Placenta growth factor expression is correlated with survival of patients with colorectal cancer

Wei, Shu–Chen; Tsao, Po‐Nien; Yu, Shan–Chi; Shun, Chia‐Tung; Tsai-Wu, Jyy-Jih; Wu, Chun‐Hsien; Su, Yi Ning; Hsieh, Fon‐Jou; Wong, Jau‐Min

doi:10.1136/gut.2004.050831

Cited by 99 publications

(90 citation statements)

References 37 publications

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“…This could be because most of the tumor tissues included in our study are from early-stage patients. This is in accordance with two recently published studies showing that PlGF expression correlates with microvessel density (19) and inversely correlates with disease progression and patient survival in non -small cell lung cancer and colorectal cancer (18).…”

Section: Discussionsupporting

confidence: 80%

“…In hypervascular germ cell tumors and hemangioblastoma tumors, VEGF is dramatically upregulated in the majority of tumors, whereas PlGF level is generally very low and is only detected in a small number of cases (14)(15)(16)(17). Several recent studies showed PlGF expression correlates with clinical prognosis in non -small cell lung cancer and in colorectal cancer (18,19). Furthermore, two recent clinical trials showed that PlGF levels are elevated in the plasma of colorectal and rectal carcinoma patients receiving bevacizumab or SU11248 (20,21).…”

Section: Introductionmentioning

confidence: 99%

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Down-Regulation of Placenta Growth Factor by Promoter Hypermethylation in Human Lung and Colon Carcinoma

Jain²

2007

Molecular Cancer Research

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Section: Discussionsupporting

confidence: 80%

Section: Introductionmentioning

confidence: 99%

Down-Regulation of Placenta Growth Factor by Promoter Hypermethylation in Human Lung and Colon Carcinoma

Jain²

2007

Molecular Cancer Research

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“…By upregulating PlGF, ECs amplify their responsiveness to VEGF during the 'angiogenic switch' in many pathological disorders. PlGF levels in plasma and tumors correlate with tumor stage, vascularity, recurrence, metastasis and survival in various tumors (48,49). Of note, PlGF is up-regulated after anti-VEGF therapy and gemcitabine (26,50,51).…”

Section: Discussionmentioning

confidence: 99%

Antiangiogenic versus cytotoxic therapeutic approaches in a mouse model of pancreatic cancer: An experimental study with a multitarget tyrosine kinase inhibitor (sunitinib), gemcitabine and radiotherapy

Casneuf

Demetter²,

Boterberg³

et al. 2009

Oncol Rep

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Abstract. This work evaluated SU11248 (sunitinib) as a potential therapeutic agent, alone or in combination with the cytotoxic agent gemcitabine or radiotherapy in a murine model of pancreatic cancer. Panc02 cells were injected subcutaneously into HsdOla/MF1 mice (n=222). Treatment was administered during 1 week: sunitinib (SUN), gemcitabine (GEM), radiotherapy (RT), RT+SUN and GEM+SUN. Mice were sacrificed 14 days after treatment. The effect on microvessel density (MVD) was measured by CD31 staining. Apoptosis (sFAS, cleaved caspase-3) and proangiogenic proteins (VEGF, PlGF, EGF) were measured with ELISA and immunohistochemistry. At day 14, tumors in all groups increased significantly despite treatment. Only after RT/SUN treatment tumor growth slowed down, although the accretion was still significant (P=0.033). Highest levels of apoptosis were seen in GEM/SUN, RT/SUN and RT treated mice (respectively P<0.001, P<0.01 and P<0.05 compared to placebo). MVD was lowest in RT/SUN treated mice [compared to placebo (P<0.05), GEM (P<0.05) and GEM/SUN (P<0.01)]. Highest VEGF levels were seen after RT and RT/SUN treatment [vs. placebo (P<0.001) and vs. other treatments (P<0.01 for all comparisons)]. GEM and SUN in monotherapy lead to an up-regulation of PlGF and EGF, respectively. In conclusion, the combination treatments RT/SUN and GEM/SUN result in a more potent antiangiogenic and antitumor effect when compared to either treatment alone. Multitargeted angiogenesis inhibitor therapy with sunitinib combined with either radiotherapy or gemcitabine may be a novel approach for human pancreatic cancer.

