Curing pancreatic cancer

Traub, Benno; Link, K. H.; Kornmann, Marko

doi:10.1016/j.semcancer.2021.05.030

Cited by 29 publications

(16 citation statements)

References 258 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The number of people who died from pancreatic cancer was 49,830 for men and 25,970 for women, respectively ( 3 ). Surgery and chemotherapy remain the mainstays of treatment for pancreatic adenocarcinoma ( 4 ). However, pancreatic cancer is aggressive with no obvious symptoms in the early stage.…”

Section: Introductionmentioning

confidence: 99%

LncRNA MALAT1 regulates METTL3-mediated PD-L1 expression and immune infiltrates in pancreatic cancer

et al. 2022

View full text Add to dashboard Cite

Pancreatic cancer is the fourth leading cause of cancer death in the United States. The main methods of treating pancreatic cancer are surgery and chemotherapy, but the treatment efficacy is low with a poor prognosis. Immunotherapy represented by PD-1/PD-L1 has brought a milestone progress in the treatment of pancreatic cancer. However, the unique tumor microenvironment of pancreatic cancer presents challenges for immunotherapy. In addition, m6A is a common RNA modification and a potential molecular target in tumor therapy. The expression pattern of m6A in pancreatic cancer is still unclear. LncRNAs also play an essential role in pancreatic cancer development and treatment. In this study, we found that some m6A regulators were significantly elevated in pancreatic cancer and associated with the expression of PD-1/PD-L1. Moreover, we observed that METTL3 can increase the expression of PD-L1. Notably, METTL3 positively regulates the expression of lncRNA MALAT1 in pancreatic cancer cells. Strikingly, lncRNA MALAT1 increased the expression of PD-L1 in pancreatic cancer cells. This finding indicated that METTL3 regulated the expression of PD-L1 possibly via targeting lncRNA MALAT1 in pancreatic cancer cells. Lastly, MALAT1 governed the viability of pancreatic cancer cells. Taken together, lncRNA MALAT1 is involved in METTL3-mediated promotion of PD-L1 expression in pancreatic cancer.

show abstract

Section: Introductionmentioning

confidence: 99%

LncRNA MALAT1 regulates METTL3-mediated PD-L1 expression and immune infiltrates in pancreatic cancer

et al. 2022

View full text Add to dashboard Cite

show abstract

“…Unfortunately, delayed diagnosis is the rule and only a small percentage of patients are offered surgical resection (7)(8)(9). There are two main ways to face this harsh reality.…”

Section: Introductionmentioning

confidence: 99%

A more radical perspective on surgical approach and outcomes in pancreatic cancer—a narrative review

Fernandes¹,

Mello²,

Braga³

et al. 2023

J Gastrointest Oncol

View full text Add to dashboard Cite

Background and Objective: Pancreatic adenocarcinoma remains a dismal disease and is expected to become an even greater burden in the near future. This review focuses on the different surgical aspects for pancreaticoduodenectomy (PD), distal and total pancreatectomy (TP), incorporating lessons from both the western and eastern visions in treating pancreatic cancer. Methods:We conducted an extensive literature review through PubMed, prioritizing papers published in the last 5 years, but older emblematic papers were also included. We included articles that explored the treatment of pancreatic adenocarcinoma, with focus on the surgical aspect and strategies to improve outcomes. References of selected articles were also reviewed to identify any missed studies. Only papers in English were included.

show abstract

“…The devastating numbers of pancreatic cancer (PC) are well known around researchers and clinicians: fourth leading cause of cancer-related mortality, estimated to rise to second position within next decade ( 1 , 2 ); no improvement in mortality rates over the last decade, unlike other malignancies ( 1 ); failure of early detection and severe side-effects in treatment ( 3 ).…”

Section: Introductionmentioning

confidence: 99%

JNK inhibitor IX restrains pancreatic cancer through p53 and p21

et al. 2022

Self Cite

View full text Add to dashboard Cite

Novel treatment options for pancreatic cancer are desperately needed. De-regulated kinases can be regularly detected in pancreatic cancer. Multiple pathway inhibitors were developed to exploit these features, among them selective inhibitors of the c-Jun N-terminal kinase isoforms 1 and 2 (JNK1 and 2). We evaluated the effectiveness of four different JNK inhibitors on pancreatic cancer cell lines. Cell mobility and migration were evaluated in scratch assay and Boyden chamber assay. Mechanism of cell death was analyzed via apoptosis assays in FACS and immunoblotting as well as cell cycle analysis via FACS, and qPCR. JNK2 knockout cells were generated using siRNA transfection. Among the inhibitors, JNK inhibitor IX (JNK-in-IX), designed as specific inhibitor against JNK2 was proven highly effective in inhibiting cell growth, mobility and migration. We were able to show that JNK-in-IX caused DNA damage resulting in G2 arrest mediated through p53 and p21. Interestingly, JNK-in-IX acted independently of its primary target JNK2. In summary, JNK-in-IX was shown highly effective in pancreatic cancer. This study underlines the need for modeling systems in testing therapeutic options as JNK2 was previously not indicated as a potential target.

show abstract

Curing pancreatic cancer

Cited by 29 publications

References 258 publications

LncRNA MALAT1 regulates METTL3-mediated PD-L1 expression and immune infiltrates in pancreatic cancer

LncRNA MALAT1 regulates METTL3-mediated PD-L1 expression and immune infiltrates in pancreatic cancer

A more radical perspective on surgical approach and outcomes in pancreatic cancer—a narrative review

JNK inhibitor IX restrains pancreatic cancer through p53 and p21

Contact Info

Product

Resources

About