Table of Contents
- Key Points
- Background: Why Cancer Stem Cells Matter
- Cancer Stem Cell Biology in Brain Tumors
- The Five Tumor Niches That Protect Cancer Stem Cells
- Cancer Stem Cells in Other Brain Tumors
- Markers Used to Identify Cancer Stem Cells
- How Researchers Study Cancer Stem Cells
- Clinical Implications for Patients
- Limitations and Open Questions
- What This Means for Patients and Families
- Frequently Asked Questions
- Source Information
Key Points
- Cancer stem cells in glioblastoma can renew themselves, resist treatment, and spread beyond the tumor margins seen on MRI scans.
- Five overlapping niches—perivascular, hypoxic, invasive, immunosuppressive, and extracellular matrix-associated—protect cancer stem cells and support treatment resistance.
- Markers like CD133, CD44, CD15, SOX2, OCT-4, and nestin are not specific to cancer stem cells and do not reliably predict tumor initiation.
- Lasting treatment will likely require combination approaches that target both cancer stem cells and the supportive microenvironments around them.
- This review is a scientific synthesis, not a clinical trial, and does not replace individualized medical advice from your neuro-oncology team.
Background: Why Cancer Stem Cells Matter
Cancer stem cells (CSCs) are a small population of tumor cells with stem-like properties. These cells can renew themselves and can change into other cell types. Researchers increasingly believe that CSCs drive tumor initiation, treatment resistance, and relapse.
The CSC hypothesis proposes that many cancers are organized in a hierarchy. A small population of stem-like cells maintains the tumor. These cells promote tumor survival and spread through self-renewal and plasticity (the ability to change state).
This idea has fundamentally shifted how scientists approach cancer. Despite major advances in targeted and cell-based therapies, patients with malignant brain tumors still rarely achieve lasting responses. This gap highlights the need to find and eliminate the specific cell populations responsible for tumor persistence.
The challenge is especially clear in aggressive central nervous system (CNS) tumors. These tumors show high variability between patients and within a single tumor. This variability lets tumors adapt and resist both standard and targeted treatments.
Ongoing research focuses on the genetic and molecular differences between CSCs and normal stem cells (SCs). The goal is to improve targeted therapies while preserving healthy tissue. This review summarizes current concepts in CSC biology, with a focus on glioblastoma (GBM), and outlines the central role of neuro-oncology in translating these discoveries into treatments.
Cancer Stem Cell Biology in Brain Tumors
Neural stem cells are multipotent progenitor cells. Their growth and development are tightly controlled by signals from their surroundings. During brain development, neural stem cells become neurons, astrocytes, and oligodendrocytes. In the adult brain, new neuron formation is largely limited to two regions: the subventricular zone (SVZ) and the subgranular zone of the dentate gyrus.
Normal neural stem cells maintain healthy tissue. CSCs, by contrast, support tumor maintenance within a specialized tumor microenvironment (TME). This environment is ruled by disrupted fate control, abnormal niche interactions, and strong stress-response adaptations. These adaptations allow tumors to survive under harsh conditions.
Neural stem cells and CSCs share core properties. Both can self-renew, both show multipotency-like differentiation programs, and both use conserved molecular signaling pathways. However, CSCs differ in important ways:
- They lack normal cell-cycle restrictions.
- They show increased asymmetric division.
- They can actively suppress antitumor immune responses.
These features contribute to the aggressive nature of CSC-driven tumors.
The concept of CSCs dates back to 19th-century observations that tumors may arise from undifferentiated cellular precursors. Later studies in embryonic tumors and teratocarcinomas supported this idea. These studies established that poorly differentiated progenitors can generate diverse malignant cell lineages.
Classical CSC theory described a rare, stable, self-renewing, one-way hierarchy. In this model, tumor-propagating capacity persists after cytotoxic stress because CSCs generate rapidly growing progeny with limited differentiation potential. Modern research has refined this framework into a plasticity model. In the plasticity model, CSCs and non-CSCs interconvert dynamically in both directions. This interconversion is shaped by internal regulatory programs and by cues from the microenvironment.
Current evidence supports a mixed model. In this model, progression and recurrence arise from two sources:
- Pre-existing quiescent (dormant) stem-like cells.
- CSC states induced by therapy or by the niche.
The relative contributions of these two sources appear to depend on anatomical niches and on the treatment context. However, the precise proportions and governing rules remain an active area of investigation.
