Cited by 2,953Angiogenesis and VEGF in CancerCancer Cells and MetastasisLymphatic System and Diseases

The DOI matches its Crossref record; 104 of the 104 references it cites were found in a registry or an index.

Modes of resistance to anti-angiogenic therapy

Open access

Bergers, Gabriele, Hanahan, Douglas·2008·Nature Reviews Cancer

Open this paper in CoChat — free account

Abstract

Angiogenesis inhibitors targeting the vascular endothelial growth factor (VEGF) signalling pathways are affording demonstrable therapeutic efficacy in mouse models of cancer and in an increasing number of human cancers. However, in both preclinical and clinical settings, the benefits are at best transitory and are followed by a restoration of tumour growth and progression. Emerging data support a proposition that two modes of unconventional resistance underlie such results: evasive resistance, an adaptation to circumvent the specific angiogenic blockade; and intrinsic or pre-existing indifference. Multiple mechanisms can be invoked in different tumour contexts to manifest both evasive and intrinsic resistance, motivating assessment of their prevalence and importance and in turn the design of pharmacological strategies that confer enduring anti-angiogenic therapies.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

Integrity signals

Registry

Crossref · 10.1038/nrc2442

Cites

104 of 104 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

The hallmarks of cancer
Hanahan, D., & Weinberg, R. A. (2000) · Cell · doi:10.1016/s0092-8674(00)81683-9 · Cited by 29,219
Self-citation
Isolation of Putative Progenitor Endothelial Cells for Angiogenesis
Asahara, T., Murohara, T., Sullivan, A., Silver, M., van der Zee, R., Li, T., Witzenbichler, B., Schatteman, G., & Isner, J. M. (1997) · Science · doi:10.1126/science.275.5302.964 · Cited by 8,725 · cited 1×
“Endothelial and pericyte progenitors differentiate into endothelial cells, which form the inner lining of blood vessel walls, or pericytes, the cells that envelop blood vessels, respectivel”
Background
Patterns and emerging mechanisms of the angiogenic switch during tumorigenesis
Hanahan, D., & Folkman, J. (1996) · Cell · doi:10.1016/s0092-8674(00)80108-7 · Cited by 6,885
Self-citation
Targeting HIF-1 for cancer therapy
Semenza, G. L. (2003) · Nature Reviews Cancer · doi:10.1038/nrc1187 · Cited by 6,717 · cited 1×
“The HIF regulatory network also holds promise as a target, given its global effects on angiogenesis, invasion and stress-adaptive cell physiolog”
Background
Normalization of Tumor Vasculature: An Emerging Concept in Antiangiogenic Therapy
Jain, R. K. (2005) · Science · doi:10.1126/science.1104819 · Cited by 5,527
Angiogenesis in life, disease and medicine
Carmeliet, P. (2005) · Nature · doi:10.1038/nature04478 · Cited by 3,551
Tumour-educated macrophages promote tumour progression and metastasis
Pollard, J. W. (2004) · Nature reviews. Cancer · doi:10.1038/nrc1256 · Cited by 3,413 · cited 1×
“By contrast, pro-angiogenic monocytes, such as tumour-associated macrophage”
Background
VEGFR1-positive haematopoietic bone marrow progenitors initiate the pre-metastatic niche
Kaplan, R. N., Riba, R. D., Zacharoulis, S., Bramley, A. H., Vincent, L., Costa, C., MacDonald, D. D., Jin, D. K., Shido, K., Kerns, S. A., et al. (2005) · Nature · doi:10.1038/nature04186 · Cited by 3,288
Paclitaxel plus Bevacizumab versus Paclitaxel Alone for Metastatic Breast Cancer
Miller, K. D., Wang, M., Gralow, J. R., Dickler, M. N., Cobleigh, M., Perez, E. A., Shenkier, T. N., Cella, D. F., & Davidson, N. E. (2007) · New England Journal of Medicine · doi:10.1056/nejmoa072113 · Cited by 3,104 · cited 1×
“aspx?CdrID=39762">paclitaxel extended progression-free survival (but not overall survival”
Background
Progenitor cell trafficking is regulated by hypoxic gradients through HIF-1 induction of SDF-1
Ceradini, D. J., Kulkarni, A. R., Callaghan, M. J., Tepper, O. M., Bastidas, N., Kleinman, M. E., Capla, J. M., Galiano, R. D., Levine, J. P., & Gurtner, G. C. (2004) · Nature Medicine · doi:10.1038/nm1075 · Cited by 2,600 · cited 1×
“Evidence that low oxygen tension triggers the recruitment of BMDCs stems from observations in experimentally induced ischaemic tissue, wherein endothelial progenitors and other CXCR4 + BMDCs are recruited, in part through increases in HIF1α and its downstream effectors SDF1α (a CXCR4 ligand) and VEGF itsel”
Background

Show all 101 references

Research works printed but not linked: 1

Berger, M. S. & Wilson, C. B. The Gliomas (W.B. Saunders, Philadelphia, 1999).

