{"id":708,"date":"2026-06-03T18:01:20","date_gmt":"2026-06-03T18:01:20","guid":{"rendered":"https:\/\/menteymanzana.com\/?p=708"},"modified":"2026-06-03T18:01:20","modified_gmt":"2026-06-03T18:01:20","slug":"hebersavax-vacuna-cubana-cancer-bevacizumab","status":"publish","type":"post","link":"https:\/\/menteymanzana.com\/en\/hebersavax-vacuna-cubana-cancer-bevacizumab\/","title":{"rendered":"HEBERSaVax: the Cuban cancer vaccine that breaks the Bevacizumab paradigm"},"content":{"rendered":"<style>\nbody.postid-708>.wp-site-blocks>main.wp-block-group{display:none!important}\nbody.postid-708 .wp-site-blocks>.wp-block-group.has-global-padding{padding-top:0!important}\nbody.postid-708 .wp-site-blocks>.wp-block-group>.wp-block-group:first-child{padding-top:0!important;margin-top:0!important}\nbody.postid-708 .entry-title{display:none!important}\nbody.postid-708 .wp-block-post-title{display:none!important}\nbody.postid-708 main{padding-top:0!important}\nbody.postid-708 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src=\"https:\/\/menteymanzana.com\/wp-content\/uploads\/2026\/06\/hebersavax-01-hero.jpeg\" alt=\"Vial de la vacuna cubana HEBERSaVax CIGB-247 contra el c\u00e1ncer\" \/><\/div>\n\n<h1 class=\"mm-custom-title\"><span class=\"accent\">HEBERSaVax<\/span>THE CUBAN CANCER VACCINE THAT BREAKS THE PARADIGM OF <span class=\"accent\">BEVACIZUMAB<\/span><\/h1>\n<p class=\"mm-subtitle\">Active anti-VEGF immunotherapy, dual mechanism and 32 months of survival in advanced ovary syndrome<\/p>\n\n<div class=\"mm-content\">\n\n<div class=\"mm-disclaimer\"><strong>Editorial note.<\/strong> This article is a peer-reviewed scientific literature review (<em>PubMed<\/em>, <em>MDPI Vaccines<\/em>, <em>Frontiers in Immunology<\/em>) and Cuban institutional communication (CIGB, CECMED, public clinical trial registries). <strong>This does not constitute individual medical advice or a treatment recommendation.<\/strong> HEBERSaVax (CIGB-247) is in phase II clinical trials and has not yet been approved by the FDA, EMA, or COFEPRIS. Any oncological treatment decision should be discussed with the treating medical team.<\/div>\n\n<p>Advanced ovarian cancer kills most patients diagnosed within three years of diagnosis. It is one of the grimtest prognoses in contemporary gynecological oncology. That is why when a phase II trial reports a <strong>median overall survival of 32.82 months<\/strong>, It is worth reading how that number was reached and, above all, what makes the drug that produced it different.<\/p>\n\n<p>The drug is called <strong>HEBERSaVax<\/strong> (development code) <em>CIGB-247<\/em>and it didn&#039;t come from a laboratory in Boston, Basel, or Cambridge. It came from <strong>Center for Genetic Engineering and Biotechnology<\/strong> (CIGB) of Havana, Cuba, after more than a decade of research led by the <strong>Dr. Yanelys Morera D\u00edaz<\/strong>, under the clinical direction of <strong>Dr. Francisco Hern\u00e1ndez Bernal<\/strong>. It is not a monoclonal antibody nor a tyrosine kinase inhibitor. It is a <em>therapeutic vaccine<\/em>: an active immunotherapy that teaches the patient&#039;s body to produce its own antibodies against the <strong>vascular endothelial growth factor<\/strong> (VEGF), the protein that tumors hijack to build their blood supply network.<\/p>\n\n<p>This post is not a pamphlet. It&#039;s a technical review of what the... <em>papers<\/em> published data, clinical trial registries, and active patents in 11 jurisdictions (including the United States, the European Union, China, and Japan). The goal is to understand why a Cuban team, with a limited budget, is accumulating clinical data that rivals the Western gold standard for cancer treatment: the <em>bevacizumab<\/em>.<\/p>\n\n<div class=\"mm-callout\"><strong>The essentials in three lines.