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FRIDAY, Jan. 23, 2026 — Brain tumors are abnormal growths of cells in or around the brain. They can be primary (originating in the brain) or secondary (metastatic, spreading to the brain from cancer elsewhere). They can also originate from the structures around the brain, like the dura (brain lining), the nerves or the bone of the skull. Not all brain tumors are cancerous. Benign tumors typically grow more slowly and may not invade nearby tissue the way malignant tumors do, but even benign tumors can cause serious problems by pressing on key nerves, arteries or the brain itself. Understanding types, symptoms, diagnosis and treatment helps patients and families navigate care. Types of brain tumors Benign tumors can be effectively treated or controlled and generally have fewer complications, but they can still cause serious problems if incompletely treated. Malignant tumors grow more aggressively, infiltrate surrounding brain or skull tissue, and can sometimes spread within the central nervous system. Metastatic tumors originate outside the brain or skull and spread to these areas. Noncancerous (benign) brain tumors Meningiomas Arising from the meninges (membranes covering the brain and spinal cord), meningiomas are the most common primary brain tumors in adults. Many are slow-growing and are incidentally discovered. Symptoms result from pressure on nearby brain or nerve tissue and may include headaches, vision changes, seizures or problems like double vision, numbness or weakness, depending on location. A rare subset of meningiomas is atypical or anaplastic (higher grade) and behaves more aggressively. Pituitary adenomas These develop in the pituitary gland at the base of the brain. Some secrete hormones (such as prolactin, growth hormone or adrenocorticotropic hormone), causing endocrine symptoms such as menstrual changes, milk production, excess levels of growth hormone or Cushing’s disease. Excess growth hormone (acromegaly) and Cushing’s disease can shorten life. Non-functioning adenomas can cause visual symptoms by compressing the optic nerves or loss of hormone function by compressing the normal pituitary gland. Treatment involves medications for prolactin-secreting types or minimally invasive surgery through the nose (endoscopic endonasal surgery). Vestibular schwannomas (acoustic neuromas) These are tumors of nerve sheath cells in the vestibular (balance) nerve. They typically cause one-sided hearing loss, tinnitus (ringing in the ear), imbalance and sometimes facial numbness or weakness if large. Depending on size and symptoms, management ranges from observation with periodic MRIs to focused radiation (Gamma Knife stereotactic radiosurgery) or microsurgical removal. Craniopharyngiomas These are other benign, often cyst-forming tumors near the pituitary gland, its stalk, or a crucial brain region called the hypothalamus, which regulates everything from sleep to hunger to thirst. Theoretically derived from normal tissue leftover from development, these tumors can cause hormone deficiencies, growth issues, excessive thirst/urination, and visual disturbances. Even after treatment, they often recur and may require a combination of surgery, radiation, targeted drug therapies and long-term endocrine care. Hemangioblastomas Hemangioblastomas are tumors that form balls of loose blood vessels and often occur in the cerebellum and spinal cord. They can be sporadic or associated with von Hippel–Lindau syndrome, which can be hereditary. Symptoms include headaches, coordination problems and water on the brain (hydrocephalus) if they obstruct cerebrospinal fluid flow. Surgical removal is typical for larger tumors and Gamma Knife is very effective for others; targeted treatments are evolving for inherited, genetic cases. Pineal region tumors (benign) Tumors arising from the pineal gland can often be benign and are typically slow-growing. They can cause headaches, visual disturbances, and hydrocephalus by blocking cerebrospinal fluid pathways. Management may include surgery and, in select cases, radiation. Pineal region cysts are very rarely symptomatic and are usually only monitored and not