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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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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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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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Qian, Chao-Nan. "Hijacking the vasculature in ccRCC—co-option, remodelling and angiogenesis." Nature Reviews Urology 10, no. 5 (March 5, 2013): 300–304. http://dx.doi.org/10.1038/nrurol.2013.26.
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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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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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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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Seano, Giorgio, and Rakesh K. Jain. "Vessel co-option in glioblastoma: emerging insights and opportunities." Angiogenesis 23, no. 1 (November 2, 2019): 9–16. http://dx.doi.org/10.1007/s10456-019-09691-z.
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Abstract Vessel co-option is the movement of cancer cells towards and along the pre-existing vasculature and is an alternative to angiogenesis to gain access to nutrients. Vessel co-option has been shown as a strategy employed by some glioblastoma (GBM) cells to invade further into the brain, leading to one of the greatest challenges in treating GBM. In GBM, vessel co-option may be an intrinsic feature or an acquired mechanism of resistance to anti-angiogenic treatment. Here, we describe the histological features and the dynamics visualized through intravital microscopy of vessel co-option in GBM, as well as the molecular players discovered until now. We also highlight key unanswered questions, as answering these is critical to improve understanding of GBM progression and for developing more effective approaches for GBM treatment.
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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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Frisch, Anne, Stefanie Kälin, Raymond Monk, Josefine Radke, Frank L. Heppner, and Roland E. Kälin. "Apelin Controls Angiogenesis-Dependent Glioblastoma Growth." International Journal of Molecular Sciences 21, no. 11 (June 11, 2020): 4179. http://dx.doi.org/10.3390/ijms21114179.
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Glioblastoma (GBM) present with an abundant and aberrant tumor neo-vasculature. While rapid growth of solid tumors depends on the initiation of tumor angiogenesis, GBM also progress by infiltrative growth and vascular co-option. The angiogenic factor apelin (APLN) and its receptor (APLNR) are upregulated in GBM patient samples as compared to normal brain tissue. Here, we studied the role of apelin/APLNR signaling in GBM angiogenesis and growth. By functional analysis of apelin in orthotopic GBM mouse models, we found that apelin/APLNR signaling is required for in vivo tumor angiogenesis. Knockdown of tumor cell-derived APLN massively reduced the tumor vasculature. Additional loss of the apelin signal in endothelial tip cells using the APLN-knockout (KO) mouse led to a further reduction of GBM angiogenesis. Direct infusion of the bioactive peptide apelin-13 rescued the vascular loss-of-function phenotype specifically. In addition, APLN depletion massively reduced angiogenesis-dependent tumor growth. Consequently, survival of GBM-bearing mice was significantly increased when APLN expression was missing in the brain tumor microenvironment. Thus, we suggest that targeting vascular apelin may serve as an alternative strategy for anti-angiogenesis in GBM.
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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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Ribatti, Domenico, Antonio Giovanni Solimando, and Francesco Pezzella. "The Anti-VEGF(R) Drug Discovery Legacy: Improving Attrition Rates by Breaking the Vicious Cycle of Angiogenesis in Cancer." Cancers 13, no. 14 (July 8, 2021): 3433. http://dx.doi.org/10.3390/cancers13143433.
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Resistance to anti-vascular endothelial growth factor (VEGF) molecules causes lack of response and disease recurrence. Acquired resistance develops as a result of genetic/epigenetic changes conferring to the cancer cells a drug resistant phenotype. In addition to tumor cells, tumor endothelial cells also undergo epigenetic modifications involved in resistance to anti-angiogenic therapies. The association of multiple anti-angiogenic molecules or a combination of anti-angiogenic drugs with other treatment regimens have been indicated as alternative therapeutic strategies to overcome resistance to anti-angiogenic therapies. Alternative mechanisms of tumor vasculature, including intussusceptive microvascular growth (IMG), vasculogenic mimicry, and vascular co-option, are involved in resistance to anti-angiogenic therapies. The crosstalk between angiogenesis and immune cells explains the efficacy of combining anti-angiogenic drugs with immune check-point inhibitors. Collectively, in order to increase clinical benefits and overcome resistance to anti-angiogenesis therapies, pan-omics profiling is key.
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Seano, G., A. Griveau, S. Shelton, S. Krishnan, N. Wang, J. Kloepper, E. Huillard, et al. "OS12.4 In vivo dynamics and targeting of vessel co-option in glioma." Neuro-Oncology 21, Supplement_3 (August 2019): iii23. http://dx.doi.org/10.1093/neuonc/noz126.076.
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Abstract BACKGROUND Gliomas comprise heterogeneous malignant glial and stromal cells. While blood vessel co-option is a potential mechanism to escape anti-angiogenic therapy, the relevance of glial phenotype in this process is unclear. MATERIAL AND METHODS Here, we intravitally study preclinical syngenetic models of glioma as well as patient-derived cells transplanted orthotopically. Moreover, we profoundly confirm our preclinical results with histological studies on patient specimens. RESULTS We show that Olig2+ oligodendrocyte precursor-like glioma cells invade by single-cell vessel co-option and preserve the blood-brain barrier (BBB). Conversely, Olig2-negative glioma cells form dense perivascular collections and promote angiogenesis and BBB breakdown, leading to innate immune cell activation. Experimentally, Olig2 promotes Wnt7b expression, a finding that correlates in human glioma profiling. Targeted Wnt7a/7b deletion or pharmacologic Wnt inhibition blocks Olig2+ glioma single-cell vessel co-option and enhances responses to temozolomide. Finally, Olig2 and Wnt7 become upregulated after anti-VEGF treatment in preclinical models and patients. CONCLUSION Here, we show that glioma is able to employ vessel co-option, i.e. the movement of tumor cells towards and along the pre-existing vasculature. Glioma oligodendrocyte-like (OPCL) cells express Wnt7 that is necessary for vessel co-option and Wnt inhibitors significantly improve survival with temozolomide. Moreover, we demonstrated that anti-VEGF-treatment of glioma selects for Olig2/Wnt7+ cells
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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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Rada, Miran, Lucyna Krzywon, Stephanie Petrillo, Anthoula Lazaris, and Peter Metrakos. "A Retrospective Study on the Role of Metformin in Colorectal Cancer Liver Metastases." Biomedicines 11, no. 3 (February 28, 2023): 731. http://dx.doi.org/10.3390/biomedicines11030731.
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Colorectal cancer liver metastases (CRCLMs) have two main histopathological growth patterns (HPGs): desmoplastic (DHGP) and replacement (RHGP). The vascularization in DHGP tumours is angiogenic, while the RHGP tumours exert vessel co-option vasculature. The presence of vessel co-option tumours is associated with poor response to anti-angiogenic agents and chemotherapy, as well as a worse prognosis. Metformin has been shown to influence the progression and vasculature of tumours in different cancers. However, its role in CRCLM is poorly understood. Herein, we conducted a retrospective cohort study to examine the role of metformin in CRCLM. A dataset of 108 patients was screened, of which 20 patients used metformin. The metformin user patients did not use metformin as an anticancer agent. We noticed a significantly lower percentage of CRCLM patients with vessel co-opting RHGP tumours in the population that used metformin compared to CRCLM patients who did not use metformin. Similar results were obtained when we compared the ratio of recurrence and extrahepatic metastases incidence. Moreover, the metformin user patients had significantly higher survival outcome compared to nonusers. Collectively, our data suggest that metformin administration is likely associated with better prognosis of CRCLM.
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Pichol-Thievend, C., O. Anezo, A. M. Pettiwala, G. Bourmeau, R. Montagne, A. Lyne, P. Guichet, et al. "OS07.5.A GLIOBLASTOMA VESSEL CO-OPTION AND TRANSITION TO A RESISTANT CELL STATE ARE INDUCED BY CHEMORADIATION." Neuro-Oncology 25, Supplement_2 (September 1, 2023): ii18. http://dx.doi.org/10.1093/neuonc/noad137.052.