Within CNS tumors, CSC biology has been studied most extensively in GBM. GBM is the most common and aggressive primary malignant brain tumor. It is defined by marked cellular and molecular heterogeneity and by near-universal recurrence despite multimodal therapy. Glioma stem cells (GSCs) have been implicated in tumor initiation, maintenance, and adaptive treatment resistance. They achieve this through enhanced DNA damage responses, metabolic adaptation, and active remodeling of the tumor microenvironment.
The Five Tumor Niches That Protect Cancer Stem Cells
The existence of spatially and functionally specialized niches within the tumor has become a central framework. This framework explains why cytoreductive therapy (treatment that reduces tumor bulk) alone rarely cures malignant CNS tumors. Together, these niches sustain temporary stem-like states, help tumors evade the immune system, and provide resistance to cytotoxic injury through coordinated signaling. The migratory and invasive properties of these cells are another important factor.
Researchers have described five niches in the literature:
- Perivascular (around blood vessels)
- Hypoxic (low oxygen)
- Invasive
- Immunosuppressive
- Extracellular matrix (ECM)-associated
The Perivascular Niche
In the perivascular niche, CSCs preserve their stemness through direct cell-to-cell interactions and paracrine signaling (signaling to nearby cells). They interact with endothelial cells (cells that line blood vessels), pericytes, and abnormal vascular remodeling.
In GBM, abnormal blood vessel formation is largely driven by vascular endothelial growth factor (VEGF) secreted from CD133+ CSCs. Endothelial cells and myeloid cells also contribute. Endothelial-derived NOTCH ligands actively strengthen CSC self-renewal. CXCL12–CXCR4 signaling helps keep CSCs within the vascular niche and supports invasion.
IL-8 and αvβ8 integrin-mediated TGFβ1 activation are complementary routes. Tumors use these routes to reinforce CSC maintenance, boost immune suppression, and remodel the extracellular matrix. CSCs can also use alternative energy sources. This lets them bypass angiogenic pathways and resist VEGF-targeted anti-angiogenic treatments.
The Hypoxic Niche
The hypoxic niche induces stem-like transcriptional states and functional resilience. In GBM, this niche is classically marked by pseudopalisading necrosis. This pattern features hypercellular regions surrounding areas of dead tissue. Necrosis formation is attributed to tumor-driven microvascular thrombosis and blood vessel blockage.
Rather than reflecting slow tumor growth, oxygen deprivation acts as a powerful regulatory signal. It works through stabilization of hypoxia-inducible factors (HIFs), notably HIF-1α and HIF-2α. These transcriptional states intertwine with STAT3, EGFR/PI3K/AKT, IGF1R, IL-8, and alarmin-RAGE signaling. Together, they support CSC tumorigenic capacity, cellular plasticity, migration, invasion, and chemoresistance.
HIF-1α enhances CSC self-renewal in part by stabilizing NOTCH intracellular domains. HIF-2α preferentially activates stemness-associated transcriptional states, including NOTCH-related and calcineurin-dependent pathways. Both factors can also promote dedifferentiation toward stem-like states through SOX2-dependent mechanisms. This reinforces the concept that stemness is an adaptive and reversible cellular program.
The Invasive Niche
The invasive niche emerges where anatomical pathways meet microenvironmental gradients of oxygen, pH, immune cells, and ECM structure. These gradients shape invasion patterns and select for specialized migratory tumor subpopulations.
In the adult brain, the SVZ is a highly vascularized neurogenic region. Its normal pro-stem-cell conditions also create a permissive hiding place for invasive GSCs. Perivascular and SVZ-associated CXCL12 gradients engage CXCR4 and CXCR7. These signals direct GSC migration along vascular and white-matter tracts, leading to tumor recurrence.
Invasion also occurs through coordinated dynamics centered on the Na+–K+–Cl− cotransporter NKCC1. This transporter modulates focal adhesion dynamics and cell contractility. At the tumor edge, GSCs face heightened metabolic and oxidative stress. Fluctuating oxygen and nutrient gradients promote selection and plasticity for stem-like states.
Integrins α6β1, αvβ3, αvβ5, and αvβ6 mediate adhesion to laminin-rich and vitronectin-rich matrices. FAK-Src dual kinase complexes activate downstream effectors that regulate motility, proliferation, and survival. Across multiple models, WNT/β-catenin, TGFβ-SMAD, and NOTCH pathways interlock with HIF signaling. This network supports an epithelial–mesenchymal-like plasticity that enables invasion.