Sorted by citations

Items 801–900 of 1,005

Breaking barriers: Neurodegenerative repercussions of radiotherapy induced damage on the blood-brain and blood-tumor barrier
Allen, B. D., & Limoli, C. L. (2021) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2021.12.002 · Cited by 66
“Clinically, anti-angiogenic agents fail to stop tumor growth because tumors have evolved multiple strategies to compensate for hypoxia and localized nutrient deprivation [81].”
Background
The characterization of a novel monoclonal antibody against CD93 unveils a new antiangiogenic target
Orlandini, M., Galvagni, F., Bardelli, M., Rocchigiani, M., Lentucci, C., Anselmi, F., Zippo, A., Bini, L., & Oliviero, S. (2014) · Oncotarget · doi:10.18632/oncotarget.1887 · Cited by 59
Phase 1 trial of tivantinib in combination with sorafenib in adult patients with advanced solid tumors
Puzanov, I. J., Sosman, J. A., Santoro, A., Saif, M. W., Goff, L. W., Dy, G. K., Zucali, P. A., Means-Powell, J. A., Ma, W. W., Simonelli, M., et al. (2014) · Investigational New Drugs · doi:10.1007/s10637-014-0167-5 · Cited by 59
Hepatocellular carcinoma treated with sorafenib: early detection of treatment response and major adverse events by contrast‐enhanced US
Sugimoto, K., Moriyasu, F., Saito, K., Rognin, N. G., Kamiyama, N., Furuichi, Y., & Imai, Y. (2013) · Liver International · doi:10.1111/liv.12098 · Cited by 59
Persistent vascular normalization as an alternative goal of anti‐angiogenic cancer therapy
Sato, Y. (2011) · Cancer Science · doi:10.1111/j.1349-7006.2011.01929.x · Cited by 59
Dovitinib demonstrates antitumor and antimetastatic activities in xenograft models of hepatocellular carcinoma
Huynh, H. T., Chow, P. K. H., Tai, W. M. D., Choo, S. P., Chung, A. Y. F., Ong, H. S., Soo, K. C., Ong, R., Linnartz, R., & Shi, M. M. (2011) · Journal of Hepatology · doi:10.1016/j.jhep.2011.09.017 · Cited by 59
“Greater antitumor activity seen in dovitinib-treated mice could also plausibly be explained by its ability to inhibit FGFR signaling pathway that is implicated in HCC development and angiogenesis [25,26].”
Background
Adding to the Mix: Fibroblast Growth Factor and Platelet-Derived Growth Factor Receptor Pathways as Targets in Non – small Cell Lung Cancer
Kono, S. A., Heasley, L. E., Doebele, R. C., & Camidge, D. R. (2012) · Current Cancer Drug Targets · doi:10.2174/156800912799095144 · Cited by 59
“Factors beyond VEGF, including the angiopoietin/TIE-2 interaction, interleukins, Notch/ delta-like ligand 4, PDGFs, and fibroblast growth factors (FGFs), influence angiogenesis [30–33].”
Background
A Novel Monoclonal Antibody to Fibroblast Growth Factor 2 Effectively Inhibits Growth of Hepatocellular Carcinoma Xenografts
Wang, L., Park, H., Chhim, S., Ding, Y., Jiang, W., Queen, C., & Kim, K. J. (2012) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-11-0813 · Cited by 59
Revisiting tumor angiogenesis: vessel co-option, vessel remodeling, and cancer cell-derived vasculature formation
Qian, C., Tan, M., Yang, J., & Cao, Y. (2016) · 癌症：英文版 · doi:10.1186/s40880-015-0070-2 · Cited by 59
“Accumulating evidence suggests that the co-opted vessels can better survive after tumor vasculature normalization, and vessel co-option is an important approach of a solid tumor to evade antiangiogenic therapy [23].”
Background
Resistance to Anti-VEGF Therapy Mediated by Autocrine IL6/STAT3 Signaling and Overcome by IL6 Blockade
Eichten, A., Su, J., Adler, A. P., Zhang, L., Ioffe, E., Parveen, A. A., Yancopoulos, G. D., Rudge, J. S., Lowy, I., Lin, H. C., et al. (2016) · Cancer Research · doi:10.1158/0008-5472.can-15-1443 · Cited by 60
“Clinical and preclinical studies suggest that resistance of tumors to anti-VEGF therapies can occur via several mechanisms: (a) changes in the tumor microenvironment resulting in upregulation of various pro-angiogenic factors, which lead to vessels that are less sensitive to VEGF blockade and/or (b) changes in the cha…”
Background
SDF-1 Blockade Enhances Anti-VEGF Therapy of Glioblastoma and Can Be Monitored by MRI
Deng, L., Stafford, J. H., Liu, S.-C., Chernikova, S. B., Merchant, M. J., Recht, L. D., & Brown, J. M. (2016) · Neoplasia · doi:10.1016/j.neo.2016.11.010 · Cited by 62
Intravital imaging of stromal cell dynamics in tumors
Lohela, M. K., & Werb, Z. (2009) · Current Opinion in Genetics & Development · doi:10.1016/j.gde.2009.10.011 · Cited by 58
“However, it has become evident that tumors do evade anti-angiogenic therapy [7].”
Background
Vascular Endothelial Growth Factor-D (VEGF-D): An Angiogenesis Bypass in Malignant Tumors
Bokhari, S. M. Z., & Hamar, P. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241713317 · Cited by 58
Anti-VEGF antibody therapy induces tumor hypoxia and stanniocalcin 2 expression and potentiates growth of human colon cancer xenografts
Miyazaki, S., Kikuchi, H., Iino, I., Uehara, T., Setoguchi, T., Fujita, T., Hiramatsu, Y., Ohta, M., Kamiya, K., Kitagawa, K., et al. (2013) · International Journal of Cancer · doi:10.1002/ijc.28686 · Cited by 58
Vessel calibre—a potential MRI biomarker of tumour response in clinical trials
Emblem, K. E., Farrar, C. T., Gerstner, E. R., Batchelor, T. T., Borra, R., Rosen, B. R., Sorensen, A. G., & Jain, R. K. (2014) · Nature Reviews Clinical Oncology · doi:10.1038/nrclinonc.2014.126 · Cited by 58
“GDC-0980; 10 mg/kg per day HM7 CRC in mice (18)184 (P <0.”
WSS25 Inhibits Growth of Xenografted Hepatocellular Cancer Cells in Nude Mice by Disrupting Angiogenesis via Blocking Bone Morphogenetic Protein (BMP)/Smad/Id1 Signaling
Qiu, H. Y., 波), B. Y. (., Pei, Z., Zhang, Z., & Ding, K. (2010) · Journal of Biological Chemistry · doi:10.1074/jbc.m110.105544 · Cited by 58
Blocking CLEC14A-MMRN2 binding inhibits sprouting angiogenesis and tumour growth
Noy, P. J., Lodhia, P., Khan, K. A., Zhuang, X. A., Ward, D. G., Verissimo, A. R., Bacon, A., & Bicknell, R. (2015) · Oncogene · doi:10.1038/onc.2015.34 · Cited by 58