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Abstract BACKGROUND Glioblastoma (GB) is one of the deadliest types of human cancer. Despite a very aggressive treatment regime, including resection of the tumor, radiation, and chemotherapy, the recurrence rate is more than 90%. Recurrence is mostly caused by the regrowth of highly invasive and resistant cells that have spread from the tumor bulk and are not removed by resection. To develop an effective therapeutic approach, we need to better understand the underlying molecular and cellular mechanisms of GB chemoradiation resistance and tumor spreading. MATERIAL AND METHODS To dynamically follow the changes occurring in GB post-therapy and investigate its relationship with vascular microenvironment, we employed multiple bulk and single-cell RNA-Seq analyses, phosphoproteome, in vitro and in vivo real-time imaging, organotypic cultures and functional assays, digital pathology, and spatial transcriptomics on patient material or preclinical models of GB. RESULTS We demonstrated that chemoradiation and the brain vasculature induce a transition to a functional cell state, which we named VC-Resist. This cell state is midway through the transcriptomic axis between proneural and mesenchymal GB cells and is closer to the AC/MES-like state. Better cell survival, G2M-arrest, activation of senescence/stemness pathways make this GB cell state more resistant to therapy. Notably, these persister GB cells are highly vessel co-opting, allowing homing to the perivascular niche, which, in turn, increases their transition to this cell state and resistance to therapy. Molecularly, the transition to the VC-Resist cell state is driven by FGF-FGFR1 signaling, which leads to the activation of DNA damage repair and YAP1 pathways. CONCLUSION These findings demonstrate that the perivascular niche and GB cell plasticity jointly generate a vicious loop that leads to resistance to therapy and brain infiltration during GB recurrence. SUPPORT This work was supported by the European Research Council (ERC) under the European Union’s Horizon 2020 (Grant Agreement No. 805225), the INSERM-CNRS ATIP-Avenir grant, the NanoTheRad grant from Paris-Saclay University, Fondation ARC pour la recherche sur le cancer, Campus France and Canceropole Ile-de-France (2022-1-EMERG-06-ICR-1).
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Takano, Shingo. "Problem and Handling of Anti-angiogenic Therapy for Glioblastoma : Vessel Co-option and Vascular Mimicry." Japanese Journal of Neurosurgery 27, no. 10 (2018): 723–35. http://dx.doi.org/10.7887/jcns.27.723.
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Ben-Tabou de-Leon, Smadar. "The Evolution of Biomineralization through the Co-Option of Organic Scaffold Forming Networks." Cells 11, no. 4 (February 9, 2022): 595. http://dx.doi.org/10.3390/cells11040595.
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Biomineralization is the process in which organisms use minerals to generate hard structures like teeth, skeletons and shells. Biomineralization is proposed to have evolved independently in different phyla through the co-option of pre-existing developmental programs. Comparing the gene regulatory networks (GRNs) that drive biomineralization in different species could illuminate the molecular evolution of biomineralization. Skeletogenesis in the sea urchin embryo was extensively studied and the underlying GRN shows high conservation within echinoderms, larval and adult skeletogenesis. The organic scaffold in which the calcite skeletal elements form in echinoderms is a tubular compartment generated by the syncytial skeletogenic cells. This is strictly different than the organic cartilaginous scaffold that vertebrates mineralize with hydroxyapatite to make their bones. Here I compare the GRNs that drive biomineralization and tubulogenesis in echinoderms and in vertebrates. The GRN that drives skeletogenesis in the sea urchin embryo shows little similarity to the GRN that drives bone formation and high resemblance to the GRN that drives vertebrates’ vascular tubulogenesis. On the other hand, vertebrates’ bone-GRNs show high similarity to the GRNs that operate in the cells that generate the cartilage-like tissues of basal chordate and invertebrates that do not produce mineralized tissue. These comparisons suggest that biomineralization in deuterostomes evolved through the phylum specific co-option of GRNs that control distinct organic scaffolds to mineralization.
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Lim, Sharon, Kayoko Hosaka, Masaki Nakamura, and Yihai Cao. "Co-option of pre-existing vascular beds in adipose tissue controls tumor growth rates and angiogenesis." Oncotarget 7, no. 25 (May 18, 2016): 38282–91. http://dx.doi.org/10.18632/oncotarget.9436.
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Auffinger, Brenda, Tanwir Hasan, Gina Lee, Alex Tobias, Marc Deheeger, Yu Han, Donna Guo, Maciej Lesniak, C. David James, and Atique Ahmed. "TMIC-24. THE CONTRIBUTION OF VASCULAR CO-OPTION AND TUMOR-DERIVED ENDOTHELIAL CELLS TO GBM RECURRENCE." Neuro-Oncology 18, suppl_6 (November 1, 2016): vi205. http://dx.doi.org/10.1093/neuonc/now212.864.
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Zhao, Chengjian, Hanshuo Yang, Huanshan Shi, Xiaofei Wang, Xiancheng Chen, Yike Yuan, Shuo Lin, and Yuquan Wei. "Distinct contributions of angiogenesis and vascular co-option during the initiation of primary microtumors and micrometastases." Carcinogenesis 32, no. 8 (April 23, 2011): 1143–50. http://dx.doi.org/10.1093/carcin/bgr076.
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S. Mashalkar, Narendra. "Resurfacing complex knee and upper third leg defect with reverse vastus lateralis muscle flap in a flap exhausted leg - A case report." IP Journal of Surgery and Allied Sciences 6, no. 1 (April 15, 2024): 33–36. http://dx.doi.org/10.18231/j.jsas.2024.007.
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Coverage of upper third leg and knee defects are complex and the main supply of pedicled flaps come from the uninjured leg. Hence planning of flaps from leg must be meticulous, because if these fail then reveres flow flaps from thigh or micro vascular surgery will become the only option. Both have their own set of complications and patients who cannot tolerate micro vascular surgery due to their prolonged duration, co morbidities, and severe atherosclerosis of vessels, end up as thigh flaps being the only resort. Thigh flaps come with a set of complications of their own and even these fail, with above knee amputation being the ultimate option, which patient hardly expects as end result with many stages of reconstruction already being done. It’s a nightmare for both surgeon and patient.
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Xuesong, Du, Xue Wei, Liu Heng, Chen Xiao, Wang Shunan, Guo Yu, and Zhang Weiguo. "Evaluation of neovascularization patterns in an orthotopic rat glioma model with dynamic contrast-enhanced MRI." Acta Radiologica 58, no. 9 (December 12, 2016): 1138–46. http://dx.doi.org/10.1177/0284185116681038.
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Background Dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) has been proved useful in evaluating glioma angiogenesis, but the utility in evaluating neovascularization patterns has not been reported. Purpose To evaluate in vivo real-time glioma neovascularization patterns by measuring glioma perfusion quantitatively using DCE-MRI. Material and Methods Thirty Sprague-Dawley rats were used to establish C6 orthotopic glioma model and underwent MRI and pathology detections. As MRI and pathology were performed at six time points (i.e. 4, 8, 12, 16, 20, and 24 days) post transplantation, neovascularization patterns were evaluated via DCE-MRI. Results Four neovascularization patterns were observed in glioma tissues. Sprout angiogenesis and intussusceptive microvascular growth located inside tumor, while vascular co-option and vascular mimicry were found in the tumor margin and necrotic area, respectively. Sprout angiogenesis and intussusceptive microvascular growth increased with Ktrans, Kep, and Vp inside tumor tissue. In addition, Kep and Vp were positively correlated with sprout angiogenesis and intussusceptive microvascular growth. Vascular co-option was decreased at 12 and 16 days post transplantation and correlated negatively with Ktrans and Kep detected in the glioma margin, respectively. Changes of vascular mimicry showed no significant statistical difference at the six time points. Conclusion Our results indicate that DCE-MRI can evaluate neovascularization patterns in a glioma model. Furthermore, DCE-MRI could be an imaging biomarker for guidance of antiangiogenic treatments in humans in the future.
