoma

Liu

et al. 2023

Preprint

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Purpose: Pyroptosis and immunogenic cell death (ICD) are two pathways of programmed cell death (PCD). The role of pyroptosis-related genes (PRGs) and immunogenic cell death-related genes (ICDGs) in the alteration of the tumor microenvironment (TME) in head and neck squamous cell carcinoma (HNSCC) remains unclear to date. Method: We used the consensus clustering analysis for the classification of subtypes from TCGA datasets.Regression analysis was performed to identify the significant genes. We analyzed the infiltration of immune cells in each patient's TME. Finally, a Nomogram model was constructed, which was related to the clinical phenotype of the patients. Result: In the consensus clustering, HNSCC patients were divided into different subtypes according to the expression levels of PRGs and ICDGs. The risk score was obtained based on 19 risk genes, and the patients were divided into a high-risk group and a low-risk group. The low-risk group was observed to be strongly associated with better survival. The Kaplan-Meier analysis revealed the risk scores of pyroptosis and ICD as independent prognostic indicators. Conclusion: It is important to type HNSCC according to PRGs and ICDGs, to develop effective treatment strategies for HNSCC.

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“…Gastric cancer (GC) is a heterogeneous malignancy and is one of the leading cancer-related mortalities across the world ( Jan et al, 2021 ; Rah et al, 2021 ). The major risk factors contributing to gastric tumorigenesis are environmental factors, geographical location, lifestyle factors, age, and chronic infection with Helicobacter pylori ( Chia and Tan, 2016 ; Jan et al, 2021 ; Karimkhani et al, 2017 ).…”

Section: Introductionmentioning

confidence: 99%

JAK/STAT Signaling: Molecular Targets, Therapeutic Opportunities, and Limitations of Targeted Inhibitions in Solid Malignancies

et al. 2022

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JAK/STAT signaling pathway is one of the important regulatory signaling cascades for the myriad of cellular processes initiated by various types of ligands such as growth factors, hormones, and cytokines. The physiological processes regulated by JAK/STAT signaling are immune regulation, cell proliferation, cell survival, apoptosis and hematopoiesis of myeloid and non-myeloid cells. Dysregulation of JAK/STAT signaling is reported in various immunological disorders, hematological and other solid malignancies through various oncogenic activation mutations in receptors, downstream mediators, and associated transcriptional factors such as STATs. STATs typically have a dual role when explored in the context of cancer. While several members of the STAT family are involved in malignancies, however, a few members which include STAT3 and STAT5 are linked to tumor initiation and progression. Other STAT members such as STAT1 and STAT2 are pivotal for antitumor defense and maintenance of an effective and long-term immune response through evolutionarily conserved programs. The effects of JAK/STAT signaling and the persistent activation of STATs in tumor cell survival; proliferation and invasion have made the JAK/STAT pathway an ideal target for drug development and cancer therapy. Therefore, understanding the intricate JAK/STAT signaling in the pathogenesis of solid malignancies needs extensive research. A better understanding of the functionally redundant roles of JAKs and STATs may provide a rationale for improving existing cancer therapies which have deleterious effects on normal cells and to identifying novel targets for therapeutic intervention in solid malignancies.

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Evaluation of biomarkers, genetic mutations, and epigenetic modifications in early diagnosis of pancreatic cancer

Cited by 7 publications

References 51 publications

Transforming Growth Factor-Beta (TGF-β) Signaling in Cancer-A Betrayal Within

Transforming Growth Factor-Beta (TGF-β) Signaling in Cancer-A Betrayal Within

Identification of Subtypes Associated with Pyroptosis and Immune Cell Death, Prediction using Prognostic Models, and Analysis of Tumor Microenvironment in Head and Neck Squamous Cell Carcinoma

JAK/STAT Signaling: Molecular Targets, Therapeutic Opportunities, and Limitations of Targeted Inhibitions in Solid Malignancies

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