Relevant bibliographies by topics / Vascular Co-option

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters

Academic literature on the topic 'Vascular Co-option'

Author: Grafiati
Published: 22 February 2025

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Journal articles on the topic "Vascular Co-option"

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García-Gómez, Pedro, and Manuel Valiente. "Vascular co-option in brain metastasis." Angiogenesis 23, no. 1 (November 7, 2019): 3–8. http://dx.doi.org/10.1007/s10456-019-09693-x.

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Takano, Shingo, Toshihide Tanaka, Eiichi Ishikawa, Youhei Yamamoto, Jun Takai, Masahide Matsuda, Takao Tsurubuchi, Hiroyoshi Akutsu, and Akira Matsumura. "ANGI-05 PATHOGENESIS OF RESISTANCE (MIMICRY AND CO-OPTION) TO ANTI-ANGIOGENIC TREATMENT FOR GLIOBLASTOMA." Neuro-Oncology Advances 1, Supplement_2 (December 2019): ii5. http://dx.doi.org/10.1093/noajnl/vdz039.020.

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Abstract PURPOSE Vessel co-option and vascular mimicry are important resistant factors with ant-angiogenic treatment for glioblastoma, but those precise evaluation is not clear. We had three types of glioblastoma surgically removed specimens treated with / without bevacizumab (Bev). Using these samples, pathogenesis of co-option and mimicry was morphometrically clarified. MATERIALS / METHODS Three types of glioblastoma specimens were analyzed; 1) Bev naive (N group, n 14), 2) Bev effective that was treated preoperative neoadjuvant Bev (E group, n 5), 3) Bev refractory that recurred with continuous Bev treatment for paired E group (R group, n 5). Vascular density was defined as a number of type IV collagen covered lumen. Vascular mimicry was measured as a ratio of CD34 negative / type IV collagen positive lumen. Vessel co-option was graded to 3 degrees (-), (+), (++) at tumor margin. RESULTS (1)Vascular density was significantly lower with E group (p<0.01) and R gr up (p<0.02) compared to N group. (2)Mimicry was significantly higher with R group compared to N and E group (p<0.01). Between paired samples, refractory case was constantly higher than effective sample. (3) Co-option was increases with R group compared to N group. DISCUSSION/CONCLUSION The effect of Bev for glioblastoma was investigated on three points (vascular density, vascular mimicry and vessel co-option) and two pathogeneses were clarified. In Bev refractory case, density was decreased, but mimicry and co-option were increased compared to Bev naive case. In Bev effective case, density was decreased, but mimicry and co-option were unchanged. Anti-angiogenic treatment for initial and Bev refractory glioblastoma should consider targeting co-option and mimicry in addition to Bev.
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Dudley, Andrew C. "Introduction to special issue: vascular co-option in cancer." Angiogenesis 23, no. 1 (December 4, 2019): 1–2. http://dx.doi.org/10.1007/s10456-019-09699-5.

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Berghoff, Anna Sophie, Orsolya Rajky, Frank Winkler, Michael Weller, Christoph Zielinski, Jens Schittenhelm, and Matthias Preusser. "Evaluation of invasion patterns and their correlation with integrin alphavbeta expression in brain metastases of solid cancers." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): 2059. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.2059.

