Laura Soucek
Barcelona, Cataluña, España
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Specialties: Cancer Research
Artículos de Laura
Actividad
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El Dr. Josep Tabernero, fundador de IOB, la Dra. Enriqueta Felip, jefa de Unidad de Tumores Torácicos, de Cabeza y Cuello de IOB, y la Dra. Ana…
El Dr. Josep Tabernero, fundador de IOB, la Dra. Enriqueta Felip, jefa de Unidad de Tumores Torácicos, de Cabeza y Cuello de IOB, y la Dra. Ana…
Recomendado por Laura Soucek
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Registration for the 2025 Gordon Research Conference on #Microproteins is OPEN. Scholarships are available! Insanely good line-up and you won't…
Registration for the 2025 Gordon Research Conference on #Microproteins is OPEN. Scholarships are available! Insanely good line-up and you won't…
Recomendado por Laura Soucek
Experiencia
Educación
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CELforPharma
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2 days course online. Understand the structure of the pharma business development process in the pharma-biotech world – Grasp the terminology, challenges, concepts & tools in each step, from analysis and planning, up to closing and following-up a deal
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Earners of this learning credential have attended the EBD Academy 3-day Advanced Business Development programme and demonstrated a competent understanding of the licensing and deal making process for the pharmaceutical and biotech industry. Covering four key areas of deal making the credential holder has participated in the continuous group exercise, practically apply their knowledge of product valuation, negotiation, intellectual property and deal structuring to successfully achieve a deal.
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Be able to decide on the best deal type for products in R&D – Know what to include in CDAs, MTAs and term sheets – Learn how to prepare product information and how to find potential partners – Know how to calculate the value of your product and optimise the deal structure. More info at: https://www.celforpharma.com/course/pharmaceutical-out-licensing-course
Publicaciones
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Inhibition of MYC attenuates tumor cell self-renewal and promotes senescence in SMARCB1 deficient Group 2 Atypical Teratoid Rhabdoid Tumors to suppress tumor growth in vivo
Int J Cancer
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Interrogating open issues in cancer medicine with patient-derived xenografts.
Nature Reviews of Cancer
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Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: the challenge ahead.
Carcinogenesis
Lifestyle factors are responsible for a considerable portion of cancer incidence worldwide, but credible estimates from the World Health Organization and the International Agency for Research on Cancer (IARC) suggest that the fraction of cancers attributable to toxic environmental exposures is between 7% and 19%. To explore the hypothesis that low-dose exposures to mixtures of chemicals in the environment may be combining to contribute to environmental carcinogenesis, we reviewed 11 hallmark…
Lifestyle factors are responsible for a considerable portion of cancer incidence worldwide, but credible estimates from the World Health Organization and the International Agency for Research on Cancer (IARC) suggest that the fraction of cancers attributable to toxic environmental exposures is between 7% and 19%. To explore the hypothesis that low-dose exposures to mixtures of chemicals in the environment may be combining to contribute to environmental carcinogenesis, we reviewed 11 hallmark phenotypes of cancer, multiple priority target sites for disruption in each area and prototypical chemical disruptors for all targets, this included dose-response characterizations, evidence of low-dose effects and cross-hallmark effects for all targets and chemicals. In total, 85 examples of chemicals were reviewed for actions on key pathways/mechanisms related to carcinogenesis. Only 15% (13/85) were found to have evidence of a dose-response threshold, whereas 59% (50/85) exerted low-dose effects. No dose-response information was found for the remaining 26% (22/85). Our analysis suggests that the cumulative effects of individual (non-carcinogenic) chemicals acting on different pathways, and a variety of related systems, organs, tissues and cells could plausibly conspire to produce carcinogenic synergies. Additional basic research on carcinogenesis and research focused on low-dose effects of chemical mixtures needs to be rigorously pursued before the merits of this hypothesis can be further advanced. However, the structure of the World Health Organization International Programme on Chemical Safety ‘Mode of Action’ framework should be revisited as it has inherent weaknesses that are not fully aligned with our current understanding of cancer biology.
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The effect of environmental chemicals on the tumor microenvironment.