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“…Although expression of PlGF in tumor tissues was proposed as prognostic marker for progression and survival in gastric, colorectal, NSCLC, hepatocellular, and breast cancer (Parr et al 2005, Wei et al 2005, Fischer et al 2008, relatively few studies evaluated circulating levels of PlGF. Results linked high circulating PlGF to adverse prognosis in renal (Matsumoto et al 2003) and oral squamous cell carcinoma (Cheng et al 2012) but not in hepatocellular cancer (Nagaoka et al 2010), and high preoperative PlGF levels predicted reduced recurrence-free and overall survival in colorectal cancer patients undergoing curative surgery (Wei et al 2009, Rahbari et al 2011.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, PlGF expression in tumor tissue and/or circulating PlGF levels correlated with tumor stage, vascularity, metastasis, survival, and recurrence in several human malignancies (Parr et al 2005, Wei et al 2005, Fischer et al 2008, Maae et al 2012. Moreover, PlGF induction occurred as a result of antiangiogenic therapies in human cancer patients and in mouse models, and (in the latter situation) constituted a functionally relevant mechanism of resistance development (Batchelor et al 2007, Fischer et al 2007, Rini et al 2008, Willett et al 2009).…”

Section: Introductionmentioning

confidence: 99%

Placental growth factor supports neuroendocrine tumor growth and predicts disease prognosis in patients

Hilfenhaus¹,

Göhrig²,

Pape³

et al. 2013

Endocrine-Related Cancer

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Placental growth factor (PlGF), a VEGF-homolog implicated in tumor angiogenesis and adaptation to antiangiogenic therapy, is emerging as candidate target in malignancies. Here, we addressed the expression, function, and prognostic value of PlGF in neuroendocrine tumors (NETs). PlGF was determined in NET patients' sera collected retrospectively (n=88) and prospectively (n=87) using Roche-Elecsys and correlated with clinicopathological data. Tumoral PlGF was evaluated by immunohistochemistry, effects of PlGF on proliferation and migration in vitro were assessed using different NET cell lines and effects on tumor growth in vivo in orthotopic xenografts. Circulating and tumoral PlGF was elevated in patients with pancreatic NETs (pNETs) compared with control sera and respective healthy tissue. De novo PlGF expression occurred primarily in the tumor stroma, suggesting paracrine stimulatory circuits. Indeed, PlGF enhanced NET proliferation and migration in vitro and, conversely, neutralizing antibodies to PlGF reduced tumor growth in vivo. Elevated circulating PlGF levels in NET patients correlated with advanced tumor grading and were associated with reduced tumor-related survival in pNETs. Subsequent determinations confirmed and extended our observation of elevated PlGF levels in a prospective cohort of grade 1 and grade 2 pNETs (n=30) and intestinal NETs (n=57). In low-grade pNETs, normal circulating PlGF levels were associated with better survival. In intestinal NETs, circulating PlGF above median emerged as an independent prognostic factor for shorter time-to-progression in multivariate analyses. These data assign to PlGF a novel function in the pathobiology of NETs and propose PlGF as a prognostic parameter and therapeutic target.

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Placenta growth factor expression is correlated with survival of patients with colorectal cancer

Cited by 99 publications

References 37 publications

Down-Regulation of Placenta Growth Factor by Promoter Hypermethylation in Human Lung and Colon Carcinoma

Down-Regulation of Placenta Growth Factor by Promoter Hypermethylation in Human Lung and Colon Carcinoma

Antiangiogenic versus cytotoxic therapeutic approaches in a mouse model of pancreatic cancer: An experimental study with a multitarget tyrosine kinase inhibitor (sunitinib), gemcitabine and radiotherapy

Placental growth factor supports neuroendocrine tumor growth and predicts disease prognosis in patients

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