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Scientific Program
16th International Conference on Cancer Stem Cell & Oncology Research, will be organized around the theme “Precision Medicine Approaches for Cancer Stem Cell Targeting”
Cancer Stem Cells 2025 is comprised of keynote and speakers sessions on latest cutting edge research designed to offer comprehensive global discussions that address current issues in Cancer Stem Cells 2025
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The tumor microenvironment plays a crucial role in cancer progression and therapy resistance, particularly in relation to cancer stem cells (CSCs). This track explores the complex interactions between CSCs and their microenvironment, including immune cells, fibroblasts, extracellular matrix (ECM), and vasculature. It examines how these components provide essential signals that promote CSC self-renewal, plasticity, and immune evasion, contributing to therapeutic failure. Special attention is given to how hypoxic conditions, metabolic shifts, and inflammatory mediators shape CSC behavior. This research seeks to identify potential therapeutic targets within the microenvironment, offering novel strategies to disrupt CSC survival and tumor propagation. Understanding these interactions is crucial for developing interventions that can reprogram the microenvironment to inhibit CSCs, rather than promote their growth.
CSCs rely on several critical signaling pathways that regulate their survival, proliferation, and ability to resist therapies. This track focuses on understanding key molecular pathways like Wnt/β-catenin, Hedgehog, Notch, and TGF-β, which govern CSC behavior. The dysregulation of these pathways often results in uncontrolled cell growth, maintenance of stemness, and enhanced survival capabilities of CSCs. Researchers aim to identify how mutations or aberrant signaling contribute to cancer initiation and metastasis. Targeting these signaling pathways holds great promise for therapies that selectively eliminate CSCs without harming normal stem cells. By understanding the molecular underpinnings of CSC regulation, novel inhibitors and therapeutic strategies can be developed to block CSC-driven tumorigenesis and overcome treatment resistance, leading to better clinical outcomes.
A major challenge in cancer treatment is the ability of CSCs to resist chemotherapy and radiation. This research track investigates the mechanisms behind this resistance, focusing on CSCs' ability to remain in a quiescent state, enhancing their DNA repair capabilities and activating drug efflux pumps to remove chemotherapeutic agents. Additionally, CSCs' high expression of survival pathways and anti-apoptotic proteins makes them less susceptible to conventional treatments. This track explores how these intrinsic properties of CSCs contribute to disease recurrence and poor patient prognosis. The aim is to discover novel therapeutic approaches that target these resistance mechanisms, ensuring that CSCs are eradicated alongside the bulk tumor cells, thereby preventing relapse and metastasis.
Epigenetic modifications play a pivotal role in maintaining CSC properties, including their self-renewal and differentiation potential. This track delves into how changes in DNA methylation, histone modifications, and non-coding RNAs regulate the stemness of CSCs. Understanding these epigenetic mechanisms is critical for identifying how CSCs evade traditional therapies and drive cancer progression. Researchers in this area explore how reversible epigenetic changes allow CSCs to adapt to different microenvironmental conditions and therapeutic pressures, leading to heterogeneity within the tumor. Epigenetic drugs, such as DNA methyltransferase inhibitors and histone deacetylase inhibitors, are being studied for their potential to disrupt CSC function and sensitize them to treatment, offering a new avenue for targeting CSC-driven cancers.
CSCs have distinct metabolic profiles that enable their survival under stress conditions, including nutrient deprivation and low oxygen. This track focuses on how CSCs exploit metabolic pathways such as glycolysis, oxidative phosphorylation, and fatty acid oxidation to fuel their growth and resistance to treatments. Researchers explore the metabolic flexibility of CSCs, which allows them to switch between energy production methods depending on environmental factors, making them highly adaptable. Targeting the unique metabolic dependencies of CSCs could offer new therapeutic strategies that impair their energy supply without affecting normal cells. This area of research is critical for developing metabolic inhibitors that selectively target CSCs, potentially improving the efficacy of cancer therapies and reducing tumor relapse.