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Rautiainen, Swarna, Timo Laaksonen, and Raili Koivuniemi. "Angiogenic Effects and Crosstalk of Adipose-Derived Mesenchymal Stem/Stromal Cells and Their Extracellular Vesicles with Endothelial Cells." International Journal of Molecular Sciences 22, no. 19 (October 8, 2021): 10890. http://dx.doi.org/10.3390/ijms221910890.
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Adipose-derived mesenchymal stem/stromal cells (ASCs) are an adult stem cell population able to self-renew and differentiate into numerous cell lineages. ASCs provide a promising future for therapeutic angiogenesis due to their ability to promote blood vessel formation. Specifically, their ability to differentiate into endothelial cells (ECs) and pericyte-like cells and to secrete angiogenesis-promoting growth factors and extracellular vesicles (EVs) makes them an ideal option in cell therapy and in regenerative medicine in conditions including tissue ischemia. In recent angiogenesis research, ASCs have often been co-cultured with an endothelial cell (EC) type in order to form mature vessel-like networks in specific culture conditions. In this review, we introduce co-culture systems and co-transplantation studies between ASCs and ECs. In co-cultures, the cells communicate via direct cell–cell contact or via paracrine signaling. Most often, ASCs are found in the perivascular niche lining the vessels, where they stabilize the vascular structures and express common pericyte surface proteins. In co-cultures, ASCs modulate endothelial cells and induce angiogenesis by promoting tube formation, partly via secretion of EVs. In vivo co-transplantation of ASCs and ECs showed improved formation of functional vessels over a single cell type transplantation. Adipose tissue as a cell source for both mesenchymal stem cells and ECs for co-transplantation serves as a prominent option for therapeutic angiogenesis and blood perfusion in vivo.
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Pombero, Ana, Raquel Garcia-Lopez, and Salvador Martínez. "Pericyte–Glioblastoma Cell Interaction: A Key Target to Prevent Glioblastoma Progression." Cells 12, no. 9 (May 5, 2023): 1324. http://dx.doi.org/10.3390/cells12091324.
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Multiple biological processes rely on direct intercellular interactions to regulate cell proliferation and migration in embryonic development and cancer processes. Tumor development and growth depends on close interactions between cancer cells and cells in the tumor microenvironment. During embryonic development, morphogenetic signals and direct cell contacts control cell proliferation, polarity, and morphogenesis. Cancer cells communicate with cells in the tumor niche through molecular signals and intercellular contacts, thereby modifying the vascular architecture and antitumor surveillance processes and consequently enabling tumor growth and survival. While looking for cell-to-cell signaling mechanisms that are common to both brain development and cancer progression, we have studied the infiltration process in glioblastoma multiforme (GBM), which is the most malignant primary brain tumor and with the worst prognosis. Cell-to-cell contacts, by means of filopodia-like structures, between GBM cells and brain pericytes (PCs) are necessary for adequate cell signaling during cancer infiltration; similarly, contacts between embryonic regions, via cytonemes, are required for embryo regionalization and development. This GBM–PC interaction provokes two important changes in the physiological function of these perivascular cells, namely, (i) vascular co-option with changes in cell contractility and vascular malformation, and (ii) changes in the PC transcriptome, modifying the microvesicles and protein secretome, which leads to the development of an immunosuppressive phenotype that promotes tumor immune tolerance. Moreover, the GTPase Cdc42 regulates cell polarity across organisms, from yeast to humans, playing a central role in GBM cell–PC interaction and maintaining vascular co-option. As such, a review of the molecular and cellular mechanisms underlying the development and maintenance of the physical interactions between cancer cells and PCs is of particular interest.
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Helm, Thomas N., and Klaus F. Helm. "Spitz Nevus Intermingling With Hemangioma, Angiomatoid Spitz Nevus, Angiotropism, and Vascular Co-option Viewed With Differing Availability Heuristics." American Journal of Dermatopathology 40, no. 6 (June 2018): 465–67. http://dx.doi.org/10.1097/dad.0000000000000870.
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Rosińska, Sara, and Julie Gavard. "Tumor Vessels Fuel the Fire in Glioblastoma." International Journal of Molecular Sciences 22, no. 12 (June 17, 2021): 6514. http://dx.doi.org/10.3390/ijms22126514.
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Glioblastoma, a subset of aggressive brain tumors, deploy several means to increase blood vessel supply dedicated to the tumor mass. This includes typical program borrowed from embryonic development, such as vasculogenesis and sprouting angiogenesis, as well as unconventional processes, including co-option, vascular mimicry, and transdifferentiation, in which tumor cells are pro-actively engaged. However, these neo-generated vascular networks are morphologically and functionally abnormal, suggesting that the vascularization processes are rather inefficient in the tumor ecosystem. In this review, we reiterate the specificities of each neovascularization modality in glioblastoma, and, how they can be hampered mechanistically in the perspective of anti-cancer therapies.
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Martinez-Morga, Marta, Daniel Garrigos, Elena Rodriguez-Montero, Ana Pombero, Raquel Garcia-Lopez, and Salvador Martinez. "Pericytes Are Immunoregulatory Cells in Glioma Genesis and Progression." International Journal of Molecular Sciences 25, no. 10 (May 7, 2024): 5072. http://dx.doi.org/10.3390/ijms25105072.
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Vascular co-option is a consequence of the direct interaction between perivascular cells, known as pericytes (PCs), and glioblastoma multiforme (GBM) cells (GBMcs). This process is essential for inducing changes in the pericytes’ anti-tumoral and immunoreactive phenotypes. Starting from the initial stages of carcinogenesis in GBM, PCs conditioned by GBMcs undergo proliferation, acquire a pro-tumoral and immunosuppressive phenotype by expressing and secreting immunosuppressive molecules, and significantly hinder the activation of T cells, thereby facilitating tumor growth. Inhibiting the pericyte (PC) conditioning mechanisms in the GBM tumor microenvironment (TME) results in immunological activation and tumor disappearance. This underscores the pivotal role of PCs as a key cell in the TME, responsible for tumor-induced immunosuppression and enabling GBM cells to evade the immune system. Other cells within the TME, such as tumor-associated macrophages (TAMs) and microglia, have also been identified as contributors to this immunomodulation. In this paper, we will review the role of these three cell types in the immunosuppressive properties of the TME. Our conclusion is that the cellular heterogeneity of immunocompetent cells within the TME may lead to the misinterpretation of cellular lineage identification due to different reactive stages and the identification of PCs as TAMs. Consequently, novel therapies could be developed to disrupt GBM-PC interactions and/or PC conditioning through vascular co-option, thereby exposing GBMcs to the immune system.
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Liu, Jianxiong, Alexander L. Fedinec, Charles W. Leffler, and Helena Parfenova. "Enteral Supplements of a Carbon Monoxide Donor CORM-A1 Protect against Cerebrovascular Dysfunction Caused by Neonatal Seizures." Journal of Cerebral Blood Flow & Metabolism 35, no. 2 (November 5, 2014): 193–99. http://dx.doi.org/10.1038/jcbfm.2014.196.
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Cerebral blood flow dysregulation caused by oxidative stress contributes to adverse neurologic outcome of seizures. A carbon monoxide (CO) donor CORM-A1 has antioxidant and cytoprotective properties. We investigated whether enteral supplements of CORM-A1 can improve cerebrovascular outcome of bicuculline-induced seizures in newborn piglets. CORM-A1 (2 mg/kg) was given to piglets via an oral gastric tube 10 minutes before or 20 minutes after seizure onset. Enteral CORM-A1 elevated CO in periarachnoid cerebrospinal fluid and produced a dilation of pial arterioles. Postictal cerebral vascular responses to endothelium-, astrocyte-, and vascular smooth muscle-dependent vasodilators were tested 48 hours after seizures by intravital microscopy. The postictal responses of pial arterioles to bradykinin, glutamate, the AMPA receptor agonist quisqualic acid, ADP, and heme were greatly reduced, suggesting that seizures cause injury to endothelial and astrocyte components of the neurovascular unit. In contrast, in the two groups of piglets receiving enteral CORM-A1, the postictal cerebral vascular responsiveness to these dilators was improved. Overall, enteral supplements of CORM-A1 before or during seizures offer a novel effective therapeutic option to deliver cytoprotective mediator CO to the brain, reduce injury to endothelial and astrocyte components of cerebral blood flow regulation and to improve the cerebrovascular outcome of neonatal seizures.
