Ductal adenocarcinoma of the pancreas usually retained SMAD4 and p53 protein status as well as expression of epithelial-to-mesenchymal transition markers and cell cycle regulators at the stage of liver metastasis

Liszka, Łukasz

doi:10.5114/pjp.2014.43959

Cited by 4 publications

(6 citation statements)

References 77 publications

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“…For example, the mitogen-activated protein kinase 3 (MAPK3) gene was revealed as an upregulated DEG in S12 vs. C12 and S24 vs. C24 (data not shown). MAPK3 serves a role in a signaling cascade that mediates various cellular processes, including proliferation, differentiation and CC progression, in response to a variety of extracellular signals (29).…”

Section: Resultsmentioning

confidence: 99%

Transcriptome analysis of pancreatic cancer cell response to treatment with grape seed proanthocyanidins

Zhan¹,

Guo

Xiang

et al. 2018

Oncol Lett

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Grape seed proanthocyanidins (GSPs) have been demonstrated to exhibit potential chemotherapeutic efficacy against various cancer types. To determine the underlying molecular mechanisms involved in GSP-induced apoptosis, the present study prepared pancreatic cancer (PC) cells samples, S3, S12 and S24, which were treated with 20 µg/ml GSPs for 3, 12 and 24 h, respectively. Control cell samples, C3, C12 and C24, were also prepared. Using RNA-sequencing, transcriptome comparisons were performed, which identified 966, 3,543 and 4,944 differentially-expressed genes (DEGs) in S3 vs. C3, S12 vs. C12 and S24 vs. C24, respectively. Gene Ontology analysis of the DEGs, revealed that treatment with GSPs is associated with disruption of the cell cycle (CC) in PC cells. Additionally, disruption of transcription, DNA replication and DNA repair were associated with GSP-treatment in PC cells. Network analysis demonstrated that the common DEGs involved in the CC, transcription, DNA replication and DNA repair were integrated, and served essential roles in the control of CC progression in cancer cells. In summary, GSPs may exhibit a potential chemotherapeutic effect on PC cell proliferation.

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Section: Resultsmentioning

confidence: 99%

Transcriptome analysis of pancreatic cancer cell response to treatment with grape seed proanthocyanidins

Zhan¹,

Guo

Xiang

et al. 2018

Oncol Lett

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“…We found that abnormal expression was closely related to the late N stage, late TNM stage, and poor tumor differentiation, which may reflect the invasive and metastatic biology of tumors with TP53 mutations 26 . We also found that p53 expression categories were superior to tumor grade, which was regularly included in pathological reports.…”

Section: Discussionmentioning

confidence: 55%

Negative p53 Expression Confers Worse Prognosis in Patients With Resected Pancreatic Ductal Adenocarcinoma

Wang

et al. 2022

Pancreas

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The aim of the study is to reinterpret the prognostic prediction of p53 expression categories in pancreatic ductal adenocarcinoma with exploration of the relationship between TP53 mutation genotype and p53 expression pattern.Methods: Data were retrospectively collected from consecutive patients who underwent primary pancreatic resection. Complete loss of function of TP53 is defined as nonsense and frameshift mutations. A tissue microarray was used to evaluate p53 expression by immunohistochemistry and was categorized as regulated, high, or negative. Results:The κ coefficient for agreement between p53 expression and TP53 was 0.761. Cox regression analyses revealed that p53 expression (high vs regulated: hazard ratio [HR], 2.225; P < 0.001; negative vs regulated: HR, 2.788; P < 0.001), tumor-node-metastasis stage (II vs I: HR, 3.471; P < 0.001; III vs I: HR, 6.834; P < 0.001), and tumor grade (G3/4 vs G1/2: HR, 1.958; P < 0.001) were independent prognostic factors in developing cohort and validation cohort. In subgroups of stage I, II, and III, compared with regulated expression, the patients with negative expression had a worse prognosis in both cohorts ( P < 0.05). Conclusions:Our findings indicate that 3-tier p53 expression in resectable pancreatic ductal adenocarcinoma provided independent prognostic information complementary to the tumor-node-metastasis staging system and facilitated patient stratification for personalized therapy.

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“…128 In cases of SMDA4-deficient PDACs, TP53 usually has a missense mutation. 129 Both TP53 and SMAD4 inactivation occur in the late stages of PDAC, but TP53 mutations occur earlier than SMAD4 loss. TP53 mutations and SMAD4 loss occur mainly in aggressive PDACs and they may be markers of high metastatic potential for tumors.…”

Section: Smad4mentioning

confidence: 99%

“…130 This findings may have potential significance for patients with PDAC and provide new ideas for treatment options to reduce local or distant tumor growth. 129…”

Section: Smad4mentioning

confidence: 99%

“…140 CDKN1A, MDM2, TP53 are included in the TP53 signal pathway in PDAC. 129 In the process of cell division, the major transcription factor of the TP53 pathway and its cofactor CDKN2A prevent the proliferating cells from repairing the damage by strongly fighting the MYC pathway, or initiate an orderly suicide if the damage cannot be repaired, in order to protect the integrity of the entire tissue. 141,142 TP53 and CDKN2A are often biallelically inactivated in human malignancies, which has a significant impact on treatment.…”

Section: Interactions In Pdacmentioning

confidence: 99%

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<p>Is there a CDKN2A-centric network in pancreatic ductal adenocarcinoma?</p>

Wu¹,

Yang²,

Liu³

et al. 2020

OTT

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Pancreatic cancer has a high mortality rate and its incidence has risen rapidly in recent years. Meanwhile, the diagnosis and treatment of this cancer remain challenging. Pancreatic ductal adenocarcinoma (PDAC) is the most common type of pancreatic cancer, but, currently, no sufficiently effective modalities for its treatment exist. The early diagnosis rate of pancreatic cancer is low and most patients have reached an advanced stage at the time of diagnosis. PDAC evolves from precancerous lesions and is highly aggressive and metastatic. It is essential to understand how the disease progresses and metastasizes. CDKN2A mutations are very common in PDAC. Therefore, here, we have performed a literature review and discuss the role of CDKN2A and some related genes in the development of PDAC, as well as the basis of gene targeting with a correlation coefficient of CDKN2A above 0.9 on the STRING website. It is noteworthy that the interaction of CDKN2A with each gene has been reported in the literature. The role of these genes and CDKN2A in PDAC may provide new directions that will advance the current knowledge base and treatment options since cancer progression is realized through interactions among cells. Our findings provide new insights into the treatment of PADC that can, to some extent, improve the diagnosis rate and quality of life of patients.

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Ductal adenocarcinoma of the pancreas usually retained SMAD4 and p53 protein status as well as expression of epithelial-to-mesenchymal transition markers and cell cycle regulators at the stage of liver metastasis

Cited by 4 publications

References 77 publications

Transcriptome analysis of pancreatic cancer cell response to treatment with grape seed proanthocyanidins

Transcriptome analysis of pancreatic cancer cell response to treatment with grape seed proanthocyanidins

Negative p53 Expression Confers Worse Prognosis in Patients With Resected Pancreatic Ductal Adenocarcinoma

<p>Is there a CDKN2A-centric network in pancreatic ductal adenocarcinoma?</p>

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