Optimizing the outcomes of pancreatic cancer surgery

Strobel, Oliver; Neoptolemos, John P.; Jäger, Dirk; Büchler, Markus W.

doi:10.1038/s41571-018-0112-1

Cited by 656 publications

(531 citation statements)

References 125 publications

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“…Pancreatic cancer (PC) is one of the deadliest human malignancies that have a median survival duration of 6 months and a 5‐year survival rate of less than 5% . The prognosis of patients remains bleak despite advances in diagnostic techniques and therapeutic strategies . Therefore, it is urgently needed to develop a better understanding of the molecular mechanisms that drive the development and progression of pancreatic cancer in order to discover more effective diagnosis and therapeutic targets for treatment of this malignance.…”

Section: Introductionmentioning

confidence: 99%

DRP1 upregulation promotes pancreatic cancer growth and metastasis through increased aerobic glycolysis

Liang

Yang²,

Bai

et al. 2020

J of Gastro and Hepatol

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Background: Mitochondrial shape is dynamically changed by fusion and fission processes in cells, and dysfunction of this process has become one of the emerging hallmarks of cancer. However, the expression patterns and biological effects of mitochondrial fission and fusion proteins in pancreatic cancer (PC) are still unclear. Methods: The expressions of mitochondrial fission and fusion proteins were first evaluated by quantitative reverse transcription polymerase chain reaction and western blot analysis in both PC cell lines and tissue samples. In addition, the biologic functions of the differentially expressed proteins in PC cell growth and metastasis both in vitro and in vivo and their potential underlying mechanisms were systematically explored. Results: We first found that DRP1 was substantially upregulated in PC cell lines and tissue samples mainly due to the downregulation of miR-29a, which contributed to the poor survival of PC patients. DRP1 promoted the growth and metastasis of PC cells both in vitro and in vivo by inducing G1-S cell cycle transition and matrix metalloproteinase 2 secretion. Mechanistic investigations revealed that increased DRP1 upregulation-mediated mitochondrial fission and subsequently enhanced aerobic glycolysis were involved in the promotion of growth and metastasis by DRP1 in PC cells. Conclusions: Our findings demonstrate that mitochondrial fusion protein DRP1 plays a critical oncogenic role in PC cells by enhancing aerobic glycolysis, which could serve as a novel therapeutic target for PC treatment. bs_bs_banner DRP1 promotes PC growth and metastasis J Liang et al. DRP1 promotes PC growth and metastasis J Liang et al.

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Section: Introductionmentioning

confidence: 99%

DRP1 upregulation promotes pancreatic cancer growth and metastasis through increased aerobic glycolysis

Liang

Yang²,

Bai

et al. 2020

J of Gastro and Hepatol

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“…The overall prognosis of pancreatic ductal adenocarcinoma (PDAC) remains poor and its therapy remains challenging . Surgical resection in combination with systemic therapy offers the only chance for long‐term survival or potential cure .…”

Section: Introductionmentioning

confidence: 99%

Local radicality and survival outcome of pancreatic cancer surgery

Niesen

Hank

Büchler

et al. 2019

Annals of Gastroent Surgery

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Pancreatic cancer remains a therapeutic challenge. Surgical resection in combination with systemic chemotherapy is the only option promising long‐term survival and potential cure. However, only about 20% of patients are diagnosed with tumors that are still in a resectable stage. Even after potentially curative resection and modern regimens for adjuvant chemotherapy, the majority of patients develop local and systemic recurrence resulting in median overall survival times of 28‐54 months. The predominance of systemic recurrence and its impact on survival may lead to the assumption that surgical radicality and local control play only minor roles in the treatment of pancreatic cancer. This review provides an overview of the recent literature on surgical radicality and survival outcome in pancreatic cancer. The current evidence on the extent of lymphadenectomy, the prognostic impact of the extent of lymph node involvement, and the impact of the resection margin status on postresection survival are reviewed. Data from recent studies performed in the context of modern surgery and adjuvant therapy provide good evidence of a considerable impact of local radicality on survival after pancreatic cancer surgery. Surgical techniques that have been developed to refine oncological resections and to increase local control as well as resectability are highlighted. These techniques include artery‐first approaches, level‐3 dissection with removal of the periarterial nerve plexus, the triangle operation, and extended resections. Local radicality and quality of surgical resection remain among the most important parameters that determine the chances for survival in patients with non‐metastatic pancreatic cancer.

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“…1 The prognosis of PDAC is associated with the tumor stage, which is determined based on the traditional tumor-node-metastasis (TNM) classification that comprises the tumor invasion depth, lymph node (LN) metastasis, and distant metastasis. The National Central Cancer Registry of China data show that PDAC leads to 79.4 thousand deaths per year in China.…”

Section: Introductionmentioning

confidence: 99%

A potential prognostic marker and therapeutic target: SPOCK1 promotes the proliferation, metastasis, and apoptosis of pancreatic ductal adenocarcinoma cells

Jin

Fang

et al. 2019

J of Cellular Biochemistry

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Pancreatic ductal adenocarcinoma (PDAC), a common malignancy originated from the digestive system worldwide, has a poor clinical outcome. SPOCK1 is a widely investigated member of the Ca2+‐binding proteoglycan family and functions as an essential driver in several cancers. However, the complex regulatory role of SPOCK1 in PDAC is unclear. Bioinformatics analysis predicted an interrelationship between increased SPOCK1 expression and the clinical characteristics of patients with PDAC. The SPOCK1 expression levels in fresh tissue samples were confirmed, and SPOCK1 expression was then knocked down by lentivirus‐mediated short hairpin RNA. Cell proliferation, metastasis, and apoptosis were detected through Cell Counting Kit‐8, colony formation assays, invasion and migration assays, flow cytometric analysis, quantitative real‐time polymerase chain reaction, and Western blot experiment. On the basis of the Cancer Genome Atlas database, we found a significantly higher level of SPOCK1 in PDAC than in adjacent nontumor tissues. Patients with PDAC with high SPOCK1 expression exhibited shorter overall survival time, as well as disease‐free survival time. The knockdown of SPOCK1 significantly decreased the proliferation and metastasis of PCNA‐1 and MIA PaCa‐2 cells. Moreover, the knockdown of SPOCK1 led to cell cycle arrest in G0/G1 phase and increased the proportion of apoptotic PDAC cells by regulating members of the caspase and Bcl‐2 families. Our data proved that SPOCK1 is a critical regulator of tumor proliferation and metastasis in PDAC cells. Therefore, SPOCK1 might be a potential prognostic and therapeutic target molecule in PDAC.

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Optimizing the outcomes of pancreatic cancer surgery

Cited by 656 publications

References 125 publications

DRP1 upregulation promotes pancreatic cancer growth and metastasis through increased aerobic glycolysis

DRP1 upregulation promotes pancreatic cancer growth and metastasis through increased aerobic glycolysis

Local radicality and survival outcome of pancreatic cancer surgery

A potential prognostic marker and therapeutic target: SPOCK1 promotes the proliferation, metastasis, and apoptosis of pancreatic ductal adenocarcinoma cells

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