treated. Choroid plexus papillomas These tumors arise from the tissue that produces cerebrospinal fluid (CSF). More common in children, these can overproduce CSF and cause hydrocephalus. Treatment usually involves surgical removal; outcomes are generally good. Smaller tumors respond well to Gamma Knife radiosurgery. Cancerous (malignant) brain tumors Low-grade gliomas (e.g., astrocytomas, oligodendrogliomas) These are slow-growing primary brain tumors that form from glial cells. They often present with seizures in young adults and can cause subtle cognitive or neurological changes. Molecular features influence prognosis and guide therapy. Even though they grow more slowly, they infiltrate brain tissue and can become higher-grade tumors over time. The lowest grade tumors can be cured with surgery or well-controlled with radiation. High-grade gliomas (e.g., glioblastoma) These rapidly growing, infiltrative tumors are the most common malignant primary brain tumors in adults. Symptoms evolve quickly and may include headaches, seizures and deficits like numbness, weakness or trouble with speech. Treatment typically combines removing as much of the tumor as possible, followed by radiation therapy and chemotherapy (for example, temozolomide), and may involve a type of cancer therapy called tumor treating fields or clinical trials. For recurrent tumors, many approaches are explored, including repeat surgery, radiosurgery and drug therapies. Ependymomas These arise from cells lining the brain’s ventricles (sacks in the brain that produce and circulate cerebrospinal fluid) or the spinal canal. They occur in children and adults. They can block the flow of cerebrospinal fluid, leading to hydrocephalus and headaches. Treatment involves surgical removal, often followed by radiation; chemotherapy is used in selected cases. Up to date classification also incorporates genetics that affect prognosis. Medulloblastomas These fast-growing tumors of the cerebellum are more common in children and can spread through cerebrospinal fluid to other parts of the brain and spinal cord. Symptoms include headaches, nausea and problems with balance and coordination. Treatment typically involves surgery, craniospinal radiation (depending on patient age) and chemotherapy. Care is tailored to the tumor’s molecular subtype and the patient’s risk. Primary central nervous system lymphoma This is a type of non-Hodgkin lymphoma confined to the brain, spinal cord and eyes. It is more common in people with compromised immunity suppression but can occur in others as well. Diagnosis often uses MRI and biopsy; treatment is based on high-dose methotrexate-containing chemotherapy regimens, with or without radiation. Pineal region malignant tumors (e.g., germinomas) These can cause hydrocephalus, vision changes and endocrine symptoms. Germinomas are typically managed through biopsy and a combination of chemotherapy and radiation, guided by precise pathology and staging. Choroid plexus carcinoma A rare malignant tumor that occurs more often in children, these can cause significant hydrocephalus and increased pressure inside the skull. Treatment includes aggressive surgical removal when possible, followed by chemotherapy and, in some cases, radiation. Metastatic brain tumors The most common of all brain malignancies, these originate from cancers elsewhere in the body — commonly lung, breast, melanoma, kidney and colorectal — that spread to the brain via the bloodstream. They may be solitary or multiple and often present with headaches, seizures or deficits like numbness, weakness of speech problems. Treatment options include surgery, stereotactic radiosurgery, whole-brain radiation and systemic therapies tailored to the primary cancer as well as corticosteroids for symptom control. Over the last 10 to 15 years, great improvements in outcomes have been achieved for many patients. Chordoma/Chondrosarcoma Chordomas and chondrosarcomas are rare tumors that can grow from the base of the skull and spine. They have a wide variety of aggressiveness, but chordomas are generally considered to be cancerous because they are very difficult to cure, even when they are slow-growing. The best outcomes