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2059 Background: Understanding the pathobiology of brain metastases (BM) could guide the establishment of new targeted therapies. Methods: We collected 57 autopsy specimens of BM (primary tumor: 27 lung cancer, 6 breast cancer, 8 melanoma, 1 kidney cancer, 2 colorectal cancer, 13 other) and histologically evaluated the patterns of invasion into the surrounding brain parenchyma. Expression of the following integrins was evaluated using immunohistochemistry: with novel antibodies for αv subunit, αvβ3, αvβ5, αvβ6 and αvβ8 integrin. Results: We observed three main invasion patterns: well-demarcated (29/57, 51%), vascular co-option (10/57, 18%) and diffuse infiltration (18/57, 32%). There was no association of invasion pattern with primary tumor type, although vascular co-option was most common in melanomas (4/10, 40%). αv subunit expression was lowest in the vascular co-option group (p = 0.05, t-test). αvβ6 levels were higher in the well-demarcated group than in the vascular co-option group (p = 0.025; t-test) and were higher in lung cancer BM than in melanoma BM (0.01, t-test). αvβ3 and αvβ5 were frequently expressed in tumoral (αvβ3: 30/57, 53%; αvβ5: 55/57, 97%) and peritumoral (αvβ3: 29/57, 51%, αvβ5: 54/57 (95%) vascular structures and 27/57 (47%) specimens showed avb5 and 6/57 (11%) αvβ3 expression on tumor cells. Prior radio- or chemotherapy did not correlate with invasion pattern or integrin expression. Conclusions: We delineate three distinct invasion patterns of BM into the brain parenchyma: well-demarcated growth, vascular co-option and diffuse infiltration. Integrin expression is frequent on tumor and vascular cells in BM and associated with distinct invasion patterns. Anti-integrin therapy could be a valid treatment option in patients with BM.
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Annese, Tiziana, Mariella Errede, Antonio d’Amati, Michelina De Giorgis, Loredana Lorusso, Roberto Tamma, and Domenico Ribatti. "Differential P-Glycoprotein/CD31 Expression as Markers of Vascular Co-Option in Primary Central Nervous System Tumors." Diagnostics 12, no. 12 (December 10, 2022): 3120. http://dx.doi.org/10.3390/diagnostics12123120.

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Background: Vascular co-option is one of the main features of brain tumor progression. It is identified using histopathological analysis, but no antibody-specific markers were found, and no universally accepted histological features were defined. Methods: We employed double immunohistochemical stainings for CD31, P-gp, S100A10, and mitochondria on formalin-fixed, paraffin-embedded human samples of IDH-WT glioblastoma, IDH-mutant astrocytoma, and meningioma to study vascular co-option across different brain tumors and across normal, peritumoral, and intratumoral areas using the Aperio colocalization algorithm, which is a valid and robust method to handle and investigate large data sets. Results: The results have shown that (i) co-opted vessels could be recognized by the presence of metabolically overactive (evaluated as mitochondria expression) and P-gp+ or S100A10+ tumor cells surrounding CD31+ endothelial cells; (ii) vascular co-option occurs in the intratumoral area of meningioma and astrocytoma; and (iii) vascular co-option is prevalent in peritumoral glioblastoma area. Conclusions: The described approach identifies new markers for cellular components of the vessel wall and techniques that uncover the order and localization of vascularization mechanisms, which may contribute to developing new and possibly more effective therapeutic strategies.
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García-Gómez, Pedro, Diana Retana, Pablo Sanz-Martínez, Irene Salgado-Crespo, Carolina Hernández-Oliver, Maria Isabel García, Oliva Sánchez, et al. "Abstract 3516: Metastatic colonization requires a proliferative pause linked to vascular co-option." Cancer Research 83, no. 7_Supplement (April 4, 2023): 3516. http://dx.doi.org/10.1158/1538-7445.am2023-3516.