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Kapelanski-Lamoureux, Audrey, Flemming Kondrup, Lucyna Krzywon, Stephanie K. Petrillo, Anthoula Lazaris, and Peter Metrakos. "Abstract 5291: Characterizing the interplay between angiogenic and immunoactive factors of hepatocellular carcinoma." Cancer Research 82, no. 12_Supplement (June 15, 2022): 5291. http://dx.doi.org/10.1158/1538-7445.am2022-5291.
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Abstract Hepatocellular carcinoma (HCC) is the fourth leading cause of cancer-related death globally. Patients typically present at an advanced stage and less than 50% reach the maximum 1-year survival rate, when given as first-line treatment, Sorafenib. This highlights the need for early detection and novel therapeutic targets crucial to increase overall survival (OS) for patients with HCC. Given the important role of angiogenesis in HCC from its early stage and its rich immune composition, anti-angiogenic and immune checkpoint inhibitors (ICI), are two therapeutic approaches when combined marked the first treatment in more than a decade to significantly improve the overall survival and progression-free survival in patients with advanced HCC compared to Sorafenib. While the combination of agents inhibiting angiogenesis and ICI have recently entered the clinic, the interplay between angiogenic factors and immunity in the context of this approach remains poorly understood. Here we focus on understanding the interplay between the vascular state of the tumor and the immune response in HCC. As a first step, we focus on defining the immune and vasculature landscape of the central tumor, peripheral tumor, adjacent liver to the tumor, and distal liver regions of each lesion by immunohistochemistry (IHC). Forty (40) formalin-fixed paraffin-embedded (FFPE) human liver tissue samples containing untreated and non-viral HCC tumors, obtained from the Liver Disease Biobank of the RI-MUHC were used to perform IHC. Images were viewed and scored using the Aperio ImageScope software. With respect to the vasculature, we observe that all tumors have a combination of both angiogenic (CD34/Ki67+ve) and co-optioning (CD31 +ve) features, with no uniform distribution. Our immune markers demonstrate that both adaptive and innate immune cells are present at the interface and different tumors demonstrate different levels of infiltration. Next, to identify the immune subtype populations (ie macrophage M1 vs M2, Treg, etc) present, we will use the NanoString Whole Transcriptome Atlas spatial profiler technology. We will also then link the vasculature to any specific immune profile. For example, it has been shown in other cancer types that macrophages are associated with co-option. This project presents preliminary evidence for the interaction of vascular factors with immune cells, thus providing insight into the biological rationale of why 30% of patients responded to combined angiogenic and immunotherapy treatment. Citation Format: Audrey Kapelanski-Lamoureux, Flemming Kondrup, Lucyna Krzywon, Stephanie K. Petrillo, Anthoula Lazaris, Peter Metrakos. Characterizing the interplay between angiogenic and immunoactive factors of hepatocellular carcinoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 5291.
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Ribatti, Domenico, Roberto Tamma, Tiziana Annese, Antonio d’Amati, Giuseppe Ingravallo, and Giorgina Specchia. "Vascular Growth in Lymphomas: Angiogenesis and Alternative Ways." Cancers 15, no. 12 (June 20, 2023): 3262. http://dx.doi.org/10.3390/cancers15123262.
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The formation of new blood vessels is a critical process for tumor growth and may be achieved through different mechanisms. Angiogenesis represents the first described and most studied mode of vessel formation, but tumors may also use alternative ways to secure blood supply and eventually acquire resistance to anti-angiogenic treatments. These non-angiogenic mechanisms have been described more recently, including intussusceptive microvascular growth (IMG), vascular co-option, and vasculogenic mimicry. Like solid tumors, angiogenic and non-angiogenic pathways in lymphomas play a fundamental role in tumor growth and progression. In view of the relevant prognostic and therapeutic implications, a comprehensive understanding of these mechanisms is of paramount importance for improving the efficacy of treatment in patients with lymphoma. In this review, we summarize the current knowledge on angiogenic and non-angiogenic mechanisms involved in the formation of new blood vessels in Hodgkin’s and non-Hodgkin’s lymphomas.
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Nakanuma, Yasuni, Zihan Li, Yasunori Sato, Motoko Sasaki, Kenichi Harada, Yuko Kakuda, and Takashi Sugino. "A Pathological Assessment of the Microvasculature of Biliary Tract Neoplasms Referring to Pre-Existing Blood Vessels and Vessel Co-Option." Cancers 16, no. 22 (November 19, 2024): 3869. http://dx.doi.org/10.3390/cancers16223869.
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There are several types of microvasculature supplying neoplasms: “newly formed blood vessels” (neoangiogenesis), which are a component of the tumor microenvironment (TME) of invasive carcinoma with wound healing-like reaction; and “pre-existing blood vessels”, which are used as tumor-supplying vessels by neoplasms (co-option vessels) and are likely to develop in hypervascularized organs. We herein review the microvasculature of neoplasms of biliary tract with reference to pre-existing vessels and vessel co-options. In the hepatobiliary system, intrahepatic large and extrahepatic bile ducts (large bile ducts) and the gallbladder as well as hepatic lobules are highly vascularized regions. In large bile ducts, the biliary lining epithelia and underlining capillaries (peribiliary capillary plexus [PCP]) form the biliary epithelia–PCP alignment, whereas the hepatocyte–sinusoid alignment composes hepatic lobules. Cholangiocarcinoma (CCA) and gallbladder carcinoma (GBC) are the main biliary tract carcinomas. CCA is subdivided into distal (d/CCA), perihilar (pCCA), and intrahepatic (iCCA), and iCCA is subdivided into small duct type (SD-iCCA) and large duct type (LD-iCCA). High-grade biliary intraepithelial neoplasm (BilIN), intraductal papillary neoplasm of the bile duct (IPNB), pyloric gland adenoma (PGA), and intracholecystic papillary neoplasm (ICPN) have recently been proposed as the precursors of LD-iCCA, p/dCCA, and GBC. In the large bile ducts and gallbladder, all cases of high-grade BilIN and PGA, about half of IPNB, and one-third of ICPN with less-complicated structure were found to have hijacked the PCP as their supporting vessels (vessel co-option), while p/dCCA, LD-iCCA, and GBC were supplied by neo-angiogenetic vessels associated with fibrous stroma. The intraluminal components of the remaining cases of ICPN and IPNB with complicated structure presented sparse capillaries without fibrous stroma, a unique microvasculature different from that of co-option or neoangiogenesis. Regarding iCCA showing invasion into the hepatic lobules, some SD-iCCAs replaced hepatocytic cords and used pre-existing sinusoids as co-opted vessels. Visualization of pre-existing vessels could be a new pathological tool for the evaluation of malignant progression and of vascular supply in CCAs and its precursors.
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Grizzi, Fabio, Mohamed A. A. A. Hegazi, Matteo Zanoni, Paolo Vota, Giovanni Toia, Maria Chiara Clementi, Cinzia Mazzieri, Maurizio Chiriva-Internati, and Gianluigi Taverna. "Prostate Cancer Microvascular Routes: Exploration and Measurement Strategies." Life 13, no. 10 (October 9, 2023): 2034. http://dx.doi.org/10.3390/life13102034.
