Antihypertensives as Novel Antineoplastics: Angiotensin-I-Converting Enzyme Inhibitors and Angiotensin II Type 1 Receptor Blockers in Pancreatic Ductal Adenocarcinoma

Arafat, Hwyda A.; Gong, Qiaoke; Chipitsyna, Galina; Rizvi, Asim; Saa, Chai T.; Yeo, Charles J.

doi:10.1016/j.jamcollsurg.2007.01.067

Cited by 104 publications

(101 citation statements)

References 39 publications

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“…Consistent with a previous report (Arafat et al 2007), the present study showed high levels of ACE in PDAC tissues. ANG II was mainly from ANG I catalyzed by ACE, and we also found the ANG II concentration was higher in the homogenate of PDAC tissues than adjacent TF tissues.…”

Section: Discussionsupporting

confidence: 94%

“…The expression of many components of the RAS in various cancers, including cancers of the pancreas, brain, lung, breast, prostate, skin, and cervix, and glioblastoma, has been previously demonstrated (Arafat et al 2007). In carcinogenesis, the ACE-ANG II-AT1R signaling pathway is associated with cell proliferation, angiogenesis, inflammation, and metastasis.…”

Section: Discussionmentioning

confidence: 96%

“…ACE and AT1R are overexpressed in the majority (approximately 75%) of PDAC patients. ACE is preferentially expressed in PDAC (Arafat et al 2007), and ACE exerts an important role in the occurrence of PDAC through the formation of ANG II. Evidence for the involvement of the ACE-ANG II-AT1R pathway in the pathogenesis of PDAC, such as growth, metastasis, and angiogenesis, has accumulated in recent reports (Egami et al 2003;Arrieta et al 2005).…”

mentioning

confidence: 99%

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Decreased Expression of Angiotensin-Converting Enzyme 2 in Pancreatic Ductal Adenocarcinoma Is Associated with Tumor Progression

Zhou

Zhang

Yao

et al. 2009

Tohoku J. Exp. Med.

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Section: Discussionsupporting

confidence: 94%

Section: Discussionmentioning

confidence: 96%

mentioning

confidence: 99%

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Decreased Expression of Angiotensin-Converting Enzyme 2 in Pancreatic Ductal Adenocarcinoma Is Associated with Tumor Progression

Zhou

Zhang

Yao

et al. 2009

Tohoku J. Exp. Med.

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“…35 Indeed, ACE and AT 1 receptor mRNA and protein levels were significantly upregulated in 19 of the 25 neoplastic tissues examined (approximately 75%), when compared with matching controls. VEGF expression was significantly higher in tissues that expressed high levels of AT 1 receptor and ACE, compared with low levels or negative cases.…”

Section: Renal Cell Carcinomamentioning

confidence: 93%

“…Addition of Ang II significantly enhanced VEGF mRNA production and protein secretion, an effect that was prevented when cells were preincubated with captopril or losartan. 35 Colon cancer Ang II receptors were detected on cells of three colorectal carcinoma cell lines. The binding assays with 125 I-labelled Ang II and ligands specific for AT 1 and AT 2 receptors showed that Ang II receptors on colorectal cancer cells are mostly of the AT 2 type.…”

Section: Renal Cell Carcinomamentioning

confidence: 99%

Angiotensin inhibition and malignancies: a review

Rosenthal

Gavras

2009

J Hum Hypertens

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After an early report that patients treated with angiotensin-converting enzyme (ACE) inhibitors had a lower than expected incidence of cancers, there was a large number of publications investigating the possible pathophysiological mechanism mediating this effect, as well as population studies comparing the incidence of cancers in patients treated with agents inhibiting the reninangiotensin system with their incidence in the general population. Several mechanisms are proposed to explain a potential anti-tumour activity of such agents in vitro in experimental animal models. However, the population studies are mostly inconclusive, although they do suggest a possible interaction between ACE genotypes and susceptibility to altered behaviour of certain tumours.

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Associations between genetically predicted levels of blood metabolites and pancreatic cancer risk

Zhong

Liu

Zhu

et al. 2023

Intl Journal of Cancer

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Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive solid malignancies, which is featured by systematic metabolism. Thus, a better understanding of metabolic dysregulation in PDAC is important to better characterize its etiology. Here, we performed a large metabolome-wide association study (MWAS) to systematically explore associations between genetically predicted metabolite levels in blood and PDAC risk. Using data from 881 subjects of European descent in the TwinsUK Project, comprehensive genetic models were built to predict serum metabolite levels. These prediction models were applied to the genetic data of 8275 cases and 6723 controls included in the PanScan (I, II and III) and PanC4 consortia. After assessing the metabolite-PDAC risk associations by a slightly modified TWAS/FUSION framework, we identified five metabolites (including two dipeptides) showing significant associations with PDAC risk at false discovery rate (FDR) <0.05. Integrated with gut microbial information, two-sample Mendelian randomization (MR) analyses were further performed to investigate the relationship among serum metabolites, gut microbiome features and PDAC. The flavonoid-degrading bacteria Flavonifractor sp90199495 was found to be associated with metabolite X-21849 and it was also shown to be associated with PDAC risk. Collectively, our study identified novel candidate metabolites for PDAC risk, which could lead to new insights into the etiology of PDAC and improved treatment options.

show abstract

Antihypertensives as Novel Antineoplastics: Angiotensin-I-Converting Enzyme Inhibitors and Angiotensin II Type 1 Receptor Blockers in Pancreatic Ductal Adenocarcinoma

Cited by 104 publications

References 39 publications

Decreased Expression of Angiotensin-Converting Enzyme 2 in Pancreatic Ductal Adenocarcinoma Is Associated with Tumor Progression

Decreased Expression of Angiotensin-Converting Enzyme 2 in Pancreatic Ductal Adenocarcinoma Is Associated with Tumor Progression

Angiotensin inhibition and malignancies: a review

Associations between genetically predicted levels of blood metabolites and pancreatic cancer risk

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