Clinically, this translates into diffuse GSC infiltration beyond MRI tumor boundaries. This infiltration undermines complete surgical resection attempts and contributes to recurrence despite adjuvant therapy.
The Immunosuppressive Niche
The immunosuppressive niche arises from vascular dysfunction and tissue damage signals. Combined with hypoxia and necrosis, these signals reshape local immunity. They stimulate infiltration of regulatory T-cells (Tregs) and recruitment of bone-marrow-derived monocytes. These monocytes differentiate into tumor-associated macrophages (TAMs). Granulocytes also arrive and mature into tumor-associated neutrophils (TANs).
This immune context suppresses antigen presentation and weakens T-cell effector activity. It does so through convergent signaling via VEGF, macrophage colony-stimulating factor 1 (CSF1), CXCL12, IL-1β, IL-6/STAT3, TGF-β, and immune checkpoint pathways such as PD-1/PD-L1.
Functionally, this niche protects CSCs from chemoradiation. It maintains CSCs in a relatively quiescent state and supports their later re-entry into the cell cycle. This process facilitates tumor regrowth and relapse.
The Extracellular Matrix-Associated Niche
The pathological ECM niche built by the tumor provides a dynamic, instructive scaffold. This scaffold helps stabilize CSCs through combined biochemical and biomechanical cues.
The glycoprotein tenascin-C is a central component. It accumulates in invasive and perivascular regions, boosting angiogenesis and tumor cell proliferation. Brain-derived chondroitin sulfate proteoglycans uphold infiltrative behavior and reinforce tumor-initiating capacity.
TAM secretion of TGF-β leads to ECM remodeling through metalloproteinases MMP2/9 and ADAMTS proteases. This remodeling amplifies EGFR activity at invasive fronts. In parallel, integrin signaling and increased matrix stiffness act together to activate the YAP/TAZ pathway. This activation stabilizes CSCs and their migratory potential.
How the Niches Work Together
These five categories overlap and should not be viewed as mutually exclusive. Despite high vessel density, the chaotic nature of GBM vasculature creates intermittent blood flow. This produces hypoxic gradients within the tumor. Immune cells and stromal elements integrate across microdomains. They upregulate the CXCL12–CXCR4 signaling axis. In this way, the niches adapt to form an interactive migratory front and an immunomodulatory sanctuary for CSCs.
Cancer Stem Cells in Other Brain Tumors
The CSC concept extends beyond GBM and appears broadly applicable to CNS tumors. Researchers have reported stem-like populations across adult and pediatric tumors. These include meningiomas, pituitary adenomas, schwannomas, oligodendrogliomas, ependymomas, and medulloblastomas. The depth of experimental validation varies among these tumors. Still, accumulating evidence suggests that stem-like compartments may contribute to tumor initiation and recurrence.
Meningiomas
Meningiomas are primary intracranial tumors that are typically benign. The evidence for distinct meningioma stem cells (MgSCs) remains less robust than for GSCs. Nonetheless, developing data suggest the presence of stem-like populations. These populations express markers shared with GSCs, such as CD133, OCT-4, SOX2, and nestin.
Transcriptomic and signaling analyses further suggest that MgSC-associated signaling contributes to aggressive features and recurrence. CXCL11 and CXCL12 have been implicated in malignant phenotypes. Clinically, meningioma management is strongly influenced by tumor location. Convexity tumors often allow wider surgical margins. Skull base tumors frequently touch or encase critical neurovascular structures, which limits the extent of resection.
Within these anatomical constraints, residual microscopic disease may persist after surgery. MgSCs residing in protective niches may also persist and contribute to recurrence. This risk is particularly relevant in higher-grade tumors or tumors that are surgically inaccessible.
Pituitary Neuroendocrine Tumors
Pituitary neuroendocrine tumors (PitNETs) arise from anterior pituitary cells. They are usually benign but can be locally invasive, recurrent, and treatment-refractory in a small subset of patients. As in meningiomas, there is limited evidence for true CSCs in PitNETs.
Researchers have identified subpopulations expressing OCT-4, SOX2, CD133, and nestin in laboratory cultures and in xenografts (human tumor tissue grown in animals). These cells show proliferative capacity and multilineage differentiation toward hormone-producing pituitary cells. This suggests a potential role in local infiltration.