Carconogenesis
Potentially carcinogenic compounds may cause cancer through direct DNA damage or through indirect cellular or physiological effects. To study possible carcinogens, the fields of endocrinology, genetics, epigenetics, medicine, environmental health, toxicology, pharmacology and oncology must be considered. Disruptive chemicals may also contribute to multiple stages of tumor development through effects on the tumor microenvironment. In turn, the tumor microenvironment consists of a complex…
Potentially carcinogenic compounds may cause cancer through direct DNA damage or through indirect cellular or physiological effects. To study possible carcinogens, the fields of endocrinology, genetics, epigenetics, medicine, environmental health, toxicology, pharmacology and oncology must be considered. Disruptive chemicals may also contribute to multiple stages of tumor development through effects on the tumor microenvironment. In turn, the tumor microenvironment consists of a complex interaction among blood vessels that feed the tumor, the extracellular matrix that provides structural and biochemical support, signaling molecules that send messages and soluble factors such as cytokines. The tumor microenvironment also consists of many host cellular effectors including multipotent stromal cells/mesenchymal stem cells, fibroblasts, endothelial cell precursors, antigen-presenting cells, lymphocytes and innate immune cells. Carcinogens can influence the tumor microenvironment through effects on epithelial cells, the most common origin of cancer, as well as on stromal cells, extracellular matrix components and immune cells. Here, we review how environmental exposures can perturb the tumor microenvironment. We suggest a role for disrupting chemicals such as nickel chloride, Bisphenol A, butyltins, methylmercury and paraquat as well as more traditional carcinogens, such as radiation, and pharmaceuticals, such as diabetes medications, in the disruption of the tumor microenvironment. Further studies interrogating the role of chemicals and their mixtures in dose-dependent effects on the tumor microenvironment could have important general mechanistic implications for the etiology and prevention of tumorigenesis.
Otros autoresVer publicación -
The estrogen receptor fusion system in mouse models: a reversible switch.
Cold Spring Harb Protoc.
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Myc inhibition is effective against glioma and reveals a role for Myc in proficient mitosis.
Nature Communications
Gliomas are the most common primary tumours affecting the adult central nervous system and respond poorly to standard therapy. Myc is causally implicated in most human tumours and the majority of glioblastomas have elevated Myc levels. Using the Myc dominant negative Omomyc, we previously showed that Myc inhibition is a promising strategy for cancer therapy. Here, we preclinically validate Myc inhibition as a therapeutic strategy in mouse and human glioma, using a mouse model of spontaneous…
Gliomas are the most common primary tumours affecting the adult central nervous system and respond poorly to standard therapy. Myc is causally implicated in most human tumours and the majority of glioblastomas have elevated Myc levels. Using the Myc dominant negative Omomyc, we previously showed that Myc inhibition is a promising strategy for cancer therapy. Here, we preclinically validate Myc inhibition as a therapeutic strategy in mouse and human glioma, using a mouse model of spontaneous multifocal invasive astrocytoma and its derived neuroprogenitors, human glioblastoma cell lines, and patient-derived tumours both in vitro and in orthotopic xenografts. Across all these experimental models we find that Myc inhibition reduces proliferation, increases apoptosis and remarkably, elicits the formation of multinucleated cells that then arrest or die by mitotic catastrophe, revealing a new role for Myc in the proficient division of glioma cells.
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The action mechanism of the Myc inhibitor termed Omomyc may give clues on how to target Myc for cancer therapy.
PlosOne
Recent evidence points to Myc – a multifaceted bHLHZip transcription factor deregulated in the majority of human cancers – as a priority target for therapy. How to target Myc is less clear, given its involvement in a variety of key functions in healthy cells. Here we report on the action mechanism of the Myc interfering molecule termed Omomyc, which demonstrated astounding therapeutic efficacy in transgenic mouse cancer models in vivo. Omomyc action is different from the one that can be…
Recent evidence points to Myc – a multifaceted bHLHZip transcription factor deregulated in the majority of human cancers – as a priority target for therapy. How to target Myc is less clear, given its involvement in a variety of key functions in healthy cells. Here we report on the action mechanism of the Myc interfering molecule termed Omomyc, which demonstrated astounding therapeutic efficacy in transgenic mouse cancer models in vivo. Omomyc action is different from the one that can be obtained by gene knockout or RNA interference, approaches designed to block all functions of a gene product. This molecule – instead – appears to cause an edge-specific perturbation that destroys some protein interactions of the Myc node and keeps others intact, with the result of reshaping the Myc transcriptome. Omomyc selectively targets Myc protein interactions: it binds c- and N-Myc, Max and Miz-1, but does not bind Mad or select HLH proteins. Specifically, it prevents Myc binding to promoter E-boxes and transactivation of target genes while retaining Miz-1 dependent binding to promoters and transrepression. This is accompanied by broad epigenetic changes such as decreased acetylation and increased methylation at H3 lysine 9. In the presence of Omomyc, the Myc interactome is channeled to repression and its activity appears to switch from a pro-oncogenic to a tumor suppressive one. Given the extraordinary therapeutic impact of Omomyc in animal models, these data suggest that successfully targeting Myc for cancer therapy might require a similar twofold action, in order to prevent Myc/Max binding to E-boxes and, at the same time, keep repressing genes that would be repressed by Myc.