<\/strong> HEBERSaVax blocks VEGF through a dual mechanism: polyclonal antibodies that cut off the tumor&#039;s blood supply + CD8+ T lymphocytes that destroy VEGF-producing cells. In the CENTAURO-4 trial (advanced ovarian cancer, n=40), it achieved <span class=\"mm-keyfig\">32.82 months median overall survival<\/span> with toxicity limited to grade 1-2. The patents are active in 11 jurisdictions until June. <strong>2032<\/strong>.<\/div>\n\n<h2>Module 1 \u2014 How it works: the dual anti-VEGF mechanism<\/h2>\n<figure class=\"mm-section-img\"><img decoding=\"async\" src=\"https:\/\/menteymanzana.com\/wp-content\/uploads\/2026\/06\/hebersavax-02-modulo1-mecanismo.jpeg\" alt=\"Mecanismo dual de HEBERSaVax: anticuerpos y linfocitos T atacando un vaso sangu\u00edneo tumoral\" \/><figcaption>The double front: antibodies that neutralize circulating VEGF and cytotoxic T cells that hunt down the producers.<\/figcaption><\/figure>\n\n<h3>Tumor angiogenesis, in a sentence<\/h3>\n<p>Solid tumors cannot grow beyond 1-2 millimeters without building their own network of blood vessels. To do this, they secrete large amounts of <strong>VEGF<\/strong>, a signaling protein that acts on receptors <em>VEGFR1<\/em> y <em>VEGFR2<\/em> (KDR) of endothelial cells and induces them to proliferate, forming new capillaries. Without VEGF, there is no tumor angiogenesis. And without tumor angiogenesis, the tumor is deprived of oxygen and nutrients.<\/p>\n\n<p>The classic clinical problem is that VEGF doesn&#039;t just build blood vessels: it also <strong>suppresses the local immune system<\/strong>. It blocks the maturation of dendritic cells, recruits tumor suppressor cells (MDSCs), and expands regulatory T lymphocytes (Tregs). By overproducing VEGF, the tumor creates an immune force field around itself that prevents cytotoxic T lymphocytes from doing their job.<\/p>\n\n<h3>HEBERSaVax&#039;s double front<\/h3>\n<p>This is what changes with Cuban active immunotherapy. When a patient receives HEBERSaVax, their own immune system begins to produce two things at once.<\/p>\n\n<p><strong>On the one hand<\/strong>, specific B cells that release torrents of <strong>polyclonal antibodies<\/strong> against multiple epitopes of circulating VEGF. Unlike a synthetic monoclonal antibody that recognizes a single site, polyclonal antibodies attack the protein from multiple angles at once, neutralizing it in the serum before it can bind to <em>VEGFR2<\/em>. The result documented in preclinical biopsies: <span class=\"mm-keyfig\">44% drop<\/span> in tumor proliferation (Ki67 marker), drastic reduction of microvessel density (CD31+), loss of pericyte support (\u03b1-SMA+).<\/p>\n\n<p><strong>On the other hand<\/strong>, the vaccine induces a response <strong>cytotoxic cell<\/strong> lymphocyte-mediated <em>T CD8+<\/em>. These lymphocytes, trained by the patient&#039;s spleen and lymph nodes, go out to hunt down and destroy the tumor stromal cells that are producing VEGF. It is not enough to neutralize VEGF in the blood; the factories that produce it must be eliminated. This is what no monoclonal antibody can do.<\/p>\n\n<p>There is a fascinating therapeutic side effect: by temporarily normalizing the tumor&#039;s vascular network, the vaccine also opens a <em>normalization window<\/em> which facilitates the entry of CD4+ and CD8+ T lymphocytes into the tumor nucleus. HEBERSaVax doesn&#039;t just attack: it also invites the rest of the immune system to join the party.<\/p>\n\n<h2>Module 2 \u2014 Molecular Engineering<\/h2>\n<figure class=\"mm-section-img\"><img decoding=\"async\" src=\"https:\/\/menteymanzana.com\/wp-content\/uploads\/2026\/06\/hebersavax-03-modulo2-proteina.jpeg\" alt=\"Estructura 3D de VEGF121 mutado del ant\u00edgeno CIGB-247\" \/><figcaption>The CIGB-247:VEGF121 antigen with the His86\u2192Glu mutation that makes it inert without losing immunological recognition.<\/figcaption><\/figure>\n\n<h3>The CIGB-247 antigen and the His86\u2192Glu mutation<\/h3>\n<p>Here&#039;s the technical problem the CIGB team had to solve: VEGF is a protein naturally found in the human body. Injecting functional VEGF as a vaccine would be suicidal\u2014it would stimulate angiogenesis and accelerate tumor growth. So how do you design a protein that is recognized by the immune system but doesn&#039;t do what natural VEGF does?