In an estradiol-benzoate-induced PitNET rat model, CSC markers were preferentially expressed in the adenoparenchyma rather than in the marginal zone. This contrasts with their distribution in normal pituitary tissue. Early evidence suggests that PitNET CSCs may migrate from marginal zones to form adenoparenchymal niches during early tumor development.
Medulloblastoma
Medulloblastoma is the most common malignant pediatric brain tumor. CSC-like cells expressing CD133, SOX2, and nestin have been linked to tumor propagation and resistance. Key developmental pathways, including SHH, WNT, NOTCH, and MYC, play central roles in maintaining stemness.
A study using orthotopic medulloblastoma xenografts (tumors grown in the brain of an animal model) demonstrated that CD133+ tumor cells can form neurospheres. These cells also participate in multilineage differentiation even after several passages. This suggests that CSCs exist in some medulloblastoma variants.
Ependymomas
Ependymomas, particularly posterior fossa subtypes, also harbor stem-like, radial glia-like compartments. These compartments are shaped by profound epigenetic dysregulation. TGF-β and WNT/β-catenin transcriptional states correlate with recurrence and poor clinical outcomes.
Single-cell analyses of all major ependymoma groups suggest three fates for ependymoma stem-like cell differentiation:
- Ependymal-like cells
- Glial-progenitor-like cells
- Neuronal-precursor-like cells
The tumors with the poorest prognosis mainly contained undifferentiated cells.
Oligodendrogliomas
Across IDH-mutant oligodendrogliomas, progenitor-like oligodendrocyte precursor cell states use IDH-dependent methylation and chromatin changes. These changes stall differentiation and enable plastic progression toward more proliferative progenitor states. Although oligodendrocyte precursor cells have distinct origins from GSCs, a single-cell study of oligodendrogliomas revealed several overlapping functions that contribute to proliferative capacity.
Schwannomas
Schwannomas are benign neural crest-derived tumors. They have been shown to express embryonic stem cell-like markers, including CD133, OCT-4, and SOX2. This is consistent with a stem-like compartment. The contribution of CSCs to schwannoma growth and recurrence is an important area for future functional work.
Common Themes Across Brain Tumors
Despite broad evidence for stem-like features in many solid tumors, the extent of strict hierarchical organization differs across CNS tumors. The degree of CSC dependence also differs, even between molecular subtypes within a given tumor type. Nonetheless, recurrent themes emerge:
- Activation of conserved developmental pathways
- Epigenetic plasticity
- Niche-mediated protection from therapy
Markers Used to Identify Cancer Stem Cells
Researchers have proposed multiple potential biomarkers for GSC identification. These include CD133, CD44, CD15, SOX2, OCT-4, and nestin. However, these markers are neither universally expressed nor specific to GSCs. There is substantial overlap across normal neural stem cells and other tumor populations.
A persistent controversy is that marker-defined CSC fractions shift with culture conditions, microenvironmental cues, and therapy-induced stress. Marker positivity does not consistently align with tumor-initiating capacity. As a result, purely marker-based CSC estimates are difficult to interpret and hard to compare across studies or tumor types. Modern efforts therefore increasingly combine marker-based enrichment with functional assays and single-cell profiling.
Single-cell RNA sequencing has been used to define transcriptional axes associated with classical and mesenchymal stem-like cellular states. These include MEOX2-NOTCH and SRGN-NFκB programs. With so many regulatory signals involved, knowledge of key factors and behaviors in CSC molecular profiles is essential for understanding their highly heterogeneous nature.
How Researchers Study Cancer Stem Cells
Stem cell-based tumor models are needed to preserve the biological features that drive tumor persistence. These models retain tumor characteristics including propagation, cellular plasticity, and clinically relevant heterogeneity. By maintaining these dynamic and diverse states, the models provide an essential framework to study CSC biology and microenvironmental dependencies. They enable researchers to identify niche-derived cues that sustain CSC survival and tumor regeneration across ex vivo (outside the body) and in vivo (inside the body) approaches.
Ex Vivo Models
Ex vivo stem cell-based models allow controlled manipulation of niche-associated variables. This allows researchers to understand the mechanisms of CSC regulation.
Historically, neuro-oncology research has relied heavily on glioma-derived immortalized cell lines. These are experimentally convenient, but their growth as two-dimensional (2D) monolayers limits cellular heterogeneity and microenvironmental gradients. Furthermore, prolonged passaging often leads to clonal drift. This yields models that progressively diverge from the original tumors.