Cancer stem cells (CSCs) within a single tumor can exhibit significant phenotypic and functional diversity, contributing to therapeutic resistance and metastasis. This track explores the heterogeneity of CSCs across different cancers and within the same tumor, examining how various CSC subpopulations respond to treatments differently. Researchers investigate how factors such as genetic mutations, epigenetic changes, and microenvironmental influences lead to this diversity. Understanding CSC heterogeneity is essential for developing personalized therapies that can target all CSC subpopulations, preventing relapse and metastasis. This track aims to uncover how CSC heterogeneity drives tumor progression and therapy resistance, offering insights into how tailored interventions could improve patient outcomes.
Identifying unique surface markers expressed by cancer stem cells (CSCs) is key to selectively targeting them without affecting normal stem cells. This track focuses on the discovery of CSC-specific markers such as CD44, CD133, and ALDH1. Researchers aim to develop targeted therapies, including monoclonal antibodies and small molecules, that can specifically recognize and eliminate CSCs. By utilizing these markers for drug delivery or immunotherapy, more precise and effective cancer treatments can be designed. The goal is to reduce tumor recurrence and improve treatment efficacy by targeting the CSC population while sparing healthy tissue, offering a promising approach to cancer therapy.
Chronic inflammation plays a significant role in cancer initiation and progression, often leading to the activation of cancer stem cells (CSCs). This track investigates the links between inflammatory signaling pathways—such as NF-κB, IL-6, and TNF-α—and the activation of CSCs. Researchers explore how inflammation within the tumor microenvironment promotes CSC self-renewal, survival, and metastasis. Targeting the inflammatory signals that support CSCs could lead to novel therapeutic strategies that disrupt this relationship, limiting tumor growth and progression. This research highlights the importance of anti-inflammatory agents in cancer treatment, offering new opportunities to inhibit CSC-driven malignancies by reducing inflammation.
The microenvironment, or niche, of cancer stem cells (CSCs) plays a pivotal role in maintaining their stemness and promoting tumor growth. Hypoxia, or low oxygen levels, is a critical feature of the CSC niche that drives their survival and resistance to therapies. This track examines how hypoxia-induced signaling pathways, such as HIF-1α, enhance CSC stemness and contribute to metastasis. Researchers aim to develop strategies to disrupt the hypoxic niche, thereby sensitizing CSCs to chemotherapy and radiation. Understanding the unique features of the CSC niche can help identify new therapeutic targets that prevent CSCs from thriving under stress conditions, improving treatment outcomes.
Cancer stem cells (CSCs) exhibit remarkable plasticity, allowing them to switch between stem-like and differentiated states in response to microenvironmental cues. This track explores the mechanisms underlying CSC plasticity and how it contributes to tumor progression, metastasis, and therapeutic resistance. Researchers study the factors that regulate transitions between CSC and non-CSC states, including epigenetic changes and signaling pathways. Targeting CSC plasticity could prevent tumors from adapting to therapies and evolving into more aggressive forms. By understanding how plasticity drives tumor heterogeneity and survival, researchers aim to develop therapies that eliminate CSCs and block tumor progression, reducing the chances of relapse.
Cancer stem cells (CSCs) can evade immune surveillance, allowing them to survive and drive tumor growth. This track focuses on the concept of immunoediting, where CSCs shape the immune response to evade detection and destruction. Researchers investigate how CSCs alter immune cell functions, such as suppressing T-cell activity and promoting regulatory T-cells, to create an immune-suppressive tumor microenvironment. Understanding the interactions between CSCs and the immune system is crucial for developing immunotherapies that can overcome immune evasion. By targeting CSC-specific mechanisms of immunoediting, researchers hope to enhance the effectiveness of cancer immunotherapies and improve patient outcomes.
Exosomes are small vesicles released by cancer stem cells (CSCs) that play a critical role in cell-to-cell communication within the tumor microenvironment. This track investigates how CSC-derived exosomes influence tumor progression, metastasis, and resistance to therapy. Exosomes carry proteins, lipids, and nucleic acids that can modulate the behavior of surrounding cells, promoting tumor growth and immune evasion. Researchers explore how blocking exosome release or altering their contents could disrupt CSC communication networks and limit tumor spread. This area of research holds potential for developing novel diagnostic markers and therapeutic strategies aimed at targeting CSC-driven communication pathways to halt cancer progression.