“7 More recent efforts to develop effective anti-angiogenic therapies have focussed on understanding and targeting the endothelial tip and stalk cells during sprouting angiogenesis.”
Changes in tumour vessel density upon treatment with anti-angiogenic agents: relationship with response and resistance to therapy
Vasudev, N. S., Goh, V., Juttla, J. K., Thompson, V. E., Larkin, J., Gore, M. E., Nathan, P., & Reynolds, A. R. (2013) · British Journal of Cancer · doi:10.1038/bjc.2013.429 · Cited by 58
“For example, tumour vessels are known to undergo a maturation process that renders them insensitive to VEGF inhibition, and tumours that have a large fraction of mature vessels are therefore less probable to respond to anti-angiogenic TKIs (Bergers and Hanahan, 2008; Sitohy et al, 2011, 2012).”
BackgroundInfluential
Vessel pruning or healing: endothelial metabolism as a novel target?
Cantelmo, A. R., Pircher, A., Kalucka, J. M., & Carmeliet, P. (2017) · Expert Opinion on Therapeutic Targets · doi:10.1080/14728222.2017.1282465 · Cited by 60
Macrophage depletion through colony stimulating factor 1 receptor pathway blockade overcomes adaptive resistance to anti-VEGF therapy
Lyons, Y. A., Pradeep, S., Wu, S. Y., Haemmerle, M., Hansen, J. M., Wagner, M. J., Villar‐Prados, A., Nagaraja, A. S., Dood, R. L., Previs, R. A., et al. (2017) · Oncotarget · doi:10.18632/oncotarget.20410 · Cited by 58
Tumor resistance to anti-VEGF therapy through up-regulation of VEGF-C expression
Li, D., Xie, K., Ding, G., Li, J., Chen, K., Li, H., Qian, J., Jiang, C., & Fang, J. (2013) · Cancer Letters · doi:10.1016/j.canlet.2013.12.004 · Cited by 59
Sequencing of Agents for Metastatic Renal Cell Carcinoma: Can We Customize Therapy?
Sonpavde, G., Choueiri, T. K., Escudier, B. J., Ficarra, V., Hutson, T. E., Mulders, P., Patard, J., Rini, B. I., Staehler, M. D., Sternberg, C. N., et al. (2011) · European Urology · doi:10.1016/j.eururo.2011.10.032 · Cited by 57
“1) [9].”
Advances in an active and passive targeting to tumor and adipose tissues
Sakurai, Y., Kajimoto, K., Hatakeyama, H., & Harashima, H. (2014) · Expert Opinion on Drug Delivery · doi:10.1517/17425247.2015.955847 · Cited by 59
“Compared to cancer cells, TECs are genetically stable, and hence TECs induce little or no resistance to chemotherapy [23].”
Arginase inhibition suppresses lung metastasis in the 4T1 breast cancer model independently of the immunomodulatory and anti-metastatic effects of VEGFR-2 blockade
Secondini, C., Coquoz, O., Spagnuolo, L., Spinetti, T., Peyvandi, S., Ciarloni, L., Botta, F., Bourquin, C., & Rüegg, C. (2017) · OncoImmunology · doi:10.1080/2162402x.2017.1316437 · Cited by 58
Design, synthesis and biological evaluation of novel 4-anilinoquinazoline derivatives as hypoxia-selective EGFR and VEGFR-2 dual inhibitors
Wei, H., Duan, Y., Gou, W., Cui, J., Ning, H., Li, D., Qin, Y. W., Liu, Q., & Li, Y. (2019) · European Journal of Medicinal Chemistry · doi:10.1016/j.ejmech.2019.07.055 · Cited by 57
Targeting PD-1 or PD-L1 in Metastatic Kidney Cancer: Combination Therapy in the First-Line Setting
Aggen, D. H., Drake, C. G., & Rini, B. I. (2020) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-19-3323 · Cited by 57
“Chronic inhibition of VEGFwith TKIs can induce a hypoxic state within the TMEwith a concomitant accumulation of HIF1a (66).”
Background
Activated FGF2 signaling pathway in tumor vasculature is essential for acquired resistance to anti-VEGF therapy
Ichikawa, K., Miyano, S. W., Minoshima, Y., Matsui, J., & Funahashi, Y. (2020) · Scientific Reports · doi:10.1038/s41598-020-59853-z · Cited by 58
Exploring the Past, Present, and Future of Anti-Angiogenic Therapy in Glioblastoma
Zhang, A. B., Mozaffari, K., Aguirre, B., Li, V., Kubba, R., Desai, N. C., Wei, D., Yang, I., & Wadehra, M. (2023) · Cancers · doi:10.3390/cancers15030830 · Cited by 57
Sequential use of targeted agents in the treatment of renal cell carcinoma
Hutson, T. E., Bukowski, R. M., Cowey, C. L., Figlin, R. A., Escudier, B. J., & Sternberg, C. N. (2010) · Critical Reviews in Oncology/Hematology · doi:10.1016/j.critrevonc.2010.07.018 · Cited by 56
The role of targeted therapy in ovarian cancer
Banerjee, S. N., & Kaye, S. B. (2011) · European Journal of Cancer · doi:10.1016/s0959-8049(11)70155-1 · Cited by 56
Quantitative fluorescent profiling of VEGFR s reveals tumor cell and endothelial cell heterogeneity in breast cancer xenografts
Imoukhuede, P. I., & Popel, A. S. (2014) · Cancer Medicine · doi:10.1002/cam4.188 · Cited by 56
“Despite significant progress into antiangiogenic therapy, anti-VEGF therapy has had only moderate effects on patient survival, ultimately leading to antiangiogenic resistance and nonresponsiveness [14].”
Background
Antiangiogenic Therapies for Advanced Hepatocellular Carcinoma
Sampat, K., & O’Neil, B. H. (2013) · The Oncologist · doi:10.1634/theoncologist.2012-0388 · Cited by 56
A dual-targeting PDGFRβ/VEGF-A molecule assembled from stable antibody fragments demonstrates anti-angiogenic activity in vitro and in vivo
Mabry, R., Gilbertson, D. G., Frank, A., Vu, T., Ardourel, D., Ostrander, C. D., Stevens, B. L., Julien, S. H., Franke, S., Meengs, B., et al. (2010) · mAbs · doi:10.4161/mabs.2.1.10498 · Cited by 56
Effects of Anti-Angiogenesis on Glioblastoma Growth and Migration: Model to Clinical Predictions
Scribner, E. Y., Saut, O., Province, P., Bag, A. K., Colin, T., & Fathallah‐Shaykh, H. M. (2014) · PLoS ONE · doi:10.1371/journal.pone.0115018 · Cited by 57
“…different mechanisms of resistance to anti-angiogenic therapy leading to revascularization; these include: 1) evasive resistance to VEGF inhibitors caused by upregulation of alternate pro-angiogenic signals, and 2) intrinsic resistance due to non-responsiveness of a tumor to bevacizumab [38].”
Influence of hepatic impairment on lenvatinib pharmacokinetics following single‐dose oral administration
Shumaker, R., Aluri, J., Fan, J., Martinez, G., Pentikis, H. S., & Ren, M. (2014) · The Journal of Clinical Pharmacology · doi:10.1002/jcph.398 · Cited by 56