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Angiogenesis is acknowledged as a pivotal feature in the pathology of human cancer. Despite the absence of universally accepted markers for gauging the comprehensive angiogenic activity in prostate cancer (PCa) that could steer the formulation of focused anti-angiogenic treatments, the scrutiny of diverse facets of tumoral blood vessel development may furnish significant understanding of angiogenic processes. Malignant neoplasms, encompassing PCa, deploy a myriad of strategies to secure an adequate blood supply. These modalities range from sprouting angiogenesis and vasculogenesis to intussusceptive angiogenesis, vascular co-option, the formation of mosaic vessels, vasculogenic mimicry, the conversion of cancer stem-like cells into tumor endothelial cells, and vascular pruning. Here we provide a thorough review of these angiogenic mechanisms as they relate to PCa, discuss their prospective relevance for predictive and prognostic evaluations, and outline the prevailing obstacles in quantitatively evaluating neovascularization via histopathological examinations.
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Pettiwala, Aafrin M., Cathy Pichol-Thievend, Oceane Anezo, Guillaume Bourmeau, Remi Montagne, Anne-Marie Lyne, Pierre-Olivier Guichet Guichet, et al. "TMIC-76. GLIOBLASTOMA VESSEL CO-OPTION OCCURS AS A RESISTANCE MECHANISM TO CHEMORADIATION VIA INDUCTION OF A NOVEL CELL STATE." Neuro-Oncology 25, Supplement_5 (November 1, 2023): v295. http://dx.doi.org/10.1093/neuonc/noad179.1141.
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Abstract Glioblastoma (GB) is one of the deadliest types of human cancer. Despite a very aggressive treatment regime-including resection, chemo-radiation, its recurrence rate is more than 90%. Recurrence is mostly caused by highly resistant and invasive cells that spread from tumor bulk and are not removed by resection. To develop an effective therapeutic approach, we need to better understand underlying molecular and cellular mechanism driving therapy resistance and invasion in GB. To dynamically track the changes post-therapy and chemoradiation-resistant cells, we employed multiple bulk and single cell transcriptomics, phosphoproteome, in vitro and in vivo real time imaging, organotypic cultures, functional analysis, digital pathology and spatial transcriptomics on patient material and preclinical models of GB. We demonstrated that the chemoradiation and brain vasculature induce a transition to invasive functional cell state, which we rename as VC-Resist. Better cell survival, G2M arrest, senescence/stemness pathway induction, makes this GB state much more resistant. Notably, these GB cells are highly vessel co-opting allowing homing to perivascular niche, which in turn increases their transition to this cell state. Molecularly, the transition to VC-Resist cell state takes place through FGF-FGFR1 signaling that leads to activation of DNA damage repair, YAP and Rho pathways. These findings demonstrate that the perivascular niche and GB cell plasticity jointly generates a vicious loop that leads to resistance and brain infiltration during GB recurrence.
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Sheng, Kevin L., Jude Raj, and Kris C. Wood. "Abstract 4591: Mechanisms of tumor-mediated endothelial cell proliferation independent of VEGF." Cancer Research 83, no. 7_Supplement (April 4, 2023): 4591. http://dx.doi.org/10.1158/1538-7445.am2023-4591.
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Abstract A hallmark of cancer is dysregulated angiogenesis and blood vessel co-option, which are often driven by vascular endothelial growth factor (VEGF). Despite the key role of VEGF signaling in promoting endothelial cell (EC) proliferation, survival, and migration, the clinical use of VEGF inhibitors has modest success and faces many challenges. In particular, patients demonstrate variable initial responses to anti-VEGF therapy, and many of those who respond to treatment subsequently develop resistance. These challenges suggest that there may be VEGF-independent mechanisms driving EC proliferation in the tumor microenvironment. To study these mechanisms, we established an in vitro model using a dual-reporter system in a co-culture model of ECs and tumor cells. Specifically, we used an immortalized endothelial cell line (SVEC4-10) expressing GFP and Renilla luciferase and a mouse renal carcinoma cell line (RENCA) expressing Tomato and Firefly luciferase. This model allowed us to independently evaluate the growth rates and cell viabilities of both ECs and tumor cells in direct co-culture. Our preliminary data revealed that ECs exhibit increased growth rates when directly co-cultured with tumor cells. Interestingly, this EC proliferation is VEGF-independent and not impacted by VEGF-A knockout in tumor cells or with treatment of a pan-VEGFR small molecule inhibitor (axitinib). To further characterize if our phenotype was due to other tumor secreted factors, we used a transwell setup to eliminate direct contact between ECs and tumor cells and found that EC growth rates were substantially mitigated. These results revealed that tumor cells induced EC proliferation through a physical cell-to-cell interaction that is independent of VEGF. Further characterizing this unknown mechanism may inform therapeutic interventions to overcome the clinical challenges of anti-VEGF therapies for cancer. To expand our understanding of this VEGF-independent EC proliferation, we aim to characterize the cell surface proteome from tumor-conditioned ECs using cell surface mass spectrometry. We will validate hits from this study using our in vitro model and translate these findings to in vivo mouse models. We expect that our current and future research will reveal new insights into tumor co-option of the vascular system and identify novel targets for developing therapies to effectively treat cancer. Citation Format: Kevin L. Sheng, Jude Raj, Kris C. Wood. Mechanisms of tumor-mediated endothelial cell proliferation independent of VEGF. [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 4591.
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Belotti, Dorina, Denise Pinessi, and Giulia Taraboletti. "Alternative Vascularization Mechanisms in Tumor Resistance to Therapy." Cancers 13, no. 8 (April 15, 2021): 1912. http://dx.doi.org/10.3390/cancers13081912.
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Blood vessels in tumors are formed through a variety of different mechanisms, each generating vessels with peculiar structural, molecular, and functional properties. This heterogeneity has a major impact on tumor response or resistance to antineoplastic therapies and is now emerging as a promising target for strategies to prevent drug resistance and improve the distribution and efficacy of antineoplastic treatments. This review presents evidence of how different mechanisms of tumor vessel formation (vasculogenesis, glomeruloid proliferation, intussusceptive angiogenesis, vasculogenic mimicry, and vessel co-option) affect tumor responses to antiangiogenic and antineoplastic therapies, but also how therapies can promote alternative mechanisms of vessel formation, contributing to tumor recurrence, malignant progression, and acquired drug resistance. We discuss the possibility of tailoring treatment strategies to overcome vasculature-mediated drug resistance or to improve drug distribution and efficacy.
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Walrand, Stephan, Michel Hesse, Philippe d’Abadie, and François Jamar. "Hepatic Arterial Buffer Response in Liver Radioembolization and Potential Use for Improved Cancer Therapy." Cancers 13, no. 7 (March 26, 2021): 1537. http://dx.doi.org/10.3390/cancers13071537.
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Liver radioembolization is a treatment option for unresectable liver cancers, performed by infusion of 90Y or 166Ho loaded spheres in the hepatic artery. As tumoral cells are mainly perfused via the liver artery unlike hepatic lobules, a twofold tumor to normal liver dose ratio is commonly obtained. To improve tumoral cell killing while preserving lobules, co-infusion of arterial vasoconstrictor has been proposed but with limited success: the hepatic arterial buffer response (HABR) and hepatic vascular escape mechanism hamper the arterioles vasoconstriction. The proposed project aims to take benefit from the HABR by co-infusing a mesenteric arterial vasodilator: the portal flow enhancement inducing the vasoconstriction of the intra sinusoids arterioles barely impacts liver tumors that are mainly fed by novel and anarchic external arterioles. Animal studies were reviewed and dopexamine was identified as a promising safe candidate, reducing by four the hepatic lobules arterial flow. A clinical trial design is proposed. A four to sixfold improvement of the tumoral to normal tissue dose ratio is expected, pushing the therapy towards a real curative intention, especially in HCC where ultra-selective spheres delivery is often not possible.
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Rana, Kush Bahadur, Afroz Ansari, Dharmendra Joshi, Apurwa Shrestha, and Madhav Ghimire. "Superficialization of the Basilic Vein in Brachiobasilic Arteriovenous Fistula: An Alternative Vascular Access for Hemodialysis- A Single Center Experience." Med Phoenix 8, no. 2 (December 31, 2023): 14–18. http://dx.doi.org/10.3126/medphoenix.v8i2.61824.