Cancer stem cells (CSCs) can enter a dormant state, allowing them to evade treatments and later reinitiate tumor growth. This track focuses on understanding the mechanisms that regulate CSC dormancy, including signals from the microenvironment and intrinsic genetic factors. Researchers explore how dormant CSCs resist conventional therapies, which typically target actively dividing cells. Developing therapies that can either awaken dormant CSCs, making them vulnerable to treatment, or eliminate them while dormant, could significantly improve long-term survival rates for cancer patients. This research aims to prevent tumor recurrence by targeting the CSCs that remain dormant but capable of causing relapse.
Cancer stem cells (CSCs) play a central role in the metastatic spread of cancer to distant organs. This track explores how CSCs possess unique abilities to invade tissues, survive in circulation, and colonize new sites, leading to secondary tumors. Researchers study the molecular and cellular mechanisms that allow CSCs to metastasize, including their interaction with the extracellular matrix, immune cells, and blood vessels. Targeting CSCs to prevent or limit metastasis could revolutionize cancer treatment by stopping the spread of the disease. This track focuses on developing therapies that specifically disrupt the metastatic potential of CSCs, improving patient prognosis and survival.
Cancer stem cells (CSCs) are notoriously resistant to standard cancer therapies, making them a major contributor to treatment failure and relapse. This track delves into the specific mechanisms that allow CSCs to resist chemotherapy and radiation, including the overexpression of drug efflux pumps, enhanced DNA repair, and activation of survival pathways. Researchers explore strategies to overcome these resistance mechanisms by developing drugs that target CSC-specific survival pathways. By identifying and inhibiting the factors that protect CSCs from treatment, this research aims to improve the efficacy of existing cancer therapies and reduce the likelihood of disease recurrence.
The potential of natural compounds to target cancer stem cells (CSCs) has garnered significant interest in recent years. This track focuses on exploring natural products, such as curcumin, resveratrol, and green tea polyphenols, for their ability to inhibit CSC self-renewal and induce differentiation or apoptosis. Researchers investigate how these compounds interfere with key signaling pathways, disrupt the CSC niche, or sensitize CSCs to conventional therapies. Natural products may offer a less toxic alternative to standard cancer treatments and could be used in combination with existing therapies to enhance their effectiveness. This research holds promise for developing novel, natural-based therapies for eradicating CSCs.
CRISPR/Cas9 technology has revolutionized cancer research, providing a powerful tool to edit genes and study their functions in cancer stem cells (CSCs). This track focuses on how CRISPR/Cas9 is being used to investigate the genetic and epigenetic regulation of CSCs, identify novel therapeutic targets, and test potential drug candidates. Researchers use CRISPR to knock out specific genes involved in CSC self-renewal, survival, and therapy resistance, revealing new insights into CSC biology. This cutting-edge research aims to develop gene-editing strategies that selectively target CSCs, offering a highly specific approach to eradicating the cells responsible for cancer progression and relapse.
Detecting cancer at an early stage is critical for improving patient outcomes, and cancer stem cells (CSCs) offer potential biomarkers for early diagnosis. This track focuses on identifying CSC-specific biomarkers, such as surface markers, secreted proteins, and genetic signatures, that can be used to detect cancer at its earliest stages. Researchers investigate how these biomarkers could be used for non-invasive screening, such as liquid biopsies, to monitor disease progression or predict therapeutic response. Early detection of CSCs could lead to more timely and targeted interventions, preventing the development of advanced, treatment-resistant tumors. This research aims to improve cancer prognosis through better diagnostic tools.
