Publications by authors named "Juan Perez-Valencia"

Article Synopsis
  • A specific group of dormant hematopoietic stem cells (dHSCs) acts as a reserve pool to protect against exhaustion, but too much dormancy can hinder responses to blood system stress.
  • Researchers discovered that CD38 serves as a key marker for identifying dHSCs and found that the cADPR signaling pathway, regulated by CD38, plays a crucial role in maintaining dHSC dormancy by influencing a protective cell cycle inhibitor.
  • Understanding this CD38/cADPR/Ca2+/c-Fos/p57Kip2 pathway could lead to new methods to enhance stem cell transplant effectiveness and promote blood recovery post-injury or illness.
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  • The Family and Community Medicine specialty (MFyC) training program, established in 2005, is being reviewed to enhance the development of specific competencies among trainees.
  • The article emphasizes the importance of values-oriented training, proposing the creation of care environments where core values can be actively experienced.
  • It suggests a focus on two core values for family physicians—commitment to individual patients and their wider community—and reorganizes competency development around five key areas related to patient care and community health.
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  • Combined inhibition of oxidative phosphorylation (OXPHOS) and glycolysis can trigger a pathway that causes tumor cell death via PP2A signaling.
  • Using specific inhibitors for mitochondrial complexes I and III, the study reveals that IACS-010759 (a complex I inhibitor) causes the release of CIP2A from PP2A, leading to the breakdown of CIP2A through autophagy.
  • The research identifies that the activation of the PP2A complex with the B56δ subunit is crucial for tumor cell death, while the suppression of cell growth from IACS-010759 treatment does not rely on this specific complex.
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Article Synopsis
  • Tumor cells exhibit distinct metabolic changes compared to normal cells, which are essential for their growth and survival by providing energy and necessary building blocks.
  • Anaplerosis helps replenish the TCA cycle, contributing to the production of important molecules; in advanced prostate cancer, increased succinate metabolism is linked to enhanced energy production and biosynthesis in malignant cells.
  • High levels of succinate in cancer cells promote tumor behaviors like migration and invasion, and the expression of certain genes (NME1 and SHMT2) associated with poor prognosis is elevated in response to succinate stimulation.
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Article Synopsis
  • - Biallelic germline pathogenic variants in mismatch repair (MMR) genes lead to constitutional MMR deficiency (CMMRD), a syndrome causing childhood cancers, which can be confused with neurofibromatosis type 1 (NF1). Testing for CMMRD in NF1-suspected children not carrying NF1/SPRED1 variants helps identify those needing monitoring before tumors develop.
  • - A study screened over 700 children suspected of having sporadic NF1 but without NF1/SPRED1 variants, using a microsatellite instability (MSI) test, and found CMMRD confirmed in 3 out of 7 positive cases, indicating a low prevalence of 0.41%.
  • - The findings
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  • Tumor cells adapt to various stresses, developing distinct metabolic profiles that reflect their levels of metastatic potential, particularly in tongue squamous cell carcinoma lines.* -
  • The study utilized nuclear magnetic resonance (NMR) spectroscopy and fluorescence lifetime imaging microscopy (FLIM) to analyze metabolites and energy metabolism in different cancer cell lines, finding variations in NAD(P)H concentrations and energy strategies.* -
  • Findings suggest that lipid metabolism, indicated by the accumulation of specific fatty acids and malonate, is linked to increased invasiveness in metastatic cells, highlighting a connection between metabolic pathways and cancer progression.*
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  • The study focuses on understanding the biochemistry of head and neck tumors to gain insights into their metastatic potential, which is linked to high mortality rates.* -
  • Researchers conducted RNA-Seq analyses on 5 different oral cancer cell lines to identify differentially expressed genes (DEGs) and their contributions to tumor invasion and metastatic progression.* -
  • Key findings include the identification of 26 consistently expressed genes throughout tumor progression, two novel metastatic markers (PIGG and SLC8B1), and several genes (MYH14, ANGPTL4, PPARD, ENPP1) that could be targeted for pharmacological interventions.*
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  • In the past decade, researchers have gained a deeper understanding of how metabolic pathways operate in cancer, revealing that tumor cells often have abnormal metabolic states.
  • Tumor cells show increased reliance on nutrients like glucose and glutamine, which are vital for energy production and cell survival.
  • The text discusses new findings on how glutamine metabolism contributes to cancer cell resilience and explores potential therapeutic approaches to target this dependency.
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  • - Tumor cells survive in harsh environments by altering gene regulation and metabolic pathways, notably relying on the Warburg effect, which promotes anaerobic glycolysis even in oxygen-rich conditions.
  • - The review reevaluates Otto Warburg's theories, showing that mitochondria in tumor cells are not dysfunctional, but rather vital for tumor growth and spread, highlighting their role in pathways like glutaminolysis.
  • - The text also discusses potential treatments targeting the unique biochemistry of tumor cells, including a case study on the effects of the drug 3BP (3-bromopyruvate) on glycolytic enzymes.
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