Targeting Olfactomedin-like 3 Inhibits Tumor Growth by Impairing Angiogenesis and Pericyte Coverage
Miljkovic‐Licina, M., Hammel, P., Garrido‐Urbani, S., Lee, B. P.-L., Meguenani, M., Chaâbane, C., Bochaton‐Piallat, M., & Imhof, B. A. (2012) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-12-0245 · Cited by 56
“and tight pericyte coverage of newly formed vessels contributes to the resistance of tumors to anti-VEGF therapy (6).”
Background
Anti-cancer and Anti-angiogenic Properties of Various Natural Pentacyclic Tri-terpenoids and Some of their Chemical Derivatives
Rufino‐Palomares, E. E., Pérez‐Jiménez, A., Reyes‐Zurita, F. J., Garcı́a-Salguero, L., Mokhtari, K., Herrera-Merchan, A., Medina, P. P., Peragón, J., & Lupiáñez, J. A. (2015) · Current Organic Chemistry · doi:10.2174/1385272819666150119225952 · Cited by 56
CXCR2 Inhibition Combined with Sorafenib Improved Antitumor and Antiangiogenic Response in Preclinical Models of Ovarian Cancer
Devapatla, B. K., Sharma, A., & Woo, S. (2015) · PLoS ONE · doi:10.1371/journal.pone.0139237 · Cited by 56
“Several mechanisms are involved in acquired resistance to anti-VEGF therapy, including activation of alternative pathways to circumvent VEGF inhibition, thereby resuming tumor angiogenesis and tumor growth [11].”
Background
Gastrointestinal cancer cells treatment with bevacizumab activates a VEGF autoregulatory mechanism involving telomerase catalytic subunit hTERT via PI3K-AKT, HIF-1α and VEGF receptors
Mahfouz, N., Tahtouh, R., Alaaeddine, N., Hajj, J. E., Sarkis, R., Hachem, R. Y., RAAD, I. I., & Hilal, G. (2017) · PLoS ONE · doi:10.1371/journal.pone.0179202 · Cited by 56
Potential of Integrin Inhibitors for Treating Ovarian Cancer: A Literature Review
Kobayashi, M., Sawada, K., & Kimura, T. (2017) · Cancers · doi:10.3390/cancers9070083 · Cited by 58
“Development of bevacizumab resistance through the intrinsic mode depends on treatment history, tumor microenvironment, or genetic makeup while that through the evasive mode depends on the activation of alternative pro-angiogenic signaling pathways, including integrin-mediated pathways [23].”
Background
Early Changes in Circulating FGF19 and Ang-2 Levels as Possible Predictive Biomarkers of Clinical Response to Lenvatinib Therapy in Hepatocellular Carcinoma
Chuma, M., Uojima, H., Numata, K., Hidaka, H., Toyoda, H., Hiraoka, A., Tada, T., Hirose, S., Atsukawa, M., Itokawa, N., et al. (2020) · Cancers · doi:10.3390/cancers12020293 · Cited by 57
“The FGF / FGFR pathway is part of an escape mechanism to VEGF-targeted anti-angiogenic therapies [17].”
The role of the tumor microenvironment in tumor cell intravasation and dissemination
Borriello, L., Karagiannis, G. S., Duran, C. L., Coste, A., Oktay, M. H., Entenberg, D. R., & Condeelis, J. S. (2020) · European Journal of Cell Biology · doi:10.1016/j.ejcb.2020.151098 · Cited by 56
Identification of diverse tumor endothelial cell populations in malignant glioma
Carlson, J. C., Gutierrez, M. E. C., Lozzi, B., Huang-Hobbs, E., Turner, W. D., Tepe, B., Zhang, Y., Herman, A. M., Rao, G., Creighton, C. J., et al. (2020) · Neuro-Oncology · doi:10.1093/neuonc/noaa297 · Cited by 56
Integrating Single-Cell and Spatial Transcriptomics to Uncover and Elucidate GP73-Mediated Pro-Angiogenic Regulatory Networks in Hepatocellular Carcinoma
Ye, J., Gao, X., Huang, X., Huang, S., Zeng, D., Luo, W., Zeng, C., Lu, C. C., Lu, L., Huang, H., et al. (2024) · Research · doi:10.34133/research.0387 · Cited by 55
“However, the initial nonresponsiveness or adaptive resistance, which are usually restricted, goes beyond the antitumor improvements in clinical practice [6].”
Background
p21-activated kinase 1 determines stem-like phenotype and sunitinib resistance via NF-κB/IL-6 activation in renal cell carcinoma
Zhu, Y., Liu, H., Xu, L., An, H., Liu, W., Liu, Y., Lin, Z., & Xu, J. (2015) · Cell Death and Disease · doi:10.1038/cddis.2015.2 · Cited by 55
“Resistance and low responsiveness to antiangiogenic tyrosine kinase inhibitors such as sunitinib is a major clinical obstacle in the treatment of mRCC.(51) Therefore, uncovering the underlying mechanisms has profound clinical significance.”
Background
HGF upregulation contributes to angiogenesis in mice with keratinocyte-specific Smad2 deletion
Hoot, K. E., Oka, M., Han, G., Böttinger, E. P., Zhang, Q., & Wang, X. (2010) · Journal of Clinical Investigation · doi:10.1172/jci43304 · Cited by 55
“Nevertheless, since cancer-associated angiogenesis involves multiple pathways and often harbors oncogene addiction (28), it remains to be determined whether blocking HGF-mediated angiogenesis can significantly slow down or starve tumor cells in Smad2-deficient SCCs.”
Background
Perivascular stem cell niche in head and neck cancer
Ritchie, K., & Nor, J. E. (2012) · Cancer Letters · doi:10.1016/j.canlet.2012.07.025 · Cited by 55
Fibroblast Growth Factor Receptor 4 Regulates Tumor Invasion by Coupling Fibroblast Growth Factor Signaling to Extracellular Matrix Degradation
Sugiyama, N., Varjosalo, M. T., Meller, P., Lohi, J., Hyytiäinen, M. M., Kilpinen, S. K., Kallioniemi, O., Ingvarsen, S., Engelholm, L. H., Taipale, J., et al. (2010) · Cancer Research · doi:10.1158/0008-5472.can-10-1223 · Cited by 55
New developments in the treatment of ovarian cancer—future perspectives
Lopez, J. S., Banerjee, S. N., & Kaye, S. B. (2013) · Annals of Oncology · doi:10.1093/annonc/mdt475 · Cited by 55
“The angiopoietin/Tie ligand/receptor system is a prototypic regulator of vessel remodelling, sprouting and maturation, and is known to be up-regulated in relapsing tumours [21, 26]).”
Background
Activin Receptor-like Kinase 1 Ligand Trap Reduces Microvascular Density and Improves Chemotherapy Efficiency to Various Solid Tumors
Hawinkels, L. J. A. C., de Vinuesa, A. G., Paauwe, M., Julio, M. K., Wiercinska, E., Pardali, E., Mezzanotte, L., Keereweer, S., Braumuller, T. M., Heijkants, R. C., et al. (2015) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-15-0743 · Cited by 54
