Functional role of matrix metalloproteinases in ovarian tumor cell plasticity

Sood, Anil K.; Fletcher, Mavis S.; Coffin, Jeremy E.; Yang, Maria C.; Seftor, Elisabeth A.; Gruman, Lynn M.; Gershenson, David M.; Hendrix, Mary J.C.

doi:10.1016/j.ajog.2004.02.011

Cited by 93 publications

(88 citation statements)

References 53 publications

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“…Hess et al (32) reported that blocking the action of tyrosine protein kinase and knocking out EphA2 can prevent the formation of VM. Sood et al (8) and Seftor et al (33) proposed that antibodies to MMPs and the laminin 5 gamma 2 chain could be used to treat tumors with VM. Chemically modified tetracycline COL-3, introduced by Seftor et al (29), can restrain the expression of genes involved in invasion and metastasis and may be useful in preventing tumors from developing vessels by VM.…”

Section: Discussionmentioning

confidence: 99%

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Vasculogenic mimicry is associated with high tumor grade, invasion and metastasis, and short survival in patients with hepatocellular carcinoma

Sun

Zhang²,

Zhang³

et al. 2006

Oncol Rep

118

124

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Abstract. Vasculogenic mimicry (VM) has increasingly been recognized as a form of angiogenesis. In VM, epithelial cells are integrated into the malignant tumor vasculature. An association has been observed between VM and poor clinical prognosis in some malignant tumors. However, whether VM is present and clinically significant in hepatocellular carcinoma (HCC) is unknown. In this study, we determined whether VM was present in HCC and whether it was associated with tumor grade, invasion and metastasis, and survival duration. We collected paraffin-embedded HCC tumor samples, along with complete clinical and pathologic data for all the cases, and performed immunohistochemical staining for CD31, CD105 (endoglin), hepatocyte, vascular endothelial growth factor, matrix metalloproteinase (MMP)-2, and MMP-9. The VM status was compared with the clinical and pathological data using statistical tests. Kaplan-Meier survival analysis and log-rank test were used to compare survival durations between patients with and without VM. The VM vessel cells were CD31 and CD105-negative and hepatocyte and vascular endothelial growth factor-positive, showing that they were not derived from endothelial cells but were HCC tumor cells. Patients with VM had a higher metastasis rate than did those without VM (P=0.003). Consistent with this finding, MMP-2 and MMP-9 were present in all the VM cases but were found less frequently in non-VM cases (P<0.05). The Kaplan-Meier survival analysis showed that patients in the VM group had a significantly shorter survival duration than did those in the non-VM group. In conclusion, VM is a marker of poor clinical prognosis in HCC: Its presence may be associated with a high tumor grade, invasion and metastasis, and short survival.

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Section: Discussionmentioning

confidence: 99%

“…VM has been reported in inflammatory breast cancer (6), prostate cancer (7), invasive ovarian cancer (8), sarcoma (9), and astrocytoma (10). VM is also involved in the invasion and metastasis of malignant tumors (6,7,11) and has been associated with poor prognosis in melanoma and sarcomas (8,9).…”

Section: Introductionmentioning

confidence: 99%

Vasculogenic mimicry is associated with high tumor grade, invasion and metastasis, and short survival in patients with hepatocellular carcinoma

Sun

Zhang²,

Zhang³

et al. 2006

Oncol Rep

118

124

View full text Add to dashboard Cite

show abstract

“…3,4 Since its discovery, VM has been described in many kinds of tumors, such as melanoma, 5 synovial sarcoma, 6 rhabdomyosarcoma, 6 osteosarcoma, 7 inflammatory and ductal breast carcinoma 8 and ovarian carcinoma. 9,10 Most of these studies have shown some association between angiogenesis or VM proliferation in relationship with the aggressiveness of the tumor. Therapeutic implications of VM have also been described in aggressive prostate cancer (PCa) in vitro.…”

Section: Introductionmentioning

confidence: 99%

Vasculogenic mimicry is a marker of poor prognosis in prostate cancer

Liu

Yang

Meng

et al. 2012

Cancer Biology & Therapy

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“…5,6 Our laboratory has begun to examine this process in detail using various strategies, resulting in the identification of several key signal transduction molecules critical for VM. 7,8 Anti-angiogenesis is a useful anticancer therapy that is widely accepted as a means for aggressive tumor therapy. However, recent findings have shown that routine single-targeted therapies using antiangiogenic drugs, such as angiostatin, endostatin and bevacizumab, which target endothelial cells have little effect on tumors exhibiting VM because of the absence of endothelial cells.…”

Section: Introductionmentioning

confidence: 99%