are achieved with complete removal, usually followed by high-dose radiation. Sinonasal Cancers Some cancers that come from the sinuses can invade the brain or skull tissue under the brain. These are managed in concert with ear, nose and throat surgeons, often combining chemo- and radiation therapy with surgery. Important caveats Some “usually benign” tumors can have atypical or anaplastic forms that behave more aggressively, necessitating closer monitoring or additional (adjuvant) therapy. Even benign tumors can be serious, because they occupy space within the skull and may compress critical brain structures. Modern classifications include molecular and genetic markers that refine diagnosis and inform prognosis and treatment across many tumor types. Discussing the specific pathology and molecular features of a tumor with the care team is essential. Symptoms of brain tumors Brain areas control specific functions, so symptoms depend on tumor location, size and growth rate. Common symptoms include: Headaches: These are often worse in the morning or with straining, new or changing patterns, and are sometimes accompanied by nausea or vomiting due to increased pressure in the skull. These can be worrisome if they are severe enough to wake someone up at night. Headaches: These are often worse in the morning or with straining, new or changing patterns, and are sometimes accompanied by nausea or vomiting due to increased pressure in the skull. These can be worrisome if they are severe enough to wake someone up at night. Seizures: New-onset seizures in adults are a common presenting sign. Seizures can be generalized (loss of consciousness, convulsions) or focal (jerking or sensations in one body part, or sudden cessation of speech). Seizures: New-onset seizures in adults are a common presenting sign. Seizures can be generalized (loss of consciousness, convulsions) or focal (jerking or sensations in one body part, or sudden cessation of speech). Focal neurological deficits: These may include weakness or numbness on one side, difficulty with coordination or problems walking, if the cerebellum is affected. Focal neurological deficits: These may include weakness or numbness on one side, difficulty with coordination or problems walking, if the cerebellum is affected. Vision and eye problems: Among these are blurred or double vision, visual field loss (e.g., losing peripheral vision) and new difficulty seeing colors or reading. Pituitary tumors, meningiomas and craniopharyngiomas may all cause progressive vision decline. Vision and eye problems: Among these are blurred or double vision, visual field loss (e.g., losing peripheral vision) and new difficulty seeing colors or reading. Pituitary tumors, meningiomas and craniopharyngiomas may all cause progressive vision decline. Speech and language changes: People may have trouble finding words, slurred speech, difficulty understanding or producing language if dominant hemisphere areas are involved. Speech and language changes: People may have trouble finding words, slurred speech, difficulty understanding or producing language if dominant hemisphere areas are involved. Cognitive and personality changes: These symptoms may include memory loss, confusion, slowed thinking, apathy, irritability, or changes in judgment and behavior — particularly with frontal lobe tumors, which can often get large before they are recognized. Cognitive and personality changes: These symptoms may include memory loss, confusion, slowed thinking, apathy, irritability, or changes in judgment and behavior — particularly with frontal lobe tumors, which can often get large before they are recognized. Hearing loss and tinnitus: These typically affect only one side, with balance issues in vestibular schwannomas. Hearing loss and tinnitus: These typically affect only one side, with balance issues in vestibular schwannomas. Nausea and vomiting: Symptoms may occur especially with increased intracranial pressure or hydrocephalus. Nausea and vomiting: Symptoms may occur especially with increased intracranial pressure or hydrocephalus. Endocrine symptoms: Among these are irregular periods, milk secretion (galactorrhea), weight changes, heat/cold