“In addition, long-term suppression of VEGF signaling gives rise to compensatory mechanisms by other angiogenic pathways (8).”
Background
The vascular landscape of human cancer
Kahn, B., Lucas, A., Alur, R. G., Wengyn, M. D., Schwartz, G. W., Li, J., Sun, K., Maurer, H. C., Olive, K. P., Faryabi, R. B., et al. (2020) · Journal of Clinical Investigation · doi:10.1172/jci136655 · Cited by 59
Measurements of adiposity as clinical biomarkers for first-line bevacizumab-based chemotherapy in epithelial ovarian cancer
Slaughter, K. N., Thai, T., Penaroza, S., Benbrook, D. M., Thavathiru, E., Ding, K., Nelson, T., McMeekin, D. S., & Moore, K. N. (2014) · Gynecologic Oncology · doi:10.1016/j.ygyno.2014.01.031 · Cited by 54
“Additional theories formechanisms of resistance include the up-regulation of inflammatory cytokines in obese patients which can offer vascular protection [16].”
Background
Overcoming resistance to tyrosine kinase inhibitors in renal cell carcinoma
Ravaud, A., & Gross‐Goupil, M. (2012) · Cancer Treatment Reviews · doi:10.1016/j.ctrv.2012.01.003 · Cited by 54
Intrinsic resistance to tyrosine kinase inhibitors is associated with poor clinical outcome in metastatic renal cell carcinoma
Busch, J. F., Seidel, C. A., Weikert, S., Wolff, I., Kempkensteffen, C., Weinkauf, L., Hinz, S., Magheli, A., Miller, K., & Grünwald, V. (2011) · BMC Cancer · doi:10.1186/1471-2407-11-295 · Cited by 54
“Alternative proangiogenic signaling pathways within the tumor, recruitment of bone marrow-derived pro-angiogenic cells, increased protection of tumor vasculature by pericytes, and increased tumor cell invasiveness to escape oxygen and nutrient deprivation may all constitute escape mechanisms in response to therapy or…”
Background
Open-label, phase I dose-escalation study of sodium selenate, a novel activator of PP2A, in patients with castration-resistant prostate cancer
Corcoran, N. M., Hovens, C. M., Michael, M., Rosenthal, M. A., & Costello, A. J. (2010) · British Journal of Cancer · doi:10.1038/sj.bjc.6605798 · Cited by 54
“In addition, given the high frequency of VHL mutations in CCRCC, angiogenesis may be much more dependent on VEGF signalling than in prostate cancer, in which multiple redundant pathways have been implicated (Gravdal et al, 2006; Kim et al, 2006; Bergers and Hanahan, 2008; Yang et al, 2008).”
Background
Inhibition of Cathepsin S by Fsn0503 enhances the efficacy of chemotherapy in colorectal carcinomas
Burden, R. E., Gormley, J. A., Kuehn, D., Ward, C., Kwok, H. F., Gazdoiu, M., McClurg, A. E., Jaquin, T. J., Johnston, J. A., Scott, C. J., et al. (2011) · Biochimie · doi:10.1016/j.biochi.2011.08.017 · Cited by 54
“However, despite the initial successes with targeting angiogenesis, it has emerged that resistance to therapy can occur resulting in more aggressive tumourswith increasedmetastases [37,38].”
Background
Vascular Normalization by Loss of Siah2 Results in Increased Chemotherapeutic Efficacy
Wong, C. S. F., Sceneay, J., House, C. M., Halse, H. M., Liu, M. C. P., George, J., Hunnam, T. C. U. P., Parker, B. S., Haviv, I., Ronai, Z. A., et al. (2012) · Cancer Research · doi:10.1158/0008-5472.can-11-3310 · Cited by 54
“The proposed reasons for tumor escape from treatment include up-regulation of alternate angiogenic molecules (either acquired or pre-existing), recruitment of pro-angiogenic cells from the bone marrow or tumor cell invasion along existing vascular networks (5).”
Background
Proteolytic Cleavages in the VEGF Family: Generating Diversity among Angiogenic VEGFs, Essential for the Activation of Lymphangiogenic VEGFs
Künnapuu, J., Bokharaie, H., & Jeltsch, M. (2021) · Biology · doi:10.3390/biology10020167 · Cited by 54
“While a multitargeted anti-VEGF-A/-C/-D therapy might result in improved survival, any progress in this area will likely be incremental since using alternative tumor angiogenesis factors is only one of many escape mechanisms that tumors can deploy [124].”
Background
Effect of small angiokinase inhibitor nintedanib (BIBF 1120) on QT interval in patients with previously untreated, advanced renal cell cancer in an open-label, phase II study
Eisen, T. G., Shparyk, Y. V., MacLeod, N. J., Jones, R. J., Wallenstein, G., Temple, G., Khder, Y., Dallinger, C., Studeny, M., Loembé, A., et al. (2013) · Investigational New Drugs · doi:10.1007/s10637-013-9962-7 · Cited by 53
Exosomes from cervical cancer cells facilitate pro-angiogenic endothelial reconditioning through transfer of Hedgehog–GLI signaling components
Bhat, A., Yadav, J., Thakur, K., Aggarwal, N., Tripathi, T., Chhokar, A., Singh, T., Jadli, M., & Bharti, A. C. (2021) · Cancer Cell International · doi:10.1186/s12935-021-02026-3 · Cited by 54
“Moreover, VEGF immunotherapy is associated with the development of either evasive or adaptive resistance [15].”
Background
Methionine secreted by tumor-associated pericytes supports cancer stem cells in clear cell renal carcinoma
Zhang, C., Du, Z., Gao, Y., Lim, K. S., Zhou, W., Huang, H., He, H., Xiao, J., Xu, D., & Li, Q. (2024) · Cell Metabolism · doi:10.1016/j.cmet.2024.01.018 · Cited by 54
Glipizide, an antidiabetic drug, suppresses tumor growth and metastasis by inhibiting angiogenesis
Qi, C., Zhou, Q., Li, B., Yang, Y., Cao, L., Ye, Y., Li, J., Ding, Y., Wang, H., Wang, J., et al. (2014) · Oncotarget · doi:10.18632/oncotarget.2483 · Cited by 53
Common Responses of Tumors and Wounds to Hypoxia
Payen, V. L., Brisson, L., Dewhirst, M. W., & Sonveaux, P. (2015) · The Cancer Journal · doi:10.1097/ppo.0000000000000098 · Cited by 55
New Targeted Therapies for Thyroid Cancer
Antonelli, A., Fallahi, P., Ferrari, S. M., Ruffilli, I., Santini, F., Minuto, M. N., Galleri, D., & Miccoli, P. (2011) · Current Genomics · doi:10.2174/138920211798120808 · Cited by 53
“Unfortunately, eventual progression despite antiangiogenic VEGFR blockade suggests emergence of alternate pathways to promote tumor growth and metastasis (including FGFR, C-MET, and angiopoietins) [54].”