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Abstract The physical interaction between metastasis-initiating cells and the pre-existing capillary network (a process known as vascular co-option) is critical during the initial stages of multi-organ metastasis in cancer. As such, this process might provide an opportunity to prevent metastasis. As part of the process of vascular co-option, we observed that brain metastatic cells in the perivascular niche temporarily enter into a novel cell state characterized by a decreased proliferation before resuming their aggressive growth to colonize the organ. Transcriptomic analysis of co-opting metastatic cells confirmed downregulation of MYC signatures, mitotic cell cycle and increased stemness properties. By focusing on one of the top upregulated transcription factors in co-opting cells: MXD4, a MYC antagonist; we have been able to dissect the relevance of this cellular state, that we termed proliferative pause, both respect to the maintenance of the interaction with the vasculature and to the ability to generate macrometastases. As such, targeting MXD4 in lung adenocarcinoma and triple-negative breast cancer metastatic models reduced multi-organ metastases to a level that translates into increased overall survival. Mechanistically, this obliged proliferative pause is linked to a cellular response to the increasing environmental pressure involved in organ colonization. For instance, we found that crossing the blood-brain barrier induced an increased DNA damage due to mechanical constrains leading to nuclear deformation. However, the MXD4-dependent proliferative pause during vascular co-option allows metastatic cells to repair this damage to continue the colonization process. Given the enormous potential to prevent metastasis and our findings dissecting the proliferative pause status, we developed a therapeutic strategy to target vascular co-opting cells. As part of the molecular profile of co-opting cells, we validated their high dependency on Bcl proteins. As such, we have used a Bcl-2 inhibitor (obatoclax) permeable to the blood-brain barrier to target these cells in preventive scenarios. Beyond the preventive therapeutic assays in vivo, we have applied additional clinically-relevant models where preventive strategies could easily translate into the clinical practice. As such, obatoclax post-surgery provided a survival benefit by preventing relapse, as the cells left behind after the local therapy are vascular co-opting cells. Furthermore, our national network of brain metastasis (RENACER) provided us with fresh neurosurgeries and, in a limited cohort of 10 surgeries with extended resections, we were able to identify invasive fronts with metastatic cells co-opting the vasculature. The use of obatoclax to target these cancer cells, which are the seeds of relapse post-surgery, confirmed that targeting vascular co-option could be a novel strategy to prevent metastasis in a clinically relevant situation. Citation Format: Pedro García-Gómez, Diana Retana, Pablo Sanz-Martínez, Irene Salgado-Crespo, Carolina Hernández-Oliver, Maria Isabel García, Oliva Sánchez, Kevin Troulé-Lozano, Verona Villar-Cerviño, Miguel Lafarga-Coscojuela, Fátima Al-Shahrour, RENACER Red Nacional de Metástasis Cerebral, Manuel Valiente. Metastatic colonization requires a proliferative pause linked to vascular co-option [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 3516.
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Valiente, Manuel, Anna C. Obenauf, Xin Jin, Qing Chen, Xiang H. F. Zhang, Derek J. Lee, Jamie E. Chaft, et al. "Serpins Promote Cancer Cell Survival and Vascular Co-Option in Brain Metastasis." Cell 156, no. 5 (February 2014): 1002–16. http://dx.doi.org/10.1016/j.cell.2014.01.040.

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Qi, Ming-Hao, Jing-Tao Li, and Bo Zhai. "Mechanisms of vascular co-option as a potential therapeutic target in hepatocellular carcinoma." World Chinese Journal of Digestology 32, no. 11 (November 28, 2024): 827–34. http://dx.doi.org/10.11569/wcjd.v32.i11.827.

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Mandelcorn, Efrem D., Alan G. Palestine, Sandor Dubovy, and Janet L. Davis. "Vascular co-option in lung cancer metastatic to the eye after treatment with bevacizumab." Journal of Ophthalmic Inflammation and Infection 1, no. 1 (November 17, 2010): 35–38. http://dx.doi.org/10.1007/s12348-010-0013-7.

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Ribatti, Domenico, and Francesco Pezzella. "Overview on the Different Patterns of Tumor Vascularization." Cells 10, no. 3 (March 13, 2021): 639. http://dx.doi.org/10.3390/cells10030639.

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Angiogenesis is a crucial event in the physiological processes of embryogenesis and wound healing. During malignant transformation, dysregulation of angiogenesis leads to the formation of a vascular network of tumor-associated capillaries promoting survival and proliferation of the tumor cells. Starting with the hypothesis formulated by Judah Folkman that tumor growth is angiogenesis-dependent, this area of research has a solid scientific foundation and inhibition of angiogenesis is a major area of therapeutic development for the treatment of cancer. Over this period numerous authors published data of vascularization of tumors, which attributed the cause of neo-vascularization to various factors including inflammation, release of angiogenic cytokines, vasodilatation, and increased tumor metabolism. More recently, it has been demonstrated that tumor vasculature is not necessarily derived by endothelial cell proliferation and sprouting of new capillaries, but alternative vascularization mechanisms have been described, namely vascular co-option and vasculogenic mimicry. In this article, we have analyzed the mechanisms involved in tumor vascularization in association with classical angiogenesis, including post-natal vasculogenesis, intussusceptive microvascular growth, vascular co-option, and vasculogenic mimicry. We have also discussed the role of these alternative mechanism in resistance to anti-angiogenic therapy and potential therapeutic approaches to overcome resistance.
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Dissertations / Theses on the topic "Vascular Co-option"

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Kerherve, Mathilde. "Étude des mécanismes d’invasion et d’expansion des cellules souches de Glioblastome." Electronic Thesis or Diss., Nantes Université, 2024. http://www.theses.fr/2024NANU1038.

