Pancreatic cancer

Güngör, Cenap; Hofmann, Bianca T.; Wolters‐Eisfeld, Gerrit; Bockhorn, Maximillian

doi:10.1111/bph.12401

Cited by 57 publications

(37 citation statements)

References 84 publications

(92 reference statements)

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“…Even with a low rate of new cases, the 7% 5-year survival rate makes pancreatic cancer the fourth leading cause of cancer-related death, and this 7% rate has not increased in the last 20 years [1,2,3,4]. PDAC is mostly treated by surgery, radiation, and chemotherapy, but only 15-20% of the patients can be successfully resected after diagnosis [5,6,7]. The lack of an effective therapy and the fact that PDAC is mostly diagnosed in advanced stages because of unspecific or late symptoms shows the need for screening programs for those high-risk individuals [8,9,10].…”

Section: Introductionmentioning

confidence: 99%

Familial Pancreatic Cancer

Benzel

Fendrich

2018

Oncol Res Treat

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Familial pancreatic cancer accounts for 10% of all patients with pancreatic cancer. Because the 5-year survival rate of pancreatic cancer is only 7%, screening programs for high-risk individuals are essential and might be advantageous. Pancreatic ductal adenocarcinoma mostly shows symptoms at an advanced state and treatment is not efficient enough to cure most patients. People with hereditary tumor syndromes or their affected relatives can also be included in such screening programs. Besides the collection of data to investigate the background of the disease, these screening programs aim to diagnose and treat precursor lesions so that more dangerous, invasive lesions are prevented. These precursor lesions can be pancreatic intraepithelial neoplasia, intraductal papillary mucinous neoplasm, and mucinous cystic neoplasm. This review summarizes the latest knowledge of pancreatic screening programs, shows the procedure of pancreatic cancer screening, and gives an overview of current guidelines.

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Section: Introductionmentioning

confidence: 99%

Familial Pancreatic Cancer

Benzel

Fendrich

2018

Oncol Res Treat

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“…Este tipo de cáncer tiene un mal pronóstico debido al diagnóstico tardío y al uso de tratamientos multimodales ineficaces 1,2 . Este mal pronóstico se ha atribuido a la desregulación de unas secuencias cortas de ARN de aproximadamente 19-21 nucleótidos de longitud, llamados microARN (miARN), los cuales regulan la expresión de proteí-nas clave que intervienen en diversos procesos celulares 3,4 .…”

Section: Introductionunclassified

Desregulación de microARN específicos en la progresión del cáncer de páncreas

Tume

Aquino-Ordinola

2015

Gaceta Mexicana de Oncología

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“…In PDAC, successive gene mutations and protein expression changes occur at various phases of tumorigenesis, including precursor conditions. Three premalignant precursor lesions of PDAC with different histological subtypes have been identified and are termed pancreatic intraepithelial neoplasia (PanIN), intraductal pancreatic mucinous neoplasia (IPMN), and mucinous cystic neoplasia (MCN) . PanIN is considered the most common precursor of PDAC, along with KRAS mutations, which occur in more than 90% of patients with PDAC and can be detected in the early PanIN stage .…”

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confidence: 99%

PRDM14 is overexpressed in chronic pancreatitis prior to pancreatic cancer

2018

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Pancreatic ductal adenocarcinoma ( PDAC ) is an aggressive and lethal cancer that is typically diagnosed at a later stage with metastases and is difficult to treat. Therefore, investigating the mechanism of PDAC initiation is important to aid early‐stage cancer detection. PRDM 14 is a transcription factor that maintains pluripotency in embryonic stem cells and is overexpressed in several cancers. We previously reported that PRDM 14 is overexpressed and regulates cancer stem‐like phenotypes in PDAC , and herein, we assess whether PRDM 14 expression increases prior to tumorigenesis. Through immunohistochemistry analyses of clinical tissues, we detected PRDM 14‐positive cells in precursor pancreatic intraepithelial neoplasia and chronic pancreatitis, which is a risk factor for PDAC , lesions. PRDM 14 staining in chronic pancreatitis was as high as that in PDAC and cancer adjacent tissues. We induced pancreatitis in mouse models by cerulein injection, and observed that PRDM 14 expression increased in chronic pancreatitis models but not in control or acute pancreatitis mice. Moreover, cerulein treatment increased PRDM 14 expression in PK ‐1 and As PC ‐1 pancreatic cancer cell lines. Our results suggest that inflammation increases the expression of PRDM 14, which regulates cancer stem‐like phenotypes, and this occurs prior to PDAC initiation and progression.

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Pancreatic cancer

Abstract: This article is part of a themed section on Midkine. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2014.171.issue-4.

Cited by 57 publications

References 84 publications

Familial Pancreatic Cancer

Familial Pancreatic Cancer

Desregulación de microARN específicos en la progresión del cáncer de páncreas

PRDM14 is overexpressed in chronic pancreatitis prior to pancreatic cancer

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