Background
Bone marrow derived cells in tumor angiogenesis and growth: are they the good, the bad or the evil?
Shaked, Y., & Voest, E. E. (2009) · Biochimica et Biophysica Acta (BBA) - Reviews on Cancer · doi:10.1016/j.bbcan.2009.07.002 · Cited by 52
Tumour vasculature and angiogenic profile of paediatric pilocytic astrocytoma; is it much different from glioblastoma?
Sie, M., de Bont, E. S. J. M., Scherpen, F. J. G., Hoving, E. W., & den Dunnen, W. F. A. (2010) · Neuropathology and Applied Neurobiology · doi:10.1111/j.1365-2990.2010.01113.x · Cited by 53
Use of bevacizumab in recurrent glioblastoma
Ghiaseddin, A. P., & Peters, K. B. (2015) · CNS Oncology · doi:10.2217/cns.15.8 · Cited by 54
NOS Inhibition Modulates Immune Polarization and Improves Radiation-Induced Tumor Growth Delay
Ridnour, L. A., Cheng, R. Y. S., Weiss, J. M., Kaur, S., Soto‐Pantoja, D. R., Basudhar, D., Heinecke, J. L., Stewart, C. A., DeGraff, W., Sowers, A. L., et al. (2015) · Cancer Research · doi:10.1158/0008-5472.can-14-3011 · Cited by 54
“Radiation-induced signaling pathways associated with cancer progression include elevated epidermal growth factor receptor, hypoxia inducible factor-1 (HIF-1), up-regulation and/or activation of matrix metalloproteinases (MMPs), and overexpression of cytokines including vascular endothelial growth factor (VEGF) and oth…”
Cyclin-dependent kinase 5 stabilizes hypoxia-inducible factor-1α: a novel approach for inhibiting angiogenesis in hepatocellular carcinoma
Herzog, J., Ehrlich, S. M., Pfitzer, L., Liebl, J., Fröhlich, T., Arnold, G. J., Mikulits, W., Haider, C., Vollmar, A. M., & Stefan Zahler, A. (2016) · Oncotarget · doi:10.18632/oncotarget.8342 · Cited by 53
COX-2 Inhibition mediated anti-angiogenic activatable prodrug potentiates cancer therapy in preclinical models
Kim, H. S., Sharma, A. K., Ren, W. X., Han, J., & Kim, J. S. (2018) · Biomaterials · doi:10.1016/j.biomaterials.2018.09.006 · Cited by 53
Personalized targeted therapy for esophageal squamous cell carcinoma
Kang, X. (2015) · World Journal of Gastroenterology · doi:10.3748/wjg.v21.i25.7648 · Cited by 54
Effects of ketoconazole on the pharmacokinetics of lenvatinib (E7080) in healthy participants
Shumaker, R., Aluri, J., Fan, J., Martinez, G., Thompson, G. A., & Ren, M. (2014) · Clinical Pharmacology in Drug Development · doi:10.1002/cpdd.140 · Cited by 52
Improving the prognosis for patients with glioblastoma: the rationale for targeting Src
de Groot, J., & Milano, V. (2009) · Journal of Neuro-Oncology · doi:10.1007/s11060-009-9916-2 · Cited by 54
“There has recently been an interest in developing combination strategies that may block the pro-invasive phenotype driven by the use of anti-VEGF therapies in glioblastoma [26, 100].”
Background
Targeted systemic therapies for hepatocellular carcinoma: Clinical perspectives, challenges and implications
Frenette, C. T. (2012) · World Journal of Gastroenterology · doi:10.3748/wjg.v18.i6.498 · Cited by 52
Evolutionary dynamics of the Warburg effect: Glycolysis as a collective action problem among cancer cells
Archetti, M. (2013) · Journal of Theoretical Biology · doi:10.1016/j.jtbi.2013.09.017 · Cited by 52
“, 2003; but see also Krtolica and Ludlow, 1996), and treatments like anti-angiogenic drugs that aim at impairing the provision of oxygen to the tumor may fail if tumors can switch to glycolysis (Bergers and Hanahan, 2008).”
Background
A PK2/Bv8/PROK2 Antagonist Suppresses Tumorigenic Processes by Inhibiting Angiogenesis in Glioma and Blocking Myeloid Cell Infiltration in Pancreatic Cancer
Curtis, V. F., Wang, H., Yang, P., McLendon, R. E., Li, X., Zhou, Q., & Wang, X. (2013) · PLoS ONE · doi:10.1371/journal.pone.0054916 · Cited by 57
Strategies to overcome therapeutic resistance in renal cell carcinoma
Siska, P. J., Beckermann, K. E., Rathmell, W. K., & Haake, S. M. (2017) · Urologic Oncology Seminars and Original Investigations · doi:10.1016/j.urolonc.2016.12.002 · Cited by 55
“Increased invasiveness is an adaptation of cancer cells to decreased angiogenesis that allows them to invade into normal tissue and rely on the normal vasculature for metabolic demands [7].”
Background
Targeted Therapy for Medullary Thyroid Cancer: A Review
Priya, S. R., Dravid, C. S., Digumarti, R., & Dandekar, M. (2017) · Frontiers in Oncology · doi:10.3389/fonc.2017.00238 · Cited by 52
“Finally, tumor cell signaling networks alterations and tumor microenvironment change which occur over time, influence disease progression as well as a drug’s effectiveness, thus resulting in secondary drug resistance (155).”
Background
The role of bevacizumab on tumour angiogenesis and in the management of gynaecological cancers: A review
Chellappan, D. K., Leng, K. H., Jia, L. J., Aziz, N. A. B. A., Hoong, W. C., Qian, Y. C., Ling, F. Y., Wei, G. S., Ying, T., Chellian, J., et al. (2018) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2018.03.061 · Cited by 53
A tightly controlled Src-YAP signaling axis determines therapeutic response to dasatinib in renal cell carcinoma
Sun, J., Wang, X., Tang, B., Liu, H., Zhang, M., Wang, Y., Ping, F., Ding, J., Shen, A., & Geng, M. (2018) · Theranostics · doi:10.7150/thno.23964 · Cited by 54
“Furthermore, the inherent occurrence of primary and acquired resistance has been observed in clinical settings [13-15].”
Antiangiogenic therapy: Markers of response, “normalization” and resistance
Alaoui‐Lasmaili, K. E., & Faivre‐Fiorina, B. (2018) · Critical Reviews in Oncology/Hematology · doi:10.1016/j.critrevonc.2018.06.001 · Cited by 52
Fatty-acid receptor CD36 functions as a hydrogen sulfide-targeted receptor with its Cys333-Cys272 disulfide bond serving as a specific molecular switch to accelerate gastric cancer metastasis
Wang, R., Tao, B., Fan, Q., Wang, S., Chen, L., Zhang, J., Hao, Y., Dong, S., Wang, Z., Wang, W., et al. (2019) · EBioMedicine · doi:10.1016/j.ebiom.2019.06.037 · Cited by 52
Tumor cell metabolism correlates with resistance to gas plasma treatment: The evaluation of three dogmas