intolerance, excessive thirst and urination from pituitary-related tumors. Endocrine symptoms: Among these are irregular periods, milk secretion (galactorrhea), weight changes, heat/cold intolerance, excessive thirst and urination from pituitary-related tumors. Fatigue and sleep disturbances: These are non-specific but common. Fatigue and sleep disturbances: These are non-specific but common. How brain tumors are diagnosed Diagnosis typically begins with a primary care physician or an emergency visit if symptoms are severe. A patient may then be referred to a neurosurgeon or neurologist for a detailed neurological exam, and to specialists such as a neuro-oncologist (medical cancer specialist for brain tumors), a neurosurgeon (surgical management), and a radiation oncologist. If hormone issues are suspected, an endocrinologist may be involved, and a neuro-ophthalmologist may be needed to evaluate vision problems. Referral to a multidisciplinary brain tumor center can usually provide all of these in one location. Key steps: Medical history and neurological examination: This includes testing nerves, strength, sensation, reflexes, coordination, vision and mental status. Medical history and neurological examination: This includes testing nerves, strength, sensation, reflexes, coordination, vision and mental status. Imaging: An MRI of the brain with and without contrast is the gold standard. Specialized sequences (perfusion, diffusion, spectroscopy) and functional MRI may be used. CT scans help in emergencies or to assess calcifications and bone involvement. For suspected metastases, imaging of the body (CT chest/abdomen/pelvis, PET) may be performed to find the primary cancer. Imaging: An MRI of the brain with and without contrast is the gold standard. Specialized sequences (perfusion, diffusion, spectroscopy) and functional MRI may be used. CT scans help in emergencies or to assess calcifications and bone involvement. For suspected metastases, imaging of the body (CT chest/abdomen/pelvis, PET) may be performed to find the primary cancer. Laboratory tests: Among these are hormone panels for pituitary tumors; basic bloodwork to assess overall health; and sometimes, viral or immune status for lymphoma. Laboratory tests: Among these are hormone panels for pituitary tumors; basic bloodwork to assess overall health; and sometimes, viral or immune status for lymphoma. Lumbar puncture (spinal tap): In select cases, this may be ordered to analyze cerebrospinal fluid for cancer cells or markers, especially in germinoma, lymphoma or medulloblastoma. The may be avoided when raised pressure in the head is suspected unless deemed safe. Lumbar puncture (spinal tap): In select cases, this may be ordered to analyze cerebrospinal fluid for cancer cells or markers, especially in germinoma, lymphoma or medulloblastoma. The may be avoided when raised pressure in the head is suspected unless deemed safe. Biopsy or surgical resection: Tissue diagnosis is often necessary. This may be via a stereotactic needle biopsy guided by imaging or removal of part/all of the tumor via craniotomy or endoscopic endonasal approach for pituitary tumors. Pathologists classify the tumor under WHO (World Health Organization) criteria and assess molecular markers, which guide prognosis and treatment. Biopsy or surgical resection: Tissue diagnosis is often necessary. This may be via a stereotactic needle biopsy guided by imaging or removal of part/all of the tumor via craniotomy or endoscopic endonasal approach for pituitary tumors. Pathologists classify the tumor under WHO (World Health Organization) criteria and assess molecular markers, which guide prognosis and treatment. How brain tumors are treated Treatment is individualized based on tumor type, size, location, molecular features and patient health. Watchful waiting (active surveillance): Small, non-cancerous tumors not causing symptoms may be monitored with periodic MRIs and exams. Watchful waiting (active surveillance): Small, non-cancerous tumors not causing symptoms may be monitored with periodic MRIs and exams. Corticosteroids: Medications like dexamethasone reduce brain swelling and improve symptoms short-term. Corticosteroids: Medications like dexamethasone reduce brain swelling and improve symptoms short-term. Anti-seizure medications: These are used to prevent or control seizures in patients who have had them. Anti-seizure medications: These are used to prevent or control seizures in patients who have had them. Surgery: The aim is to remove as much tumor as safely possible. Techniques include craniotomy (opening the skull); awake mapping to preserve speech or movement; and endoscopic endonasal surgery for many tumors at the base of the skull (meningiomas, craniopharyngioma, chordomas) or pituitary adenomas. Complete removal may be possible for some benign tumors.Malignant tumors that have invaded into nearby tissue sometimes require partial removal. Surgery: The aim is to remove as much tumor as safely possible. Techniques include craniotomy (opening the skull); awake mapping to preserve speech or movement; and endoscopic endonasal surgery for many tumors at the base of the skull (meningiomas, craniopharyngioma, chordomas) or pituitary adenomas. Complete removal may be possible for some benign tumors.Malignant tumors that have invaded into nearby tissue sometimes require partial removal. Radiosurgery or radiotherapy: External beam radiation (including IMRT) targets residual tumor cells. Stereotactic radiosurgery (Gamma Knife, CyberKnife) delivers precise, high-dose radiation to small tumors or metastases. Proton therapy may spare surrounding tissue in certain cases. Radiation use is common after surgery for high-grade gliomas, chordomas and for many metastases and benign tumors that cannot be safely removed. Radiosurgery or radiotherapy: External beam radiation (including IMRT) targets residual tumor cells. Stereotactic radiosurgery (Gamma Knife, CyberKnife) delivers precise, high-dose radiation to small tumors or metastases. Proton therapy may spare surrounding tissue in certain cases. Radiation use is common after surgery for high-grade gliomas, chordomas and for many metastases and benign tumors that cannot be safely removed. Chemotherapy: Drugs like temozolomide are standard for glioblastoma; PCV (procarbazine, lomustine, vincristine) for oligodendroglioma; high-dose methotrexate-based regimens for CNS lymphoma; various pediatric protocols for medulloblastoma and ependymoma. Side effects and schedules vary. Chemotherapy: Drugs like temozolomide are standard for glioblastoma; PCV (procarbazine, lomustine, vincristine) for oligodendroglioma; high-dose methotrexate-based regimens for CNS lymphoma; various pediatric protocols for medulloblastoma and ependymoma. Side effects and schedules vary. Targeted and biologic therapies: Bevacizumab (anti-VEGF) can reduce swelling and symptoms in recurrent glioblastoma. Some tumors respond to BRAF or MEK inhibitors when specific mutations are present. Tumor treating fields, which are wearable devices delivering low-intensity electrical fields, can be used in glioblastoma. Tumors can be tested for specific defects to see what targeted therapies can be used. Targeted and biologic therapies: Bevacizumab (anti-VEGF) can reduce swelling and symptoms in recurrent glioblastoma. Some tumors respond to BRAF or MEK inhibitors when specific mutations are present. Tumor treating fields, which are wearable devices delivering low-intensity electrical fields, can be used in glioblastoma. Tumors can be tested for specific defects to see what targeted therapies can be used. Clinical trials: These offer access to investigational therapies and combinations that may improve outcomes. Many times these are free of charge as part of a study. Clinical trials: These offer access to investigational therapies and combinations that may improve outcomes. Many times these are free of charge as part of a study. Supportive procedures: These include ventriculoperitoneal shunt or endoscopic third ventriculostomy to relieve hydrocephalus; rehabilitation therapies (physical, occupational, speech) to improve function; and endocrine therapy for pituitary-related hormone imbalances. Supportive procedures: These include ventriculoperitoneal shunt or endoscopic third ventriculostomy to relieve hydrocephalus; rehabilitation therapies (physical, occupational, speech) to improve function; and endocrine therapy for pituitary-related hormone imbalances. What causes brain tumors? For most brain tumors, the exact cause is unknown. They result from genetic changes that alter cell growth and survival, and are sometimes influenced by inherited syndromes or environmental exposures. Unlike many other cancers, brain tumors are rarely linked to lifestyle factors (such as diet or alcohol use). Metastatic brain tumors are caused by cancer cells spreading through the bloodstream or cerebrospinal fluid from a primary tumor elsewhere. Brain tumor risk factors Age: Some tumors (medulloblastoma, ependymoma) are more common in children; others (glioblastoma, meningioma) occur more often in older adults. Age: Some tumors (medulloblastoma, ependymoma) are more common in children; others (glioblastoma, meningioma) occur more often in older adults. Sex: Meningiomas are more common in women; glioblastoma is slightly more common in men. Sex: Meningiomas are more common in women; glioblastoma is slightly more common in men. Ionizing radiation: Prior therapeutic radiation to the head increases risk years later. Ionizing radiation: Prior therapeutic radiation to the head increases risk years later. Family history/genetic syndromes: Neurofibromatosis type 1 and 2 (schwannomas, meningiomas, gliomas); Li-Fraumeni (various tumors); von Hippel–Lindau (hemangioblastomas); tuberous sclerosis (subependymal giant cell astrocytomas); Cowden/PTEN hamartoma syndrome (meningiomas); Lynch/Turcot (medulloblastoma, gliomas). Family history/genetic syndromes: Neurofibromatosis type 1 and 2 (schwannomas, meningiomas, gliomas); Li-Fraumeni (various tumors); von Hippel–Lindau (hemangioblastomas); tuberous sclerosis (subependymal giant cell astrocytomas); Cowden/PTEN hamartoma syndrome (meningiomas); Lynch/Turcot (medulloblastoma, gliomas). Immune suppression: HIV/AIDS, organ transplantation or immunosuppressive medications increase risk of CNS lymphoma. Immune suppression: HIV/AIDS, organ transplantation or immunosuppressive medications increase risk of CNS lymphoma. Certain occupational exposures: High-dose solvents or chemicals have been studied, but evidence is mixed and often inconclusive. Certain occupational exposures: High-dose solvents or chemicals have been studied, but evidence is mixed and often inconclusive. Previous cancers: People with aggressive cancers (lung, melanoma, breast, kidney) have higher risk of brain metastases. Previous cancers: People with aggressive cancers (lung, melanoma, breast, kidney) have higher risk of brain metastases. Obesity and hormones: Obesity is linked to higher risk of meningioma; prolonged hormones from pills or implants (progesterone) may influence some meningiomas. Obesity and hormones: Obesity is linked to higher risk of meningioma; prolonged hormones from pills or implants (progesterone) may influence some meningiomas. Radiation from everyday devices: Typical cell phone use has not been conclusively linked; large studies remain ongoing and generally reassuring. Radiation from everyday devices: Typical cell phone use has not been conclusively linked; large studies remain ongoing and generally reassuring. Living with a brain tumor: Complications and long-term considerations Living with a brain tumor can involve navigating both the effects of the tumor and side effects of treatment. Possible complications include: Neurological deficits: These may include persistent weakness, sensory changes, speech or language problems, vision or hearing loss, and coordination difficulties, depending on tumor location and treatment. Neurological deficits: These may include persistent weakness, sensory changes, speech or language problems, vision or hearing loss, and coordination difficulties, depending on tumor location and treatment. Seizure disorder: Even after treatment, some patients continue to have seizures and must take anti-epileptic medications and follow safety precautions. Seizure disorder: Even after treatment, some patients continue to have seizures and must take anti-epileptic medications and follow safety precautions. Cognitive and emotional changes: Memory problems, slowed