Cancer immunotherapy has shown great promise in recent years, but its effectiveness against cancer stem cells (CSCs) remains a challenge. This track explores how immunotherapy approaches, such as CAR T-cells, immune checkpoint inhibitors, and cancer vaccines, can be used to target and eliminate CSCs. Researchers study the immune evasion strategies employed by CSCs and how these cells can be made more vulnerable to immune-mediated destruction. By developing immunotherapies that specifically target CSCs, this research aims to enhance the overall success of cancer treatments, reduce the risk of recurrence, and improve long-term survival rates for cancer patients.
Angiogenesis, the formation of new blood vessels, is essential for tumor growth and metastasis. Cancer stem cells (CSCs) play a key role in promoting angiogenesis by secreting pro-angiogenic factors like VEGF. This track investigates how CSCs drive the formation of new vasculature to support their growth and survival in the tumor microenvironment. Researchers explore therapeutic strategies that inhibit CSC-induced angiogenesis, potentially starving tumors of the blood supply they need to grow and spread. Targeting CSCs' role in angiogenesis could lead to more effective anti-angiogenic therapies that not only shrink tumors but also prevent their recurrence and metastasis.
The epithelial-mesenchymal transition (EMT) is a process by which cancer stem cells (CSCs) acquire enhanced migratory and invasive properties, contributing to metastasis. This track explores the role of EMT in CSC plasticity and how it allows CSCs to switch between epithelial and mesenchymal states. Researchers investigate how EMT-related signaling pathways, such as TGF-β and ZEB1, regulate CSC behavior and promote tumor progression. Targeting EMT in CSCs could help prevent metastasis and improve treatment responses by limiting the cells’ ability to adapt and spread. This research aims to develop novel therapies that block EMT in CSCs, reducing their metastatic potential.
Cancer stem cells (CSCs) are adept at creating an immunosuppressive microenvironment, enabling them to evade immune attack. This track focuses on how CSCs manipulate immune cells, such as T-cells, macrophages, and dendritic cells, to suppress anti-tumor immune responses. Researchers explore how CSCs produce immunosuppressive factors like IL-10, TGF-β, and PD-L1, which inhibit immune cell activation and function. By targeting these immunosuppressive mechanisms, new therapeutic strategies could be developed to enhance the immune system’s ability to recognize and eliminate CSCs. This research highlights the importance of combining immunotherapy with CSC-targeted approaches to improve cancer treatment outcomes.
Cancer stem cells (CSCs) possess the unique ability to self-renew and differentiate into various cell types within the tumor. This track explores the molecular mechanisms that govern CSC fate determination, including how signals from the tumor microenvironment and intrinsic genetic factors influence whether a CSC remains stem-like or differentiates. Researchers study how manipulating CSC differentiation pathways could force CSCs to lose their stemness and become more susceptible to treatment. By inducing CSC differentiation, therapies could target the more differentiated, less resistant cells, potentially preventing tumor growth and recurrence. This research aims to develop new strategies that alter CSC fate and improve cancer therapy outcomes.
Nanotechnology offers a promising approach for selectively targeting cancer stem cells (CSCs) with greater precision. This track focuses on the development of nanoparticle-based drug delivery systems that can specifically target CSCs while minimizing damage to normal cells. Researchers explore how nanoparticles can be engineered to deliver therapeutic agents directly to CSCs by recognizing specific surface markers or responding to the unique microenvironment of CSCs. Nanotechnology also enables the delivery of combination therapies, such as chemotherapy and immunotherapy, to effectively eliminate CSCs and prevent tumor recurrence. This research holds the potential to revolutionize cancer treatment by improving the specificity and efficacy of CSC-targeted therapies.
Radiotherapy is a common treatment for cancer, but cancer stem cells (CSCs) are often resistant to radiation, leading to treatment failure and tumor recurrence. This track investigates the mechanisms by which CSCs resist radiotherapy, including enhanced DNA repair, activation of survival pathways, and antioxidant defenses. Researchers explore strategies to sensitize CSCs to radiation by targeting these resistance mechanisms, improving the overall effectiveness of radiotherapy. By overcoming CSC-driven radioresistance, this research aims to reduce the likelihood of cancer recurrence and improve patient survival rates. This track highlights the importance of developing combination therapies that target CSCs to enhance the success of radiotherapy.