Next-generation stem-like cultures incorporate ECM substrates, microfluidic gradient systems, and multicellular co-cultures. These approaches partially replicate structural and biochemical niche features. They also address the progressive divergence seen in progenitor cell lines.
Given the central role of three-dimensional (3D) architecture in glioma aggressiveness, 3D tumor models represent a major advance in neuro-oncology research. Among these models, patient-derived tumor organoids (PDTOs) and neurosphere cultures are established directly from surgical specimens. They are maintained under serum-free conditions. These models can retain aspects of intratumoral heterogeneity linked to stemness. In this way, they mimic clinically relevant variability in treatment responses.
PDTOs preserve native cell-to-cell interactions. In some cases, they maintain infiltrating immune or stromal elements from the original tumor. Organoids often show selective radiosensitivity. Differentiated tumor cells are preferentially eliminated while adjacent GSCs persist. This mirrors clinical patterns of incomplete eradication and relapse.
Additionally, the cerebral organoid glioma (GLICO) model provides a human neural-like scaffold. In this model, GSCs infiltrate in patterns that closely resemble disease in living organisms. They form tumor foci with microtube-associated networks implicated in infiltration.
Clinical Implications for Patients
This research reframes how doctors and scientists think about treating glioblastoma and other CNS tumors. The key message is that lasting therapeutic response will likely require multimodal approaches. Treatment must target both CSC-intrinsic pathways and the supportive microenvironments around them.
Several specific implications stand out:
- CSCs extend beyond radiographic margins. CSCs populate peritumoral regions beyond the contrast-enhancing tumor margins seen on imaging. This provides a biological basis for near-universal recurrence.
- Longitudinal outcomes depend on CSC eradication. Long-term therapeutic outcomes are increasingly dictated by the success or failure of total CSC eradication.
- Surgery must balance two goals. The findings highlight the need for function-preserving maximal resection. Surgeons aim to remove as much tumor as possible while protecting healthy brain function.
- Single-target therapies are unlikely to succeed. Because CSCs use multiple resistance mechanisms and multiple protective niches, sustained response will likely require combination approaches.
The five niches cooperate to enforce stemness, metabolic adaptability, immune evasion, and phenotypic plasticity. This cooperation enables CSC persistence despite maximal surgical resection and standard-of-care therapy. Advances in multiparametric imaging, stem cell-based ex vivo and in vivo models, and single-cell and spatial profiling have refined insight into CSC heterogeneity, niche dependence, and treatment resistance.
Limitations and Open Questions
The review identifies several important limitations and unresolved questions in the field.
First, the precise proportions and governing rules of CSC dynamics remain an active area of investigation. Researchers do not yet know exactly how much recurrence comes from pre-existing dormant stem-like cells versus therapy-induced or niche-induced CSC states.
Second, CSC markers are not reliable on their own. Markers such as CD133, CD44, CD15, SOX2, OCT-4, and nestin are neither universally expressed nor specific to GSCs. Marker positivity does not consistently align with tumor-initiating capacity. This makes purely marker-based CSC estimates difficult to interpret and compare across studies.
Third, the strength of evidence varies widely across tumor types. Evidence for CSCs is most extensive in glioblastoma. For meningiomas and pituitary neuroendocrine tumors, evidence for true CSCs remains limited. For schwannomas, the functional contribution of CSCs to growth and recurrence is not yet established.
Fourth, the extent of strict hierarchical organization and the degree of CSC dependence differ across CNS tumors. They even differ between molecular subtypes within a given tumor type.
Fifth, the five niches overlap and should not be viewed as mutually exclusive. This overlap makes it difficult to study each niche in isolation.
What This Means for Patients and Families
This review is a scientific synthesis, not a clinical trial. It does not test a new drug or report patient outcomes from a new treatment. However, its findings offer several practical takeaways for patients and families navigating a brain tumor diagnosis.
- Understand why recurrence is common. In glioblastoma, cancer stem cells spread beyond the tumor margins visible on MRI scans. This is a biological reason why the tumor so often returns, even after successful-looking surgery and standard therapy. Recurrence is not a failure of the patient or the surgical team.
- Ask about the extent of resection. The review supports function-preserving maximal resection. This means removing as much tumor as safely possible while protecting brain function. Patients can ask their surgical team how the planned resection balances tumor removal against neurological risk.
