Gastrointestinal hormones as potential adjuvant treatment of exocrine pancreatic adenocarcinoma

Fisher, William E.; Muscarella, Peter; Boros, László G.; Schirmer, William J.

doi:10.1007/bf02788419

Cited by 13 publications

(3 citation statements)

References 71 publications

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“…Somatostatin receptors also may play an important role in regulating apoptosis in combination with tumor necrosis factors (TNFs) [120, 121]. Activation of the somatostatin pathway has shown potential for use as adjuvant therapy in pancreatic cancer and has inhibited tumor growth in animal models [114, 122]. Moreover, transfection of pancreatic cancer cells with somatostatin receptor (SSTR)‐1 or SSTR‐2 inhibits proliferation and increases susceptibility to treatment with somatostatin analogues [117, 118].…”

Section: Pdx‐1 Embryologic Transcription Factors and Pancreatic Cancermentioning

confidence: 99%

“…In addition to its relationship with the pathways listed above, PDX-1 also interacts with the somatostatin pathway which also plays a key role in pancreatic cancer. The somatostatin signaling pathway has been shown to downregulate the growth of pancreatic cancer [113][114][115][116].…”

Section: Pdx-1 Embryologic Transcription Factors and Pancreatic Cancermentioning

confidence: 99%

“…In addition to its relationship with the pathways listed above, PDX‐1 also interacts with the somatostatin pathway which also plays a key role in pancreatic cancer. The somatostatin signaling pathway has been shown to downregulate the growth of pancreatic cancer [113–116]. Somatostatin receptors are G‐protein‐coupled receptors that control pathways responsible for cell growth and proliferation, with both SSTR1 and SSTR2 transfection into pancreatic cancer cells leading to decreased cell growth [117–119].…”

Section: Pdx‐1 Embryologic Transcription Factors and Pancreatic Cancermentioning

confidence: 99%

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Defining the Cancer Master Switch

et al. 2011

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Defining useful targets for therapy depends on identifying pathways that are crucial for tumor growth, survival, and metastasis. Because not all signaling cascades are created equal, selecting master switches or targets for intervention needs to be done in a systematic fashion. This discussion proposes a set of criteria to define what it means to be a cancer master switch and provides examples to illustrate their application.

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Section: Pdx‐1 Embryologic Transcription Factors and Pancreatic Cancermentioning

confidence: 99%

Section: Pdx-1 Embryologic Transcription Factors and Pancreatic Cancermentioning

confidence: 99%

Section: Pdx‐1 Embryologic Transcription Factors and Pancreatic Cancermentioning

confidence: 99%

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Defining the Cancer Master Switch

et al. 2011

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Gastrointestinal carcinoid tumors and second primary malignancies

2000

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The development of second primary malignancies (SPM) in patients with gastrointestinal carcinoid tumors is a well-described phenomenon, with reported rates as high as 55%. There is a predilection for gastrointestinal and genitourinary adenocarcinomas, but a variety of other malignancies have been reported as well. The etiology of this malignant predisposition may be rooted in the tumorigenic properties of the various neuroendocrine peptides elaborated and secreted by neuroendocrine cells. Peptides such as secretin, gastrin, bombesin, cholecystokinin (CCK), and vasoactive intestinal peptide (VIP) are believed to promote the growth of tumor cells. As many as 30 peptides and amines identified in neuroendocrine cells may have similar properties. This review of the literature on carcinoid-associated second primary malignancies is accompanied by a case report of metastatic carcinoid identified during surgical exploration for a perforating colon adenocarcinoma.

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G protein-coupled receptor signaling in human ductal pancreatic cancer cells: Neurotensin responsiveness and mitogenic stimulation

Ryder¹,

Guha²,

Hines³

et al. 2000

J. Cell. Physiol.

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Neuropeptides and their corresponding G protein-coupled receptors (GPCRs) are increasingly implicated in the autocrine/paracrine stimulation of growth of human cancers. We report that neurotensin induced rapid Ca2+ mobilization from intracellular stores followed by Ca2+ influx in five human ductal pancreatic cancer cell lines: HPAF-II, Capan-1, Capan-2, PANC-1, and MIA PaCa-2. In addition, most cell lines exhibited Ca2+ responses to multiple neuropeptides including bombesin, bradykinin, cholecystokinin, and vasopressin and to bioactive lipids, including lysophosphatidic acid (LPA), that also act via GPCRs. The well-differentiated line HPAF-II responded to at least seven independent GPCR agonists. The concentrations of neurotensin required to induce half-maximal effects (EC50) in HPAF-II and PANC-1 cells were 5 and 8nM, respectively. Digital fluorescence image analysis to measure Ca2+ responses in single cells revealed that 90% or more of HPAF-II and PANC-1 cells responded to 10nM neurotensin. Addition of neurotensin to PANC-1 cells also induced rapid and dose-dependent extracellular-regulated protein kinase (ERK-1 and ERK-2) activation and subsequently, stimulated DNA synthesis. The signaling complexity of GPCRs uncovered by these studies reveals a new aspect in the biology of human pancreatic cancer and could offer the basis for new approaches to the treatment of this disease.

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Gastrointestinal hormones as potential adjuvant treatment of exocrine pancreatic adenocarcinoma

Cited by 13 publications

References 71 publications

Defining the Cancer Master Switch

Defining the Cancer Master Switch

Gastrointestinal carcinoid tumors and second primary malignancies

G protein-coupled receptor signaling in human ductal pancreatic cancer cells: Neurotensin responsiveness and mitogenic stimulation

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