<\/p>\n\n<p>The answer was a subtle but surgical genetic re-engineering. The pharmacological core of HEBERSaVax is a recombinant variant of the human isoform. <em>VEGF121<\/em>, produced in bacterial fermentation systems (allowing for scalable manufacturing). This protein was then introduced <strong>three amino acid substitutions<\/strong>, the most critical being the mutation <strong>His86 \u2192 Glu<\/strong>: histidine at position 86 was replaced by glutamic acid.<\/p>\n\n<p>The biological effect is categorical. This substitution changes the three-dimensional conformation of the receptor-binding domain and <strong>completely abrogates<\/strong> the antigen&#039;s ability to bind to <em>VEGFR1<\/em> y <em>VEGFR2<\/em>. The CIGB-247 antigen is <em>inert<\/em> In terms of pro-angiogenic signaling: it doesn&#039;t stimulate endothelial proliferation, it doesn&#039;t feed the tumor. But it preserves intact the epitopes that the immune system needs to recognize. It&#039;s the difference between a key that opens a door and a deformed key that no longer fits but that the immune system still identifies as a key.<\/p>\n\n<h3>The adjuvant transition<\/h3>\n<p>A therapeutic vaccine is not just the antigen. It is the antigen plus a <strong>adjuvant<\/strong>. For years, the CIGB used the <em>Very Small Proteoliposome<\/em> (VSSP), derived from modified membrane <em>Neisseria meningitidis<\/em>, which in murine models induced a more potent Th1-type response.<\/p>\n\n<p>But the VSSP is complex, difficult to scale, and unfamiliar to regulators. When the project needed to be scaled to phases II and III, the team migrated to <strong>Aluminum Phosphate<\/strong> (AP), pre-approved by the FDA. Human trials revealed that the immunogenic differences between VSSP and AP were <em>marginal<\/em>. What dictated the strength of the response was not the adjuvant, but the <span class=\"mm-keyfig\">escalation to 800 \u00b5g antigen<\/span>. That discovery simplified manufacturing and paved the way for international regulation.<\/p>\n\n<h2>Module 3 \u2014 Clinical data: the CENTAURO program<\/h2>\n<figure class=\"mm-section-img\"><img decoding=\"async\" src=\"https:\/\/menteymanzana.com\/wp-content\/uploads\/2026\/06\/hebersavax-04-modulo3-clinico.jpeg\" alt=\"Vial de HEBERSaVax sobre expedientes cl\u00ednicos del ensayo CENTAURO-4\" \/><figcaption>CENTAURO-4: Phase II trial with six years of follow-up, 32.82 months of overall survival.<\/figcaption><\/figure>\n\n<h3>From phase I to phase II: the chronology<\/h3>\n<p>The CIGB clinical trials program is named after <strong>CENTAUR<\/strong>. The following table summarizes the most relevant published phases.<\/p>\n\n<table>\n<thead><tr><th>Phase<\/th><th>Population<\/th><th>Dosage and adjuvant<\/th><th>Key finding<\/th><\/tr><\/thead>\n<tbody>\n<tr><td><strong>CENTAUR<\/strong> (Phase I)<\/td><td>30 patients with advanced refractory solid tumors<\/td><td>Escalation 50 \u2192 100 \u2192 400 \u00b5g with VSSP<\/td><td>Systemic safety confirmed. Dose-response correlation via ELISPOT.<\/td><\/tr>\n<tr><td><strong>CENTAURO-2<\/strong> (Phase Ib)<\/td><td>Expanded cohorts<\/td><td>200 \u2192 400 \u2192 <strong>800 \u00b5g<\/strong>, VSSP vs AP<\/td><td>Validation of 800 \u00b5g as the optimal dose. Equivalent tolerance between adjuvants.<\/td><\/tr>\n<tr><td><strong>CENTAURO-4<\/strong> (Phase II)<\/td><td>40 patients with advanced epithelial ovarian cancer<\/td><td>800 \u00b5g + chemotherapy (carboplatin\/paclitaxel)<\/td><td><strong>Median PFS: 18 months. Median OS: 32.82 months.<\/strong> Adverse effects grade 1-2 local.<\/td><\/tr>\n<tr><td><strong>CENTAURO-6<\/strong> (Phase II)<\/td><td>Hepatocellular carcinoma<\/td><td>800 \u00b5g under hospital conditions<\/td><td>Ongoing at CIMEQ in Havana. Reductions in liver tumor activity reported.