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Le glioblastome (GB) est le cancer le plus courant et le plus agressif du système nerveux central chez l'adulte. Malgré un traitement multimodal incluant chirurgie, radiothérapie, et chimiothérapie, la survie médiane reste limitée a environ 15 mois. Cette issue défavorable s'explique par ('infiltration tumorale dans des régions cérébrales critiques, et, par la résistance aux traitements et les capacités d'expansion des cellules tumorales. Parmi celles-ci, les cellules de type souche de glioblastome (GSCs) jouent un rôle central dans la croissance, l'invasion, et la récidive. Localisées dans des niches spécifiques, telles que la niche périvasculaire, les GSCs interagissent directement avec les cellules endothéliales pour préserver leur état indifférencié et leur capacité d'auto-renouvellement. Mon travail de these a notamment permis d'identifier deux protéines transmembranaires, NRP1 et JAMC, comme des régulateurs clés de l'invasion et de la co-option vasculaire via le contrôle des intégrines dans les GSCs. Par ailleurs, les GSCs présentent une grande hétérogénéité transcriptionnelle, formant des sous-types aux etats parfois transitoires. Cette plasticité leur permettrait ainsi de générer différents phénotypes a partir d'une seule cellule. Dans ce contexte, j'ai montre que la kinase IKKE module non seulement les capacités d'auto-renouvellement des GSCs, mais aussi leur destin de différenciation. Bien que les mécanismes moléculaires sous-jacentes restent à décrypter, mes travaux ont permis de révéler trois nouveaux acteurs modulant l'invasion et l'expansion des cellules de GB
Glioblastoma (GB) is the most common and aggressive cancer of the adult central nervous system. Despite multimodal treatment including surgery, radiotherapy and chemotherapy, median survival remains limited to around 15 months. This unfavorable outcome is explained by tumor infiltration into critical brain regions, and by the resistance to treatments and the expansion of tumor cells. Among these, glioblastoma stem-like cells (GSCs) play a central role in growth, invasion, and recurrence. These GSCs, localized in specific niches such as the perivascular niche, interact directly with endothelial cells to preserve their undifferentiated state and capacity for self-renewal. My thesis notably identified two transmembrane proteins, NRP1 and JAMC, as key regulators of invasion and vascular co-option via integrin control in GSCs. Furthermore, GSCs display considerable transcriptional heterogeneity, forming subtypes that may display transient states. This plasticity could enable them to generate different phenotypes from a single cell. In this context, I have demonstrated that the kinase IKKE modulates not only the self-renewal capacities of GSCs, but also their differentiation fate. Overall, although the underlying molecular mechanisms remain to be deciphered, my work has revealed three new actors modulating the invasion and expansion of GB cells
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Book chapters on the topic "Vascular Co-option"

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Wang, Sarah, and Andrew C. Dudley. "Vascular Co-option in the Brain Tumor Microenvironment." In Biomarkers of the Tumor Microenvironment, 537–47. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-98950-7_32.

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Annese, Tiziana, Mariella Errede, Michelina De Giorgis, Loredana Lorusso, Roberto Tamma, and Domenico Ribatti. "Double Immunohistochemical Staining on Formalin-Fixed Paraffin-Embedded Tissue Samples to Study Vascular Co-option." In Methods in Molecular Biology, 101–16. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2703-7_8.

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García-Gómez, Pedro, and Manuel Valiente. "Vascular co-option." In Tumor Vascularization, 33–47. Elsevier, 2020. http://dx.doi.org/10.1016/b978-0-12-819494-2.00003-1.

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Herzig, Samuel, Elilary Montilla Medrano, and Karina Gritchenko. "Regional Anesthesia." In Vascular Anesthesia Procedures, 209–24. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780197506073.003.0015.

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Patients presenting for vascular surgery typically have significant comorbidities. Procedures can vary from minor to quite large with significant blood loss and fluid shifts, and can be elective or emergent. Perioperative morbidity and mortality in the context of co-existing cardiovascular disease, diabetes, dementia and other factors all provide great concern to the anesthesiologist in their approach towards the vascular patient. The anesthetic approach to such patients must therefore be taken with great forethought. Many times, these procedures can be localized to a particular extremity or well-defined set of dermatomes, and regional anesthesia has become one important option for the complicated vascular patient. In this chapter, the risks, benefits, and feasibility of various regional techniques are discussed in the context of patients presenting for carotid endarterectomy, vascular access placement, and major lower extremity vascular surgery.
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Journal articles
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