- Expect combination approaches. Because CSCs use multiple resistance mechanisms and hide in multiple protective niches, single-target therapies are unlikely to produce lasting responses. Patients may be offered combinations of treatments, and this reflects the biology described in this review.
- Ask about clinical trials. The review highlights the need for multimodal therapies that target both CSCs and their supportive microenvironments. Clinical trials are where these new combination strategies are tested.
- Recognize that research is advancing. New imaging methods, stem cell-based laboratory models, and single-cell and spatial profiling techniques are refining how researchers understand CSC heterogeneity and treatment resistance. These tools are building the foundation for future therapies.
Patients should discuss all treatment decisions with their neuro-oncology team. The findings in this review describe the biology behind the disease. They do not replace individualized medical advice.
Frequently Asked Questions
Why does glioblastoma often come back after surgery and treatment?
Cancer stem cells spread beyond the tumor margins visible on MRI scans. This means microscopic tumor cells remain after surgery and standard therapy. These cells can renew themselves, resist treatment, and hide in protective environments called niches. Recurrence is not a failure of the patient or the surgical team; it reflects the biology of the disease.
What are the five niches that protect cancer stem cells?
The five niches are perivascular (around blood vessels), hypoxic (low oxygen), invasive, immunosuppressive, and extracellular matrix-associated. These overlapping environments keep cancer stem cells in a stem-like state, help them evade the immune system, and provide resistance to treatment. They work together to support tumor survival and regrowth.
What does it mean if my tumor has cancer stem cell markers like CD133?
Markers such as CD133, CD44, CD15, SOX2, OCT-4, and nestin are used to identify cancer stem cells, but they are not specific. They can appear on normal neural stem cells and other tumor cells. Marker positivity does not always mean a cell can start a tumor. Researchers now combine markers with functional tests and single-cell profiling for clearer results.
Why are single-target therapies unlikely to work for glioblastoma?
Cancer stem cells use multiple resistance mechanisms and hide in several protective niches. A therapy that targets only one pathway or one niche may leave other cancer stem cells untouched. Lasting treatment will likely require combination approaches that target both the cancer stem cells themselves and the supportive environments around them.
What should I ask my surgeon about removing my brain tumor?
You can ask how the planned resection balances removing as much tumor as safely possible against protecting healthy brain function. This is called function-preserving maximal resection. Because cancer stem cells can spread beyond the visible tumor margins, complete removal is difficult. Your surgical team can explain the goals and risks for your specific case.
Are clinical trials important for brain tumor treatment?
Clinical trials are where new combination strategies that target cancer stem cells and their supportive microenvironments are tested. Because single-target therapies are unlikely to produce lasting responses, trials of multimodal approaches are needed. You can ask your neuro-oncology team whether a clinical trial is appropriate for your situation.
I was just diagnosed with glioblastoma — when should I seek a second opinion about surgery and treatment?
A second opinion is worth considering at diagnosis, before surgery, and whenever a treatment plan is proposed. Cancer stem cells spread beyond the tumor margins visible on MRI scans, which is a biological reason glioblastoma so often returns even after successful-looking surgery and standard therapy. Because these cells use multiple resistance mechanisms and hide in five overlapping protective niches, single-target therapies are unlikely to produce lasting responses. A second opinion can review imaging, pathology, and whether the planned resection balances tumor removal against neurological risk. Diagnostic Detectives Network provides independent expert second opinions.
Source Information
Original article title: Neuro-Oncological Perspectives on Cancer Stem Cell Biology in Glioblastoma: Implications for Resection, Recurrence, Targeted Therapy, and Other CNS Tumors.
Authors: Salmeron-Moreno K, Papisetty K, Kim CD, McCaffery T, Kashlan R, Theodore J, Kim JM, Buclez J, Duggireddy H, Maldonado J, Guerrero-Cázares H, Pradilla G, Garzon-Muvdi T.
Author affiliations: Department of Neurological Surgery, Emory University, Atlanta, GA, USA; Neurosurgery Department, Mayo Clinic, Jacksonville, FL, USA
Journal: Cells, 2026, volume 15, article 413
Publication dates: Received 6 February 2026; Revised 24 February 2026; Accepted 25 February 2026; Published 27 February 2026
DOI: https://doi.org/10.3390/cells15050413
Article type: Review article, open access under the Creative Commons Attribution (CC BY) license
This patient-friendly article is based on peer-reviewed research. It is intended for educational purposes and does not replace consultation with a qualified medical professional.