<\/td><\/tr>\n<\/tbody>\n<\/table>\n\n<h3>32.82 months: the figure that rewrites the forecast<\/h3>\n<p>The number that matters is in the CENTAURO-4 row. To understand why this is relevant, it needs to be put into context: advanced epithelial ovarian cancer with suboptimal surgery or unresectable disease historically has a median overall survival of <strong>20 to 24 months<\/strong> with standard treatment (chemotherapy + bevacizumab). To reach <strong>32.82 months<\/strong> Adding subcutaneous injections of very low toxicity places HEBERSaVax at a clinical level clearly superior to the standard.<\/p>\n\n<p>The study was published in a peer-reviewed journal (<em>PubMed<\/em> 41099583) after six years of follow-up. The median PFS was 18 months, and the OS was 32.82 months. Adverse events were limited to grade 1-2 local injection site reactions\u2014nothing comparable to the refractory hypertension, bleeding, and gastrointestinal perforations documented with conventional bevacizumab.<\/p>\n\n<p>In it <strong>Compassionate Use Program<\/strong> (CUP) approved by CECMED, real-world practice data confirmed the findings: polyclonal production of IgM, IgA, and IgG specifically directed against VEGF, without cross-reactivity with other isoforms (VEGF-C, VEGF-D). In long-term survivors, a <em>class-switching<\/em> from IgG1 to <strong>IgG4<\/strong>, the molecular hallmark of an immunological memory that confers sustained protection.<\/p>\n\n<h2>Module 4 \u2014 HEBERSaVax vs Bevacizumab<\/h2>\n<figure class=\"mm-section-img\"><img decoding=\"async\" src=\"https:\/\/menteymanzana.com\/wp-content\/uploads\/2026\/06\/hebersavax-05-modulo4-acceso.jpeg\" alt=\"Comparaci\u00f3n HEBERSaVax vs Bevacizumab: subcut\u00e1neo vs infusi\u00f3n intravenosa\" \/><figcaption>Two paradigms: passive immunity (bevacizumab IV) versus active immunity (HEBERSaVax subcutaneous).<\/figcaption><\/figure>\n\n<h3>Passive immunity versus active immunity<\/h3>\n<p>He <em>bevacizumab<\/em> (trade names) <em>Avastin<\/em>, <em>Mvasi<\/em>, <em>Zirabev<\/em>) is the global standard for VEGF blocking. It works, but it belongs to the paradigm of <strong>passive immunity<\/strong>The patient receives intravenous infusions of monoclonal antibodies manufactured in industrial bioreactors. Plasma levels are extremely high, effectively neutralizing circulating VEGF, but they also damage healthy endothelium. Hence the range of toxicities: severe hypertension, hemorrhage, renal dysfunction, and intestinal perforation.<\/p>\n\n<p>HEBERSaVax establishes the opposite paradigm: <strong>active immunity<\/strong> modulated and persistent. The patient does not receive the finished antibody; they receive the modified antigen that teaches their own body to produce it. The result is endogenous secretion. <em>metronomic<\/em>, sustained, at low concentrations but with high affinity.<\/p>\n\n<table>\n<thead><tr><th>Variable<\/th><th>Bevacizumab<\/th><th>HEBERSaVax<\/th><\/tr><\/thead>\n<tbody>\n<tr><td><strong>Mechanism<\/strong><\/td><td>Passive immunity: exogenous antibody<\/td><td>Active immunity: polyclonal antibodies + CD8+ T cells<\/td><\/tr>\n<tr><td><strong>Via<\/strong><\/td><td>Hospital intravenous infusion<\/td><td>Outpatient subcutaneous injection<\/td><\/tr>\n<tr><td><strong>Kinetics<\/strong><\/td><td>High peaks and rapid falls<\/td><td>Levels sustained for months<\/td><\/tr>\n<tr><td><strong>Epitopes<\/strong><\/td><td>One (monoclonal)<\/td><td>Multiple (polyclonal)<\/td><\/tr>\n<tr><td><strong>Action on VEGF producers<\/strong><\/td><td>None<\/td><td>Active cytotoxicity via CD8+ T cells<\/td><\/tr>\n<tr><td><strong>Toxicity<\/strong><\/td><td>Hypertension, hemorrhages, GI perforations<\/td><td>Local reactions grade 1-2<\/td><\/tr>\n<tr><td><strong>Cost<\/strong><\/td><td>Tens of thousands of USD per cycle<\/td><td>Scalable bacterial fermentation<\/td><\/tr>\n<\/tbody>\n<\/table>\n\n<p>There is one piece of experimental data that deserves to be highlighted: the trials <em>in vitro<\/em> Using serum from vaccinated patients, they demonstrated that endogenously generated antibodies <strong>They compete for the same VEGF domains<\/strong> which bevacizumab attacks, and even <strong>completely inhibit<\/strong> The ability of bevacizumab to bind to its target when mixed. The natural immune machinery activated by the vaccine produces antibodies that match the affinity of those created in the laboratory.