Laura Soucek

Laura Soucek

Barcelona, Cataluña, España
5 mil seguidores Más de 500 contactos

Acerca de

Specialties: Cancer Research

Artículos de Laura

Actividad

Unirse para ver toda la actividad

Experiencia

  • Gráfico referentsfemenins.cat
  • -

  • -

    Catalunya, Spain

  • -

    Barcelona, Catalunya, Spain

  • -

  • -

    Vall d'Hebron Institute of Oncology (VHIO)

  • -

  • -

  • -

  • -

Educación

  • Gráfico CELforPharma

    CELforPharma

    -

    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

  • -

    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.

  • -

  • -

  • -

  • 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

  • Structural and Biophysical Insights into the Function of the Intrinsically Disordered Myc Oncoprotein

    Cells

    Otros autores
  • MYC, MYCL and MYCN as therapeutic targets in lung cancer

    Expert Opin Ther Targets

    Otros autores
  • Epigenetic SMAD3 repression in tumor-associated fibroblasts impairs fibrosis and response to the antifibrotic drug nintedanib in lung squamous cell carcinoma

    Cancer Res

    Otros autores
  • Myc instructs and maintains pancreatic adenocarcinoma phenotype

    Cancer Discov

    Otros autores
  • Blocking Myc to Treat Cancer: Reflecting on Two Decades of Omomyc

    Cells

    Otros autores
  • A spotlight on cancer researchers in Spain: new paradigms and disruptive ideas

    Clin Transl Oncol

    Otros autores
  • Targeting antitumoral proteins to breast cancer by local administration of functional inclusion bodies

    Advanced Sciences

    Otros autores
  • Editorial Overview: Peptides in Cancer

    Current Opinion in Pharmacology

    Otros autores
  • 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

  • Intrinsic cell-penetrating activity propels Omomyc from proof of concept to viable anti-Myc therapy

    Sci Trans Med

  • Finding MYCure

    Mol Cell Oncology

    Otros autores
  • Myc and Ras, the Bonnie and Clyde of immune evasion

    Translational Cancer Research

    Otros autores
  • 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.

    Otros autores
    Ver publicación
  • 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 autores
    Ver publicación
  • Tamoxifen administration to mice.

    Cold Spring Harb Protoc.

  • 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.

    Otros autores
    Ver publicación
  • The Myc world within reach.

    Methods Mol Biol.

    Otros autores
    Ver publicación
  • 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.

    Otros autores
    Ver publicación

Patentes

  • EP19382195

    Presentada el EU EP19382194

    Otros inventores
  • METHODS FOR THE DIAGNOSIS OF LUNG CANCER

    Presentada el EU EP19382195

    Otros inventores
  • Methods and compositions for the treatment of cancer

    Expedida EU EP 13382167 A 20130507

    Otros inventores
  • METHODS AND COMPOSITIONS FOR THE TREATMENT OF CANCER

    Presentada el EU EP16382339.6

    Otros inventores
  • Methods of treating fibrosis

    Presentada el US 62/086,945

    Otros inventores

Idiomas

  • English

    Competencia bilingüe o nativa

  • Italian

    Competencia bilingüe o nativa

  • Spanish

    Competencia bilingüe o nativa

  • Catalan

    Competencia básica

Recomendaciones recibidas

Más actividad de Laura

Ver el perfil completo de Laura

  • Descubrir a quién conocéis en común
  • Conseguir una presentación
  • Contactar con Laura directamente
Unirse para ver el perfil completo

Perfiles similares

Otras personas con el nombre de Laura Soucek

Añade nuevas aptitudes con estos cursos