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Introduction: The use of basilic vein to create brachiobasilic arteriovenous fistula (BBAVF) is the vascular access option of choice for hemodialysis when cephalic veins are not available. To create BBAVF, the basilic vein should be superficialized and lateralized. The study aims to highlight the outcome and morbidity of BBAVF at the tertiary referral center and aims to improve the results of the procedure in patients with chronic renal failure.Materials and Methods: This is prospective, descriptive study conducted at College of Medical Sciences Teaching Hospital from January 2019 to December 2022.The demographic data, morbidities, results were analyzed using the Statistical Package for Social Sciences (SPSS) version 23.0 (SPSS).Results: We evaluated outcome of total forty patients who underwent BBAVF with transposition of basilic vein. The mean age of patients was 61 ± 10.85 years and male:female ratio was 2.07:1. The mean size of basilic vein was 3.05 ± 0.84mm and brachial artery was 4.11 ± 0.99mm. The most common co-morbidities in this study was Diabetes Mellitus and hypertension both was present in 52.5% of patients, only hypertension in 27.5%, only Diabetes Mellitus in 5%, HTN with PVD in 2.5% and HTN, Diabetes Mellitus with PVD in 2.5% of patients. The postoperative complications were bleeding in 25% (10), infection 10% (4), primary failure 7.5% (3), pseudoaneurysm 5% (2), and oedema 7.5% (3).Total 82.5% (33) of cases were able to start dialysis in 45 days. The failure rate was 12.5% (5) due to thrombosis and pseudoaneurysm.Conclusion: BBAVF is a suitable option for vascular access in patients with failed previous AVF or patients with small cephalic vein. Relocation of basilic vein for AVF is feasible, safe and with good patency and complication rates are acceptable.
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Lyons, Caomhán J., and Timothy O'Brien. "The Functionality of Endothelial-Colony-Forming Cells from Patients with Diabetes Mellitus." Cells 9, no. 7 (July 20, 2020): 1731. http://dx.doi.org/10.3390/cells9071731.
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Endothelial-colony-forming cells (ECFCs) are a population of progenitor cells which have demonstrated promising angiogenic potential both in vitro and in vivo. However, ECFCs from diabetic patients have been shown to be dysfunctional compared to ECFCs from healthy donors. Diabetes mellitus itself presents with many vascular co-morbidities and it has been hypothesized that ECFCs may be a potential cell therapy option to promote revascularisation in these disorders. While an allogeneic cell therapy approach would offer the potential of an ‘off the shelf’ therapeutic product, to date little research has been carried out on umbilical cord-ECFCs in diabetic models. Alternatively, autologous cell therapy using peripheral blood-ECFCs allows the development of a personalised therapeutic approach to medicine; however, autologous diabetic ECFCs are dysfunctional and need to be repaired so they can effectively treat diabetic co-morbidities. Many different groups have modified autologous diabetic ECFCs to improve their function using a variety of methods including pre-treatment with different factors or with genetic modification. While the in vitro and in vivo data from the literature is promising, no ECFC therapy has proceeded to clinical trials to date, indicating that more research is needed for a potential ECFC therapy in the future to treat diabetic complications.
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Tomarchio, Stefania, Anna Portale, Stefano Catanzaro, Agata Polizzi, Giuseppe Belfiore, Concetta Pirrone, Carmelo Schepis, et al. "Wyburn-Mason Syndrome." Journal of Pediatric Neurology 16, no. 05 (August 20, 2018): 297–304. http://dx.doi.org/10.1055/s-0038-1667133.
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AbstractWyburn–Mason syndrome is a very rare neurocutaneous disorder characterized by unilateral arteriovenous malformations of the midbrain associated with vascular abnormalities of eye and optic pathways, as well as multiple cutaneous nevi, reddish-bluish in color. The co-occurrence of such anomalies can be explained by an embryonic anomaly occurring in common ancestor cells, with the more severe cases related to development errors in the very early phases of gestation. Central nervous system and vision may be severely impaired: affected individuals may present with acute headache, hemiplegia, and homonymous hemianopsia in half of the cases. Seizures, cerebellar dysfunction, acute psychiatric signs, hallucinations, and temporal/spatial disorientation are reported more rarely. A progressive mental illness can become evident later in up to 30% of cases. Surgical removal is indicated only in superficially located arteriovenous malformations, while nonsurgical strategies (i.e., embolization and radiation therapy) are indicated for most of the lesions and represent the gold standard option in the treatment of this syndrome.
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Seropian, Ignacio M., Germán E. González, Sebastián M. Maller, Daniel H. Berrocal, Antonio Abbate, and Gabriel A. Rabinovich. "Galectin-1 as an Emerging Mediator of Cardiovascular Inflammation: Mechanisms and Therapeutic Opportunities." Mediators of Inflammation 2018 (November 5, 2018): 1–11. http://dx.doi.org/10.1155/2018/8696543.
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Galectin-1 (Gal-1), an evolutionarily conserved β-galactoside-binding lectin, controls immune cell homeostasis and tempers acute and chronic inflammation by blunting proinflammatory cytokine synthesis, engaging T-cell apoptotic programs, promoting expansion of T regulatory (Treg) cells, and deactivating antigen-presenting cells. In addition, this lectin promotes angiogenesis by co-opting the vascular endothelial growth factor receptor (VEGFR) 2 signaling pathway. Since a coordinated network of immunomodulatory and proangiogenic mediators controls cardiac homeostasis, this lectin has been proposed to play a key hierarchical role in cardiac pathophysiology via glycan-dependent regulation of inflammatory responses. Here, we discuss the emerging roles of Gal-1 in cardiovascular diseases including acute myocardial infarction, heart failure, Chagas cardiomyopathy, pulmonary hypertension, and ischemic stroke, highlighting underlying anti-inflammatory mechanisms and therapeutic opportunities. Whereas Gal-1 administration emerges as a potential novel treatment option in acute myocardial infarction and ischemic stroke, Gal-1 blockade may contribute to attenuate pulmonary arterial hypertension.
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Cui, Qi, Yingmei Zhang, Ning Tian, Jiaxin Yang, Dongshan Ya, Wenjing Xiang, Zixian Zhou, et al. "Leptin Promotes Angiogenesis via Pericyte STAT3 Pathway upon Intracerebral Hemorrhage." Cells 11, no. 17 (September 3, 2022): 2755. http://dx.doi.org/10.3390/cells11172755.
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Angiogenesis is a vital endogenous brain self-repair processes for neurological recovery after intracerebral hemorrhage (ICH). Increasing evidence suggests that leptin potentiates angiogenesis and plays a beneficial role in stroke. However, the proangiogenic effect of leptin on ICH has not been adequately explored. Moreover, leptin triggers post-ICH angiogenesis through pericyte, an important component of forming new blood vessels, which remains unclear. Here, we reported that exogenous leptin infusion dose-dependent promoted vascular endothelial cells survival and proliferation at chronic stage of ICH mice. Additionally, leptin robustly ameliorated pericytes loss, enhanced pericytes proliferation and migration in ICH mice in vivo, and in ICH human brain microvascular pericytes (HBVPC) in vitro. Notably, we showed that pericytes-derived pro-angiogenic factors were responsible for enhancing the survival, proliferation and tube formation followed leptin treatment in human brain microvascular endothelial cells (HCMEC/D3)/HBVPC co-culture models. Importantly, considerable improvements in neurobehavioral function and hostile microenvironment were observed in leptin treatment ICH mice, indicating that better vascular functionality post ICH improves outcome. Mechanistically, this study unveiled that leptin boost post-ICH angiogenesis potentially through modulation of leptin receptor (leptinR)/Signal Transducer and Activator of Transcription 3 (STAT3) signaling pathway in pericyte. Thus, leptin may be a lucrative option for the treatment of ICH.
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Hajjar, Katherine A., Jia Ruan, Guangzhi Sui, Arunkumar B. Deora, Sarah Church, Leona Cohen-Gould, Shahin Rafii, David C. Lyden, and Qi Ling. "Annexin 2 Mediates Plasminogen-Related Recruitment of Neovascular Mural Cells in Lymphoma Angiogenesis." Blood 110, no. 11 (November 16, 2007): 3708. http://dx.doi.org/10.1182/blood.v110.11.3708.3708.