Bekeschus, S., Liebelt, G., Menz, J., Berner, J., Sagwal, S. K., Wende, K., Weltmann, K., Boeckmann, L., von Woedtke, T., Metelmann, H., et al. (2021) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2021.02.035 · Cited by 56
Physical supports from liver cancer cells are essential for differentiation and remodeling of endothelial cells in a HepG2-HUVEC co-culture model
Chiew, G. G. Y., Fu, A., Low, K. P., & Luo, K. Q. (2015) · Scientific Reports · doi:10.1038/srep10801 · Cited by 52
VEGFR-2 redirected CAR-T cells are functionally impaired by soluble VEGF-A competition for receptor binding
Lanitis, E., Kosti, P., Ronet, C., Cribioli, E., Rota, G., Spill, A., Reichenbach, P., Zoete, V., Laniti, D. D., Coukos, G., et al. (2021) · Journal for ImmunoTherapy of Cancer · doi:10.1136/jitc-2020-002151 · Cited by 51
Natural products targeting tumour angiogenesis
Lu, X., Friedrich, L. J., & Efferth, T. (2023) · British Journal of Pharmacology · doi:10.1111/bph.16232 · Cited by 56
“…resistance related to natural products can be divided into two main mechanisms: One possible mechanism is the upregulation of alternative angiogenesis pathways or promoting tumour cell survival, such as the recruitment of bone marrow-derived cells to promote tumour growth (Bergers & Hanahan, 2008).”
Single-cell transcriptomic analysis reveals tumor cell heterogeneity and immune microenvironment features of pituitary neuroendocrine tumors
Yan, N., Xie, W., Wang, D., Fang, Q., Guo, J., Chen, Y., Li, X., Gong, L., Wang, J., Guo, W., et al. (2024) · Genome Medicine · doi:10.1186/s13073-023-01267-3 · Cited by 51
“These changes implied that the PitNET cells could be shielded by increased pericytes coverage [50, 51].”
Background
Molecular communication between tumor-associated fibroblasts and head and neck squamous cell carcinoma
Leef, G. C., & Thomas, S. M. (2013) · Oral Oncology · doi:10.1016/j.oraloncology.2012.12.014 · Cited by 51
“Since TAFs produce pro-angiogenic factors besides VEGF, they may be also involved in ‘‘evasive resistance’’, a phenomenon where tumors develop resistance to VEGF inhibitors by exploiting alternative angiogenic pathways.(58) Targeting pro-angiogenic factors produced by TAFs could complement existing anti-angiogenic the…”
Background
Progress on Antiangiogenic Therapy for Patients with Malignant Glioma
Ahluwalia, M. S., & Gladson, C. L. (2010) · Journal of Oncology · doi:10.1155/2010/689018 · Cited by 55
Glutamate as chemotactic fuel for diffuse glioma cells: Are they glutamate suckers?
van Lith, S. A. M., Navis, A. C., Verrijp, K. N., Niclou, S. P., Bjerkvig, R., Wesseling, P., Tops, B. B. J., Molenaar, R. J., Noorden, C. J. F. V., & Leenders, W. P. J. (2014) · Biochimica et Biophysica Acta (BBA) - Reviews on Cancer · doi:10.1016/j.bbcan.2014.04.004 · Cited by 51
A novel antiangiogenic and vascular normalization therapy targeted against human CD160 receptor
Chabot, S., Jabrane‐Ferrat, N., Bigot, K., Tabiasco, J., Provost, A. C., Golzio, M., Noman, M. Z., Giustiniani, J., Bellard, E., Brayer, S., et al. (2011) · The Journal of Experimental Medicine · doi:10.1084/jem.20100810 · Cited by 51
“After a period of clinical benefit, however, this mAb fails to produce an enduring clinical response in most patients as a result of adaptive resistance and compensatory mechanisms (Dorrell et al., 2007; Bergers and Hanahan, 2008).”
Background
Genetic variability of VEGF pathway genes in six randomized phase III trials assessing the addition of bevacizumab to standard therapy
de Haas, S., Delmar, P., Bansal, A. T., Moisse, M., Miles, D. W., Leighl, N. B., Escudier, B. J., Cutsem, E. V., Carmeliet, P., Scherer, S. J., et al. (2014) · Angiogenesis · doi:10.1007/s10456-014-9438-1 · Cited by 51
The Spatial Organization of Proton and Lactate Transport in a Rat Brain Tumor
Grillon, E., Farion, R., Fablet, K., WAARD, M. M. D., Tse, C., Donowitz, M., Remy, C. C., & Coles, J. A. (2011) · PLoS ONE · doi:10.1371/journal.pone.0017416 · Cited by 51
“given disappointing results in the long term [1].”
Result
Oral delivery of a potent anti-angiogenic heparin conjugate by chemical conjugation and physical complexation using deoxycholic acid
Alam, F., Al-Hilal, T. A., Chung, S. W., Seo, D.-H., Mahmud, F., Kim, H. S., Kim, S. Y., & Byun, Y. (2014) · Biomaterials · doi:10.1016/j.biomaterials.2014.04.050 · Cited by 51
Circulating endothelial cells as biomarkers in clinical oncology
Mancuso, P., & Bertolini, F. (2010) · Microvascular Research · doi:10.1016/j.mvr.2010.02.007 · Cited by 51
Multiscale Models of Breast Cancer Progression
Chakrabarti, A., Verbridge, S. S., Stroock, A. D., Fischbach, C., & Varner, J. D. (2012) · Annals of Biomedical Engineering · doi:10.1007/s10439-012-0655-8 · Cited by 52
M2-like tumor-associated macrophages drive vasculogenic mimicry through amplification of IL-6 expression in glioma cells
Zhang, L., Xu, Y., Sun, J., Chen, W., Zhao, L., Ma, C., Wang, Q., Sun, J., Huang, B., Zhang, Y., et al. (2016) · Oncotarget · doi:10.18632/oncotarget.13661 · Cited by 51
Hypoxia-Inducible PIM Kinase Expression Promotes Resistance to Antiangiogenic Agents
Casillas, A. L., Toth, R. K., Sainz, A. G., Singh, N., Desai, A. A., Kraft, A. S., & Warfel, N. A. (2017) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-17-1318 · Cited by 51
Glycosylation as new pharmacological strategies for diseases associated with excessive angiogenesis
Bousseau, S., Vergori, L., Soleti, R., Lenaers, G., Martínez, M. C., & Andriantsitohaina, R. (2018) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2018.06.003 · Cited by 51
Myricetin Inhibits Breast Tumor Growth and Angiogenesis by Regulating VEGF/VEGFR2 and p38MAPK Signaling Pathways
Zhou, Z., Mao, W., Li, Y., Qi, C., & He, Y. (2019) · The Anatomical Record · doi:10.1002/ar.24222 · Cited by 52
“© 2019 American Association for Anatomy process that mediates the invasion and metastasis of cancer cells in vital organs (Carmeliet, 2005).”
Background

