Antiangiogenic cancer treatment: The great discovery and greater complexity (Review)

Maj, Ewa; Papiernik, Diana; Wietrzyk, Joanna

doi:10.3892/ijo.2016.3709

Cited by 119 publications

(98 citation statements)

References 115 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The first concept of antiangiogenic therapy aimed to destroy tumour vessels, while it turned out that, paradoxically, antiangiogenic drugs normalised vasculature and as a result offered an improvement in chemotherapeutic delivery [13, 14]. The results of the present study support the positive importance of the normalisation of tumour vasculature rather than destruction.…”

Section: Discussionsupporting

confidence: 71%

The changes of tumour vascular endothelial growth factor expression after neoadjuvant chemoradiation in patients with rectal adenocarcinoma

Buka

Dvořák

Sitorová

et al. 2017

View full text Add to dashboard Cite

Aim of the studyThe aim was to examine the effects of neoadjuvant chemoradiotherapy on VEGF expression in patients with locally advanced rectal cancer.Materials and methodsA total of 53 patients with locally advanced rectal cancer were retrospectively studied. Neoadjuvant treatment comprised external beam radiation (50.4 Gy/28 fractions) with continuous infusion of 5-fluorouracil. Four to 6 weeks after the chemoradiotherapy, the patients underwent surgical resection. Immunohistochemistry was performed to assess VEGF expression in the pretreatment biopsies and in resected specimens.ResultsResection with microscopic residual tumour (R1) was performed in two patients while in the remaining 51 patients radical resection with microscopically negative margins (R0) was possible. Downstaging after preoperative chemoradiotherapy was observed in 34 patients (64%). After chemoradiotherapy 24 patients (45%) had decreased VEGF expression, in 20 patients (38%) there was no change, and in two patients it was not possible to assess the dynamics of VEGF expression due to pathologic complete response after chemoradiotherapy. The five-year overall survival (OS) rate was 56% (95% CI: 43–70%). Although the median OS was 2.5 times shorter in patients who experienced decreased VEGF expression during therapy, this difference did not reach statistical significance. VEGF expression was not significant in Cox regression analysis or log-rank test. VEGF expression decreased after neoadjuvant chemoradiotherapy in most patients with rectal adenocarcinoma examined. This decrease was associated with a trend of inferior prognosis.ConclusionsVEGF expression decreased after neoadjuvant chemoradiotherapy in most patients examined. This decrease was associated with a trend of inferior prognosis.

show abstract

Section: Discussionsupporting

confidence: 71%

The changes of tumour vascular endothelial growth factor expression after neoadjuvant chemoradiation in patients with rectal adenocarcinoma

Buka

Dvořák

Sitorová

et al. 2017

View full text Add to dashboard Cite

show abstract

“…The discovery of tumour angiogenesis opened a new path in fighting cancer that increased the effectiveness of standard chemotherapy, or even replaced it, by offering better patient outcomes [32]. Over the past decade, extensive studies of 3D cultures have demonstrated differences compared to the behaviour of cells on 2D surfaces [33].…”

Section: Discussionmentioning

confidence: 99%

Growth of MCF-7 breast cancer cells and efficacy of anti-angiogenic agents in a hydroxyethyl chitosan/glycidyl methacrylate hydrogel

et al. 2017

View full text Add to dashboard Cite

BackgroundBreast cancer negatively affects women’s health worldwide. The tumour microenvironment plays a critical role in tumour initiation, proliferation, and metastasis. Cancer cells are traditionally grown in two-dimensional (2D) cultures as monolayers on a flat solid surface lacking cell–cell and cell–matrix interactions. These experimental conditions deviate from the clinical situation. Improved experimental systems that can mimic the in vivo situation are required to discover new therapies, particularly for anti-angiogenic agents that mainly target intercellular factors and play an essential role in treating some cancers.MethodsChitosan can be modified to construct three-dimensional (3D) tumour models. Here, we report an in vitro 3D tumour model using a hydroxyethyl chitosan/glycidyl methacrylate (HECS–GMA) hydrogel produced by a series of chitosan modifications. Parameters relating to cell morphology, viability, proliferation, and migration were analysed using breast cancer MCF-7 cells. In a xenograft model, secretion of angiogenesis-related growth factors and the anti-angiogenic efficacy of Endostar and Bevacizumab in cells grown in HECS–GMA hydrogels were assessed by immunohistochemistry.ResultsHydroxyethyl chitosan/glycidyl methacrylate hydrogels had a highly porous microstructure, mechanical properties, swelling ratio, and morphology consistent with a 3D tumour model. Compared with a 2D monolayer culture, breast cancer MCF-7 cells residing in the HECS–GMA hydrogels grew as tumour-like clusters in a 3D formation. In a xenograft model, MCF-7 cells cultured in the HECS–GMA hydrogels had increased secretion of angiogenesis-related growth factors. Recombinant human endostatin (Endostar), but not Bevacizumab (Avastin), was an effective anti-angiogenic agent in HECS–GMA hydrogels.ConclusionsThe HECS–GMA hydrogel provided a 3D tumour model that mimicked the in vivo cancer microenvironment and supported the growth of MCF7 cells better than traditional tissue culture plates. The HECS–GMA hydrogel may offer an improved platform to minimize the gap between traditional tissue culture plates and clinical applicability. In addition, the anti-angiogenic efficacy of drugs such as Endostar and Bevacizumab can be more comprehensively studied and assessed in HECS–GMA hydrogels.

show abstract

“…It differs from other chemotherapeutic strategies by targeting the tumour vasculature rather than neoplastic cells. However, the response to anti‐angiogenic therapy is variable because angiogenic activity differs among tumour types and at different locations within the same tumour, caused, in part at least, by multiple vascularisation mechanisms being utilised at these different sites …”

Section: Control Of Angiogenesismentioning

confidence: 99%

Tumour angiogenesis, anti‐angiogenic therapy and chemotherapeutic resistance

Mander

Finnie

2018

Aust Veterinary J

View full text Add to dashboard Cite

In order for a tumour to continue to grow and disseminate, it must acquire a new blood supply. Neovascularisation can be enacted by a number of different mechanisms. This dependence of tumour progression on an augmented vascular supply has been exploited by the development of anti‐angiogenic drugs, which are designed to inhibit new blood vessel formation or disrupt existing tumour‐associated vasculature, both leading to ischaemic–hypoxic tumour cell death. However, the clinical benefits of these therapeutic approaches are frequently variable and often transient, the neoplasm sometimes being able to use other neovascularisation mechanisms to maintain its blood supply and thus evade the current anti‐angiogenic therapy. Tumours may also develop a more malignant phenotype following this treatment. Clinical outcomes may be improved by simultaneously inhibiting different angiogenic pathways, abetted by more effective drug delivery regimens such as metronomic chemotherapy and the concurrent use of other antitumour modalities.

show abstract

Antiangiogenic cancer treatment: The great discovery and greater complexity (Review)

Cited by 119 publications

References 115 publications

The changes of tumour vascular endothelial growth factor expression after neoadjuvant chemoradiation in patients with rectal adenocarcinoma

The changes of tumour vascular endothelial growth factor expression after neoadjuvant chemoradiation in patients with rectal adenocarcinoma

Growth of MCF-7 breast cancer cells and efficacy of anti-angiogenic agents in a hydroxyethyl chitosan/glycidyl methacrylate hydrogel

Tumour angiogenesis, anti‐angiogenic therapy and chemotherapeutic resistance

Contact Info

Product

Resources

About