<\/p>\n\n<h3>Patents and global access<\/h3>\n<p>The CIGB secured a worldwide monopoly on CIGB-247 technology through a dossier of patents active until June. <strong>2032<\/strong> in: <strong>European Union<\/strong> (EPO), <strong>USA<\/strong> (USPTO), <strong>Canada<\/strong>, <strong>Mexico<\/strong>, <strong>Japan<\/strong>, <strong>South Korea<\/strong>, <strong>China<\/strong>, <strong>Russian Federation<\/strong>, <strong>Australia<\/strong> y <strong>South Africa<\/strong>. The <em>Technology Innovation Agency<\/em> South Africa has already documented the bilateral Cuba-South Africa collaboration for local production.<\/p>\n\n<h2>Balance<\/h2>\n\n<p><strong>First<\/strong>, The published clinical data are robust for their category. CENTAURO-4 is a phase II trial, n=40, with six years of follow-up and publication in a peer-reviewed journal. It is not a phase III trial, it does not have FDA or EMA approval, and that should be made clear. But the <span class=\"mm-keyfig\">32.82 months<\/span> Median overall survival in a cancer population with a very poor prognosis is not a minor fact.<\/p>\n\n<p><strong>Second<\/strong>, Molecular design is elegant. Mutation <em>His86 \u2192 Glu<\/em> It solved the central technical problem of how to vaccinate against a self-protein without triggering iatrogenic effects. The transition from the VSSP adjuvant to aluminum phosphate resolved the logistical problem of scalability. These are engineering decisions that a team with a limited budget had to make with particular rationality, and the data suggest that they made them well.<\/p>\n\n<p><strong>Third<\/strong>, The contrast with bevacizumab is not merely rhetorical. HEBERSaVax is subcutaneous (not IV), polyclonal (not monoclonal), has a dual mechanism of action (antibodies + cytotoxic T cells), exhibits a toxicity profile limited to grade 1-2, and is produced by scalable bacterial fermentation. If the phase II data are replicated in phase III, the cost-benefit analysis for public health systems in the Global South and Europe changes radically.<\/p>\n\n<p><strong>Room<\/strong>, A sober reading. This is not a declaration that the Cuban vaccine \u201ccures cancer.\u201d No serious researcher at the CIGB makes that claim. What is documented is that a dual-pathway active immunotherapy, developed outside the traditional pharmaceutical system, is accumulating clinical evidence that fully justifies advancing to a multicenter, international Phase III trial. For patients with advanced ovarian, hepatocellular, colorectal, and renal cancer, the mere possibility of incorporating HEBERSaVax into the treatment algorithm deserves sustained attention. The dossier is open, and the data continues to arrive.<\/p>\n\n<div class=\"mm-refs\"><h3>Selected references<\/h3><ol>\n<li>Hern\u00e1ndez-Bernal F, et al. (2026). <em>HEBERSaVax immunotherapy combined with first-line chemotherapy in advanced ovarian cancer: Phase II CENTAURO-4 trial results.<\/em> PubMed 41099583.<\/li>\n<li>Morera Y, et al. (2026). <em>Anti-VEGF immunotherapy with HEBERSaVax suppresses melanoma growth and metastasis.<\/em> Frontiers in Immunology \/ PMC12757277.<\/li>\n<li>Morera Y, et al. (2026). <em>Longitudinal Assessment of an 800 \u00b5g Dose of HEBERSaVax in Non-Human Primates.<\/em> MDPI Vaccines 14(3):230.<\/li>\n<li>Gavilondo JV, Hern\u00e1ndez-Bernal F, et al. <em>Specific active immunotherapy with the HEBERSaVax VEGF-based cancer vaccine: From bench to bedside.<\/em> PubMed 30318086.<\/li>\n<li>Morera Y, et al. (2012). <em>CIGB-247: a VEGF-based therapeutic vaccine that reduces experimental and spontaneous lung metastasis.