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Abstract Malignant tumor progression requires the development of tumor-associated blood vessels through co-option of nearby host vascular cells, recruitment of marrow-derived progenitor cells, or both. The annexin 2 (A2)/p11 heterotetramer is a cell surface co-receptor for the fibrinolytic proteins plasminogen (Plg) and tPA, and strongly augments the catalytic efficiency of vascular cell plasmin generation. We showed previously that A2−/ − mice display impaired postnatal angiogenesis in the corneal pocket, oxygen-induced retinopathy, and Matrigel plug assays. Here, we examined neovascularization of experimental lymphoma in mice with fibrinolytic deficiency states. For both EL4, a T cell lymphoma, and B6RV2, a B cell lymphoma, growth of implanted tumor cells was rapid in wildtype and tPA−/ − mice, but nearly flat in both A2−/ − and Plg−/ − mice. Immunohistochemical staining of EL4 tissue on day 8 revealed reduced vascular density, frequent intravascular fibrin thrombi, and dilated microvessels in A2−/ −, compared with A2+/+, mice. Electron microscopy and immunofluorescence revealed a striking paucity of pericytes and secondary dropout of endothelial cells within A2−/ − tumor microvessels. Flow cytometric analysis of circulating progenitor cells showed reduced recruitment of VEGFR1+/CD11b+ hematopoietic precursors from bone marrow to blood in A2−/ − versus A2+/+ tumor-bearing mice. In lethally irradiated A2−/ − mice, moreover, tumor growth was rescued completely upon engraftment with A2+/+ marrow. Transplantation of green fluorescent protein (GFP)-labeled A2+/+ bone marrow revealed the appearance of abundant marrow-derived CD11b+/CD68+ cells closely apposed to developing tumor neovessels. Many of these cells also express the pericyte marker, NG2. Transplantation of A2+/+ marrow, finally, restored the investment of tumor microvessels with α-smooth muscle actin-positive pericytes. These data suggest that A2 contributes critically to tumor angiogenesis in experimental lymphoma in mice, by enabling recruitment of A2+ myelomonocytic cells that promote neovascular stabilization by pericyte-like cells. The data suggest further that targeting the A2/p11 system could offer a novel strategy for the treatment of malignant lymphoma.
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Mueller, Thomas, Juana Freystein, Henrike Lucas, and Hans-Joachim Schmoll. "Efficacy of a Bispecific Antibody Co-Targeting VEGFA and Ang-2 in Combination with Chemotherapy in a Chemoresistant Colorectal Carcinoma Xenograft Model." Molecules 24, no. 16 (August 7, 2019): 2865. http://dx.doi.org/10.3390/molecules24162865.
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Vascular endothelial growth factor (VEGF) inhibition by the addition of bevacizumab to the chemotherapy regimen of metastatic colorectal cancer leads to an improved outcome. However, anti-angiogenic tumor therapy targeting a single factor may be limited by complementary mechanisms. Angiopoietin-2 (Ang-2, ANGPT2) is another important factor that cooperates with VEGF to drive tumor angiogenesis. It was shown that high Ang-2 levels are associated with a poor clinical outcome of colorectal cancer patients treated with bevacizumab-containing therapy. Therefore, combined inhibition of VEGF and Ang-2 was supposed to improve anti-angiogenic therapy. Here, we evaluated the efficacy of a bispecific antibody (CrossMab) co-targeting VEGF and Ang-2 in combination with chemotherapy in a chemoresistant colorectal carcinoma model. Antitumor activity was evaluated in athymic nude mice bearing subcutaneous DLD1 xenograft tumors and treated with anti-VEGF (B20), anti-Ang-2 (LC06) and anti-VEGF/Ang-2 (CrossMab) antibodies. Chemotherapy consisted of 5-FU and irinotecan. Resected tumors were analyzed immunohistochemically. First, an impact of targeting each single factor but also a clear advantage of co-targeting both factors could be demonstrated. Accordingly, tumor tissue showed strong staining for VEGF and Ang-2. Chemotherapy alone was less effective. Efficient tumor growth inhibition could be achieved by treatment with anti-VEGF/chemotherapy, single CrossMab and CrossMab/chemotherapy, which resulted in 3 out of 10, 6 out of 10 and 10 out of 10 complete responses, respectively, during seven weeks. Complete retarded tumors were characterized by massive intratumoral necrosis surrounded by layers of vital tumor cells and connective tissue with CD31-positive vessels at the periphery. In some cases, a distinct feature known as vessel co-option could be observed. In conclusion, the data from this model clearly support the strategy of co-targeting VEGF and Ang-2 and further demonstrate the beneficial impact of co-treatment with chemotherapy. The clear superiority of the CrossMab-containing regimen compared to clinical standard anti-VEGF/chemotherapy warrants further analyses in other models.
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Степанов, И. А., В. А. Белобородов, and М. А. Шамеева. "Molecular and cellular mechanisms of glioblastoma resistance to vascular endothelial growth factor inhibitors." ZHurnal «Patologicheskaia fiziologiia i eksperimental`naia terapiia», no. 3() (September 16, 2020): 137–45. http://dx.doi.org/10.25557/0031-2991.2020.03.137-145.
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Представлен обзор современных источников литературы, посвященных изучению молекулярных и клеточных механизмов резистентности глиобластомы к антиангиогенным лекарственным средствам. Ангиогенез представляет собой важнейший патофизиологический механизм роста и прогрессирования глиобластомы за счет активного развития микрососудистой сети. Ускоренное развитие микрососудистой сети в глиобластоме происходит благодаря синтезу опухолевыми клетками большого количества фактора роста эндотелия сосудов (Vascular Endothelial Growth Factor, VEGF). Среди основных молекулярных и клеточных механизмов лекарственной устойчивости глиобластомы к анти-VEGF агентам принято относить VEGF-независимые пути ангиогенеза, активность клеток костного мозга и перицитов, а также сосудистую кооперацию, периваскулярную инвазию и феномен аутофагии. Изложены современные данные о рациональном и наиболее эффективном использовании анти-VEGF-лекарственных средств у пациентов с глиомами высокой степени злокачественности. Обозначены актуальные, остающиеся нерешенными вопросы, что обусловливает необходимость проведения дальнейших экспериментальных и клинических исследований, посвященных изучению механизмов лекарственной устойчивости глиобластомы к анти-VEGF-препаратам. This state-of-the-art review focuses on molecular and cellular factors associated with glioblastoma resistance to antiangiogenic drugs. Angiogenesis is an important pathophysiological mechanism for the growth and progression of glioblastoma facilitated by active development of microvasculature. The accelerated development of the microvascular network in glioblastoma occurs due to the synthesis of a large number of vascular endothelial growth factor (VEGF) by tumor cells Among the major molecular and cellular factors, glioblastoma drug resistance to anti-VEGF agents is commonly attributed to VEGF-independent pathways of angiogenesis, bone marrow cell and pericyte activity as well as to vascular co-option, perivascular invasion, and the phenomenon of autophagy. The authors provided current data on the rational and most effective use of anti-VEGF drugs for patients with high-grade gliomas. Relevant unsolved problems associated with drug resistance of glioblastoma to anti-VEGF drugs were highlighted.
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Restivo, Ignazio, Alessandro Attanzio, Luisa Tesoriere, Mario Allegra, Guadalupe Garcia-Llatas, and Antonio Cilla. "Anti-Eryptotic Activity of Food-Derived Phytochemicals and Natural Compounds." International Journal of Molecular Sciences 23, no. 6 (March 11, 2022): 3019. http://dx.doi.org/10.3390/ijms23063019.