Authors: Bergers, G., & Hanahan, D.
Affiliations: University of California, San Francisco (US)
ORCID: Bergers, Gabriele
Hanahan, Douglas
Venue: Nature Reviews Cancer
Publisher: Springer Science and Business Media LLC
Published: 2008-08
Volume: 8
Issue: 8
Pages: 592-603
ISSN: 1474-175X (ISSN-L)
1474-1768
DOI: 10.1038/nrc2442
PMC: PMC2874834
OpenAlex: W2017322644
Cited by: 2,953
References: 101
Citations by year: 2026: 70 · 2025: 77 · 2024: 97 · 2023: 130 · 2022: 95 · 2021: 172 · 2020: 133 · 2019: 152 · 2018: 148 · 2017: 202 · 2016: 217 · 2015: 228 · 2014: 241 · 2013: 248 · 2012: 215
FWCI: 13.60
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springer.com/tdm (tdm)
Locations: Nature reviews. Cancer (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Cancer Institute (R01CA099948)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
Health Sciences › Medicine › Oncology › Lymphatic System and Diseases
Keywords: anti-angiogenic therapy, drug resistance, vascular endothelial growth factor, VEGF signaling, tumor angiogenesis, intrinsic resistance, combination therapy
MeSH terms: Humans, Neoplasms, Neovascularization, Pathologic, Signal Transduction, Drug Resistance, Neoplasm, Angiogenesis Inhibitors, Vascular Endothelial Growth Factors

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review

Modes of resistance to anti-angiogenic therapy

Abstract

Overview

Integrity signals

Verification

Claims the paper makes

Claims other papers make about this one

Self-check

Citations

Cites

Cited by

Related

Metadata

Record

About these checks