processing, attention difficulties, depression, anxiety and personality changes may occur. Neuropsychological evaluation and cognitive rehabilitation may help. Cognitive and emotional changes: Memory problems, slowed processing, attention difficulties, depression, anxiety and personality changes may occur. Neuropsychological evaluation and cognitive rehabilitation may help. Hydrocephalus and intracranial pressure: Some patients need long-term shunt management or monitoring for fluid buildup. Hydrocephalus and intracranial pressure: Some patients need long-term shunt management or monitoring for fluid buildup. Endocrine issues: Pituitary and hypothalamic tumors or their treatments can cause chronic hormone deficiencies, requiring replacement therapy. Endocrine issues: Pituitary and hypothalamic tumors or their treatments can cause chronic hormone deficiencies, requiring replacement therapy. Treatment side effects: Radiation can cause fatigue, skin changes, hair loss and late effects like tissue damage or cognitive decline. Chemotherapy may cause nausea, low blood counts, increased infection risk and neuropathy. Steroids can lead to weight gain, mood changes, high blood sugar and bone loss. Treatment side effects: Radiation can cause fatigue, skin changes, hair loss and late effects like tissue damage or cognitive decline. Chemotherapy may cause nausea, low blood counts, increased infection risk and neuropathy. Steroids can lead to weight gain, mood changes, high blood sugar and bone loss. Functional impacts: These may include driving restrictions after seizures, challenges with work or school, and the need for assistive devices or home modifications. Functional impacts: These may include driving restrictions after seizures, challenges with work or school, and the need for assistive devices or home modifications. Recurrence and surveillance: Many tumors require long-term MRI monitoring. Recurrence may necessitate additional surgery, radiation or systemic therapy. Recurrence and surveillance: Many tumors require long-term MRI monitoring. Recurrence may necessitate additional surgery, radiation or systemic therapy. Thromboembolism: Certain tumors and treatments increase risk of blood clots, requiring vigilance for swelling or chest symptoms. Thromboembolism: Certain tumors and treatments increase risk of blood clots, requiring vigilance for swelling or chest symptoms. Fertility and family planning: Treatments can affect fertility; consultation with reproductive specialists before therapy may be helpful. Fertility and family planning: Treatments can affect fertility; consultation with reproductive specialists before therapy may be helpful. Palliative and supportive care: Symptom management, advance care planning,and psychosocial support improve quality of life. Social workers, rehabilitation therapists, support groups and counseling can be invaluable. Palliative and supportive care: Symptom management, advance care planning,and psychosocial support improve quality of life. Social workers, rehabilitation therapists, support groups and counseling can be invaluable. If you or a loved one is experiencing new neurological symptoms, prompt evaluation is essential. Early diagnosis and a coordinated care team — including neurosurgery, neuro-oncology, radiation oncology, neurology, endocrinology and rehabilitation — provide the best chance for effective treatment and symptom control. About the experts Paul A. Gardner, MD, is vice chair of clinical innovation for the Department of Neurosurgery at NYU Grossman School of Medicine and director of the NYU Langone Skull Base Surgery Center. Douglas Kondziolka, MD, is vice chair of clinical research for the Department of Neurosurgery at NYU Grossman School of Medicine and director of the NYU Langone Center for Advanced Radiosurgery and the Gamma Knife Program.