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Patentes
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English
Competencia bilingüe o nativa
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Italian
Competencia bilingüe o nativa
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Spanish
Competencia bilingüe o nativa
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Catalan
Competencia básica
Recomendaciones recibidas
2 personas han recomendado a Laura
Unirse para verloMás actividad de Laura
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CRIS contra el Cáncer se ha incorporado a nuestro patronato, el máximo órgano de gobierno del centro, junto a Generalitat de Catalunya, Fundación…
CRIS contra el Cáncer se ha incorporado a nuestro patronato, el máximo órgano de gobierno del centro, junto a Generalitat de Catalunya, Fundación…
Recomendado por Laura Soucek
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Ver a seis miembros de FERO en este ranking es para nosotros un gran orgullo porque nos indica que vamos en la buena dirección para nuestra única…
Ver a seis miembros de FERO en este ranking es para nosotros un gran orgullo porque nos indica que vamos en la buena dirección para nuestra única…
Recomendado por Laura Soucek
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STAb Therapeutics participated in the #ASEICAMED retreat organized by ASEICA - Asociación Española de Investigación sobre el Cáncer with our CEO…
STAb Therapeutics participated in the #ASEICAMED retreat organized by ASEICA - Asociación Española de Investigación sobre el Cáncer with our CEO…
Recomendado por Laura Soucek
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🎉 Congratulations to Karin de Visser, who will be awarded the prestigious 2025 Pezcoller-Marina Larcher Fogazzaro-EACR Women in Cancer Research…
🎉 Congratulations to Karin de Visser, who will be awarded the prestigious 2025 Pezcoller-Marina Larcher Fogazzaro-EACR Women in Cancer Research…
Recomendado por Laura Soucek
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💡Las investigadoras del grupo de investigación #Diamet del #IISPV, Sonia Fernandez Veledo (IP) e Isabel Huber Ruano forman parte del…
💡Las investigadoras del grupo de investigación #Diamet del #IISPV, Sonia Fernandez Veledo (IP) e Isabel Huber Ruano forman parte del…
Recomendado por Laura Soucek
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🏥👏 El Grupo de Factores de Crecimiento del Vall d'Hebron Institute of Oncology (VHIO) y el Hospital del Mar Research Institute (HMRI) han…
🏥👏 El Grupo de Factores de Crecimiento del Vall d'Hebron Institute of Oncology (VHIO) y el Hospital del Mar Research Institute (HMRI) han…
Recomendado por Laura Soucek
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El passat cap de setmana el Dr. Tabernero, professor i catedràtic d'Oncologia de la Facultat de #Medicina de la Universitat de Vic – Universitat…
El passat cap de setmana el Dr. Tabernero, professor i catedràtic d'Oncologia de la Facultat de #Medicina de la Universitat de Vic – Universitat…
Recomendado por Laura Soucek
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Treatment for one of the world's deadliest cancers has remained largely unchanged for over 20 years. Samy Lamouille hopes a spinoff company he…
Treatment for one of the world's deadliest cancers has remained largely unchanged for over 20 years. Samy Lamouille hopes a spinoff company he…
Recomendado por Laura Soucek
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Several Vall d'Hebron Institute of Oncology (VHIO) researchers and medical staff were last night at the III Gala fundraising Dinner of #Alipanc…
Several Vall d'Hebron Institute of Oncology (VHIO) researchers and medical staff were last night at the III Gala fundraising Dinner of #Alipanc…
Compartido por Laura Soucek
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Our lab focuses on the infamous oncogene MYC and the therapeutic effect of its inhibition in cancer, but MYC is involved in many other diseases! We…
Our lab focuses on the infamous oncogene MYC and the therapeutic effect of its inhibition in cancer, but MYC is involved in many other diseases! We…
Recomendado por Laura Soucek
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Células con GPS incorporado para llegar a donde queramos.🗺️📍 Eso es lo que se hace en las terapias CAR-T: se utilizan marcadores específicos de…
Células con GPS incorporado para llegar a donde queramos.🗺️📍 Eso es lo que se hace en las terapias CAR-T: se utilizan marcadores específicos de…
Recomendado por Laura Soucek
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