<\/em> PubMed 22240345.<\/li>\n<li>Hern\u00e1ndez-Bernal F, et al. (2014). <em>Specific active immunotherapy with a VEGF vaccine in patients with advanced solid tumors. CENTAURO phase I.<\/em> PubMed 24530151.<\/li>\n<li>P\u00e9rez-S\u00e1nchez L, et al. (2020). <em>Specific humoral response in cancer patients treated within a compassionate use program.<\/em> PMC 7071683.<\/li>\n<li>CIMEQ. <em>CENTAURO-6 Study \u2014 Hepatocellular Carcinoma.<\/em> RPCEC00000237.<\/li>\n<li>SciELO Cuba (2022). <em>New contributions to the study of immunological effectors induced with CIGB-247.<\/em><\/li>\n<li>Granma (May 2026). <em>HEBERSaVax: The story of a Cuban product unique in the world.<\/em><\/li>\n<li>Radio Angulo (May 2026). <em>Cuba Showcases Results of HEBERSaVax Cancer Vaccine Candidate.<\/em><\/li>\n<li>Technology Innovation Agency South Africa (2025). <em>South Africa-Cuba Biotechnology Collaboration.<\/em><\/li>\n<li>CIGB. <em>HEBERSaVax product profile.<\/em> cigb.edu.cu.<\/li>\n<li>Morera Y, et al. <em>Experimental studies of a vaccine formulation of recombinant human VEGF.<\/em> Tandfonline 10.1080\/21645515.2015.1029213.<\/li>\n<\/ol><\/div>\n\n<\/div>","protected":false},"excerpt":{"rendered":"<p>HEBERSaVax (CIGB-247) is the Cuban therapeutic cancer vaccine that targets VEGF through a dual mechanism. Six-year data from the CENTAURO-4 trial in advanced ovarian cancer: 32.82 months of overall survival. How does it compare to Bevacizumab and why does it change the landscape of cancer treatment?.<\/p>","protected":false},"author":1,"featured_media":707,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"footnotes":""},"categories":[51,45],"tags":[],"class_list":["post-708","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-longevidad-metricas","category-noticias"],"acf":{"hallazgo_clave":"HEBERSaVax (CIGB-247): vacuna cubana anti-VEGF con 32,82 meses de supervivencia global mediana en ovario avanzado.","tiempo_lectura":14,"nivel_evidencia":"moderado","fuente_original":"https:\/\/pubmed.ncbi.nlm.nih.gov\/41099583\/","protocolo_aplicable":false,"referencias_texto":"","tags_cientificos":"HEBERSaVax, CIGB-247, vacuna terap\u00e9utica, VEGF, angiog\u00e9nesis tumoral, inmunoterapia activa, CENTAURO-4, c\u00e1ncer de ovario, Bevacizumab, CIGB, oncolog\u00eda"},"hallazgo_clave":"HEBERSaVax (CIGB-247): vacuna cubana anti-VEGF con 32,82 meses de supervivencia global mediana en ovario avanzado.","tiempo_lectura":"14","nivel_evidencia":"moderado","fuente_original":"https:\/\/pubmed.ncbi.nlm.nih.gov\/41099583\/","protocolo_aplicable":false,"referencias_texto":null,"tags_cientificos":"HEBERSaVax, CIGB-247, vacuna terap\u00e9utica, VEGF, angiog\u00e9nesis tumoral, inmunoterapia activa, CENTAURO-4, c\u00e1ncer de ovario, Bevacizumab, CIGB, oncolog\u00eda","_links":{"self":[{"href":"https:\/\/menteymanzana.com\/en\/wp-json\/wp\/v2\/posts\/708","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/menteymanzana.com\/en\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/menteymanzana.com\/en\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/menteymanzana.com\/en\/wp-json\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"https:\/\/menteymanzana.com\/en\/wp-json\/wp\/v2\/comments?post=708"}],"version-history":[{"count":2,"href":"https:\/\/menteymanzana.com\/en\/wp-json\/wp\/v2\/posts\/708\/revisions"}],"predecessor-version":[{"id":710,"href":"https:\/\/menteymanzana.com\/en\/wp-json\/wp\/v2\/posts\/708\/revisions\/710"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/menteymanzana.com\/en\/wp-json\/wp\/v2\/media\/707"}],"wp:attachment":[{"href":"https:\/\/menteymanzana.com\/en\/wp-json\/wp\/v2\/media?parent=708"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/menteymanzana.com\/en\/wp-json\/wp\/v2\/categories?post=708"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/menteymanzana.com\/en\/wp-json\/wp\/v2\/tags?post=708"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}