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Human red blood cells (RBCs), senescent or damaged due to particular stress, can be removed by programmed suicidal death, a process called eryptosis. There are various molecular mechanisms underlying eryptosis. The most frequent is the increase in the cytoplasmic concentration of Ca2+ ions, later exposure of erythrocytes to oxidative stress, hyperosmotic shock, ceramide formation, stimulation of caspases, and energy depletion. Phosphatidylserine (PS) exposed by eryptotic RBCs due to interaction with endothelial CXC-Motiv-Chemokin-16/Scavenger-receptor, causes the RBCs to adhere to vascular wall with consequent damage to the microcirculation. Eryptosis can be triggered by various xenobiotics and endogenous molecules, such as high cholesterol levels. The possible diseases associated with eryptosis are various, including anemia, chronic kidney disease, liver failure, diabetes, hypertension, heart failure, thrombosis, obesity, metabolic syndrome, arthritis, and lupus. This review addresses and collates the existing ex vivo and animal studies on the inhibition of eryptosis by food-derived phytochemicals and natural compounds including phenolic compounds (PC), alkaloids, and other substances that could be a therapeutic and/or co-adjuvant option in eryptotic-driven disorders, especially if they are introduced through the diet.
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Cordova, Leonardo Zandavalli, Jennifer Martins, and Patricia Terrill. "Negative pressure wound therapy in the management of complex lower limb wounds: a case series highlighting outpatient care with small single-use devices." Wound Practice and Research 27, no. 3 (September 2019): 116–21. http://dx.doi.org/10.33235/wpr.27.3.116-121.
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Background: Traditionally, the treatment of exposed tendon has required vascularised tissue coverage, usually with complex surgical intervention. The introduction of negative pressure wound therapy (NPWT) has challenged this traditional reconstructive concept. Unfortunately, standard NPWT units are usually bulky, noisy and curtail the mobility and lifestyle of patients. The introduction of small, modern, lightweight, portable, single-use NPWT units have therefore revitalised the use of NPWT and provided a solution to the many problems encountered with the larger devices. Case series: This study highlights three cases of patients with complex lower limb wounds with tendon exposure who were successfully treated with single-use NPWT in an outpatient setting. The median time for complete wound granulation was 5–10 weeks. Minor sharp debridement of wounds was required to encourage granulation tissue formation and this was well tolerated in the outpatient setting. Conclusion: Portable NPWT units provide an alternative to surgical reconstruction in patients with lower limb wounds with exposed tendon. These devices can be utilised in a purely outpatient setting, thus avoid long-term hospitalisation. Older patients with high anaesthesia risk or who lack alternative reconstructive options due to vascular co-morbidities are the most appropriate candidates for this treatment option.
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Markus, Birgit, Julian Kreutz, Giorgios Chatzis, Styliani Syntila, Jannis Kuchenbuch, Charlotte Mueller, Maryana Choukeir, Bernhard Schieffer, and Nikolaos Patsalis. "Mitral Valve Transcatheter Edge-to-Edge Repair (MV-TEER) in Patients with Secondary Mitral Regurgitation Improves Hemodynamics, Enhances Renal Function, and Optimizes Quality of Life in Patients with Advanced Renal Insufficiency." Biomedicines 12, no. 11 (November 20, 2024): 2648. http://dx.doi.org/10.3390/biomedicines12112648.
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Background/Objectives: Secondary mitral regurgitation (MR) is a common valvular heart disease burdening the prognosis of patients with co-existing chronic heart failure. Transcatheter edge-to-edge mitral valve repair (MV-TEER) is a minimally invasive treatment option for high-risk patients. However, the effects of MV-TEER on expanded hemodynamics, tissue perfusion, and quality of life, particularly in patients with advanced renal failure, remain underexplored. Methods: This prospective, single-center study evaluated the impact of MV-TEER on hemodynamics, renal function, and quality of life in 45 patients with severe MR. Non-invasive bioimpedance monitoring with NICaS® was used to assess hemodynamics pre- and 3–5 days post-procedure. Quality of life was assessed using the EQ-5D-3L questionnaire before and 3 months post-procedure. For further analysis, patients were divided into subgroups based on the estimated baseline glomerular filtration rate (eGFR < 35 mL/min vs. eGFR ≥ 35 mL/min). Results: A significant reduction in systemic vascular resistance (SVR; p = 0.003) and an increase in eGFR (p = 0.03) were observed in the entire cohort after MV-TEER, indicating improved tissue perfusion. Notably, particularly patients with eGFR < 35 mL/min showed a significant increase in cardiac output (CO; p = 0.035), cardiac index (CI; p = 0.031), and eGFR (p = 0.018), as well as a reduction in SVR (p = 0.007). Consistent with these findings, quality of life significantly improved, with the EQ-5D-3L index and EQ-VAS score increasing from 0.44 to 0.66 (p < 0.001) and from 51.7% to 62.9% (p < 0.001).
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Munson, Teresa, Jun Zhao, Esther Elise Knapp, Charmaine Du Toit, Ashok Raj, and Kerry McGowan. "Single Needle Option: An Alternative to Dual-Needle Access in Erythrocytapheresis in Patients with Sickle Cell Disease." Blood 138, Supplement 1 (November 5, 2021): 4284. http://dx.doi.org/10.1182/blood-2021-154080.
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Abstract Background: Erythrocytapheresis or red cell exchange (RCE) is an invaluable treatment option for patients with complications related sickle cell disease, including acute stroke, stroke prevention, acute chest syndrome, and recurrent pain crisis. The procedure entails the removal of each patient's red blood cells containing the abnormal sickle hemoglobin and replacing them with normal red blood cells carrying non-sickled hemoglobin. Adequate vascular access is essential for erythrocytapheresis to allow for high flow rates and various forms of access are used including peripheral veins and central venous access devices. Our center typically uses a single vortex port (Angiodynamics, Walnut Creek, CA) with placement of a peripheral IV at time of procedure in order to maintain a circuit for exchange. Using peripheral access reliably becomes particularly difficult in young patients and those that require multiple access over time due to scaring. To ensure a successful procedure in patients with poor peripheral access, a single-needle (SN) option for TPE (SN-TPE) that is available on Spectra Optia (Terumo BCT, Lakewood, CO) was used. The single-needle procedure utilizes intermittent, rather than continuous, flow, and thus requires extra procedure run time. One discontinuous cycle consists of "exchanging red cells," which is the drawing of blood and removal of the red cells, and "adjusting the volume in the reservoir," which is the returning of blood. These cycles continue until the procedure is complete. This procedure allows us to continue RCE in a select number of patients with poor vascular access. Methods: We evaluated our institutional experience on patients treated using single-needle RCE. In addition, information regarding each RCE session was collected including duration of procedure and inlet flow rate. Results: An average of 45 RCE procedures are performed each month. Patients are scheduled every 3 to 8 weeks, with an average of every 4-5 week frequency. We started the Single Needle option in July of 2019 on 3 patients: one adult aged patient and 2 pediatric patients. By the end of 2019 we had perform a total of 27 SN procedures. In 2020, we performed a total of 112 SN procedures, average of 9 procedures each month. As of the first 6 months of 2021, we have completed 35 SN procedures, averages 6 a month. In patients undergoing single needle exchange we were able to increase inlet flow rates from an average of 30-50ml/min to 60-80ml/min. This decreased the duration of run times from 120-198 min to 77- 119 min. Pre and post hemoglobin S% was comparable between dual and single exchange patients and there was no change in the interval between RCE sessions. Conclusion: With our increasing experience with single-needle RCE, our findings suggest that RCE can be successfully completed using the single-needle option with no impact on pre- and post-exchange hemoglobin S% levels. There was a reduction in the total length of procedure due to ability to maintain higher inlet rates and decreased time to obtain access for RCE. The single needle option also improved patient satisfaction due to more reliable access and negating need for peripheral IV access. Disclosures Munson: Terumo Medical Corporation: Consultancy, Honoraria, Speakers Bureau. Raj: Forma therapeutics: Consultancy; Terumo Medical Corporation: Honoraria, Speakers Bureau; Global biotherapeutics: Speakers Bureau.