中华医学会放射肿瘤治疗学分会. 脑胶质瘤放射治疗专家共识（2025版）[J]. 中华放射肿瘤学杂志, 2026, 35(1): 20-33. DOI: 10.3760/cma.j.cn113030-20250608-00217. 脑胶质瘤放射治疗专家共识（2025版） 中华医学会放射肿瘤治疗学分会 基金信息： 国家医学高层次人才计划（2024年优秀青年医师）；四川省干部保健课题（川干研ZH2023‐801）；成都市科技局重点研发支撑计划（2024‐YF05‐02377‐SN，2024‐YF05‐00948‐SN） 实践指南注册：国际实践指南注册与透明化平台（PREPARE‐2025CN1375） 摘 要 脑胶质瘤是指发生在脑神经胶质的肿瘤，是最常见的原发性颅内肿瘤，年发病率约为6.4/10万人口。放疗是脑胶质瘤重要的局部治疗手段，不同级别和类型的脑胶质瘤放疗原则不同。2017年，中华医学会放射肿瘤治疗学分会发布了国内首部脑胶质瘤放疗共识，为国内放疗同行提供了脑胶质瘤的放疗参考，规范了我国脑胶质瘤的放疗实践。2021年版世界卫生组织中枢神经系统肿瘤分类更新了脑胶质瘤的分子病理亚型。随着分子病理学、显微外科学、功能影像学、放射治疗学等学科的发展，脑胶质瘤的多学科诊疗手段不断丰富，脑胶质瘤临床疗效有所提高。基于上一版放疗共识，胶质瘤的分子病理、电场治疗，室管膜瘤、儿童胶质瘤、老年胶质瘤的放疗等问题的共识需要进一步地更新和丰富。因此，中华医学会放射肿瘤治疗学分会组织全国脑胶质瘤领域的专家，围绕脑胶质瘤放疗临床关切的实际问题，遵守循证医学原则与高质量临床研究依据，结合我国国情和临床可及性等多个因素，制定了本共识。以期更加规范脑胶质瘤的放疗实践，为临床工作提供参考，推动我国脑胶质瘤的诊疗规范和综合治疗效果提升。 关键词 神经胶质瘤；放射疗法；共识 脑胶质瘤（glioma）是指发生在脑神经胶质的肿瘤，是最常见的原发性颅内肿瘤，占所有颅内原发肿瘤的60%~70%。脑胶质瘤年发病率约为6.4/10万人口，其中胶质母细胞瘤（glioblastoma，GBM）发病率最高，约为4.03/10万［1］，中国人群低级别胶质瘤［世界卫生组织（World Health Organization，WHO）2级］、间变性胶质瘤（WHO 3级）和胶质母细胞瘤（WHO 4级）的中位生存时间分别约为78.1、37.6和14.4个月［2］。2017年，中华医学会放射肿瘤治疗学分会发布了国内首部脑胶质瘤放疗专家共识，为国内放疗同行提供脑胶质瘤的放疗参考［3］。本版共识对成人弥漫性胶质瘤、高级别脑胶质瘤的电场治疗，室管膜瘤、儿童胶质瘤、老年胶质瘤的放疗进行了更新和补充，围绕低级别及高级别脑胶质瘤、儿童及老年脑胶质瘤、复发胶质瘤、室管膜瘤的放疗共识、放射性脑损伤共7个板块，从临床关切的实际临床问题出发，遵守循证医学原则与高质量临床研究依据，结合我国国情和临床可及性等多个因素，以期推动我国脑胶质瘤的诊疗规范和综合治疗疗效提高。共识制订机构为中华医学会放射肿瘤治疗学分会，专家组由国内脑胶质瘤放疗领域的专家共42人组成，旨在为国内脑胶质瘤放疗同行和从事脑胶质瘤诊疗的相关专业人员提供诊疗参考，推动脑胶质瘤放疗的规范化和整体疗效提高。 共识专家组基于现有循证医学证据，先后召开了10余次线上线下会议，对相关证据进行评估、讨论，按照循证医学原则定义推荐意见的证据级别，结合我国专家的临床实践经验，形成初步的共识意见、证据级别和推荐级别（如表1），并对共识意见的陈述进行投票，每一个推荐条目设置“非常同意”“基本同意”“不同意或不确定”3个选项，通过投票结果专家共识度≥80%的专家意见定义为达成共识。基于专家投票结果，最终形成本共识。 表1   证据级别和推荐等级 一、成人型弥漫性胶质瘤（WHO 2级少突胶质瘤，WHO 2级星型细胞瘤）放疗共识 根据2021年WHO中枢神经系统肿瘤分类标准，本文的WHO 2级成人型弥漫性胶质瘤包括2级星形细胞瘤（IDH突变）和2级少突胶质瘤（IDH突变和1p/19q共缺失）。 1.WHO 2级成人型弥漫性胶质瘤的术后影像学评价 专家共识1：WHO 2级成人型弥漫性胶质瘤术后建议72 h内进行影像学复查，切除程度主要依据术前与术后MRI的T2或液体抑制反转恢复（fluid attenuated inversion recovery，FLAIR）序列综合判定［证据级别：Ⅰ级；推荐级别：强］。有条件的单位可选择性将MRI与功能影像学新技术相结合，更好地判断肿瘤边界、术后残留及肿瘤浸润等情况，有利于准确勾画靶区［证据级别：Ⅳ~Ⅴ级；推荐级别：中等］。 2.WHO 2级成人型弥漫性胶质瘤术后风险分层及治疗策略：主要依据美国肿瘤放射治疗协作组（Radiation Therapy Oncology Group，RTOG） 9802和欧洲癌症治疗研究组织（European Organisation for Research and Treatment of Cancer，EORTC） 22844标准进行风险分层［4-5］。RTOG 9802标准中，低风险特征为≤40岁和肿瘤全切除，高风险特征为>40岁或肿瘤非全切除。EORTC 22844试验数据建立的低级别胶质瘤风险预测模型，最终将年龄≥40岁、星形细胞瘤、肿瘤最大径≥6 cm、肿瘤跨中线和术前神经功能受损5项指标确定为独立预后因素，其中低风险组（包含0~2个危险因素）预后明显优于高风险组（包含3~5个危险因素）。 专家共识2：需要综合RTOG 9802和EORTC 22844标准进行风险分层，临床中需个体化分析，才能更准确地判断疾病风险。无任何高危因素患者可选择术后观察，对于高风险WHO 2级成人型弥漫性胶质瘤，推荐术后放疗+辅助替莫唑胺化疗，放疗+丙卡巴肼/洛莫司汀/长春新碱（procarbazine /lomustine / vincristine，PCV）辅助化疗或个体化考虑同步放化疗［证据级别：Ⅰ~Ⅱ级；推荐级别：强］。 3. WHO 2级成人型弥漫性胶质瘤的术后放疗指征及时机：对于高风险组应尽早开始放疗及辅助化疗，建议术后4~8周内［5］。对于肿瘤全切、年龄<40岁的WHO 2级成人型少突胶质瘤患者，除了肿瘤残留以及年龄等因素外，还需要同其他低级别胶质瘤患者一样加入相关危险因素进行综合评价（如肿瘤最大径≥6 cm、肿瘤跨中线、术前神经功能受损等）［6-7］。 专家共识3：低风险组可密切观察，每3~6个月复查MRI［证据级别：Ⅰ~Ⅱ级；推荐级别：强］；高风险组应尽早放疗及辅助化疗，建议术后4~8周内开始放疗［证据级别：Ⅰ~Ⅱ级；推荐级别：强］。 4. WHO 2级成人型弥漫性胶质瘤的术后放疗剂量分割方案：术后放疗总剂量为45~54 Gy，单次剂量1.8~2.0 Gy，单次剂量超过2 Gy会增加发生远期认知障碍的风险。残留病灶的放疗剂量>50 Gy，提高残留病灶区的剂量需要开展进一步临床研究。 专家共识4：术后放疗剂量总量为45~54 Gy，单次剂量1.8~2.0 Gy［证据级别：Ⅰ级；推荐级别：强］；提高放疗剂量需要进一步开展临床研究。 5. WHO 2级成人型弥漫性胶质瘤的术后靶区勾画原则：依据术前和术后的MR影像，采用FLAIR序列和T2序列高信号的区域定义为大体肿瘤区（gross tumor volume，GTV），在GTV外放1~2 cm作为临床靶区（clinical target volume，CTV），超出解剖屏障的部分可仅包括0.5 cm的解剖屏障外的结构。对于弥漫多病灶建议在放疗45 Gy左右时复查MRI，残留病灶周围外放1 cm，加量至54 Gy［5，7-8］。囊性肿瘤占位效应较大，可根据术后放疗前MRI和CT模拟定位显示的残腔勾画GTV，不需要包全术前囊腔的范围。 专家共识5：依据术前和术后的MR影像，采用FLAIR序列和T2序列中高信号的区域定义GTV，GTV外放1~2 cm作为CTV，超出解剖屏障的部分可仅包括0.5 cm的解剖屏障外的结构［证据级别：Ⅰ级；推荐级别：强］；对于弥漫多病灶的低级别胶质瘤建议在放疗45 Gy左右时复查MRI，残留病灶周围外放1 cm，加量至54 Gy［证据级别：Ⅱ~Ⅲ级；推荐级别：中等］。 6.WHO 2级成人型弥漫性胶质瘤的药物治疗 专家共识6：对于初治高风险患者，应积极考虑放疗联合化疗。推荐化疗方案包括PCV、替莫唑胺同步和/或辅助化疗［证据级别：Ⅰ~Ⅱ级；推荐级别：强］。对于伴有BRAF基因V600E突变（第600位缬氨酸被谷氨酸替代）或NTRK融合的WHO 2级成人型弥漫性胶质瘤患者可考虑相应的靶向药物治疗［证据级别：Ⅲ~Ⅳ级；推荐级别：中等］［8-11］。 二、高级别胶质瘤 高级别胶质瘤（high grade glioma，HGG）是指WHO中枢神经系统肿瘤分类中规定的3或4级胶质瘤，主要包括3级星形细胞瘤（IDH突变）、3级少突胶质瘤（IDH突变和1p/19q共缺失）、4级星形细胞瘤（IDH野生型）和胶质母细胞瘤（glioblastoma，GBM）。手术仍是HGG的基础治疗，放疗是不可或缺的重要治疗手段，术后放疗可以取得显著生存获益。 1.新诊断HGG的放疗时机：近几年的研究显示，术后42 d内放疗能有获益，而超过42 d生存期显著缩短［12］。根据临床试验数据推算GBM术后残余肿瘤的倍增时间为24 d［13］，目前建议HGG术后4~6周放疗可能最合适。 专家共识7：高级别胶质瘤生存时间与放疗开始时间密切相关，术后早期放疗能有效延长高级别胶质瘤患者生存期［12，14］，强烈推荐术后尽早（手术后2~6周）开始放疗［证据级别：Ⅲ~Ⅳ级；推荐级别：强］。同时评估放疗时替莫唑胺同步化疗的必要性。 2.新诊断HGG的放疗剂量：早期研究证实60 Gy以上的放疗剂量并未延长HGG患者生存期，且生活质量明显下降［12-13］。推荐放疗总剂量为54~60 Gy分30~33次，1.8~2.0 Gy/次，每日1次，肿瘤体积较大和/或位于重要功能区及WHO 3级胶质瘤，可适当降低照射总剂量。考虑到水肿区照射体积较大，可分二程放疗，首程一般46 Gy或45~50.4 Gy，缩野后二程14 Gy或9~14.4 Gy。随着现代磁共振影像技术、新的分子病理诊断及放疗技术的提高，更高剂量的照射是否有获益值得重新评估。 专家共识8：照射总剂量为54~60 Gy分30~33次，1.8~2.0 Gy/次，每日1次，肿瘤体积较大和/或位于重要功能区及WHO 3级胶质瘤，可适当降低照射总剂量［证据级别：Ⅲ~Ⅳ级；推荐级别：强］。尽管调强放疗能提高靶区适形度、减少正常组织受照剂量，最大限度缩小照射体积，给予靶区更高的放疗剂量，但提高剂量后的疗效尚未得到大型临床试验证实，盲目提高照射总剂量或分次剂量，应慎重。 3.新诊断HGG的靶区勾画：HGG的GTV建议参考术前和术后MRI的FLAIR序列和T1增强序列确定。参考肿瘤侵犯具体情况，GTV外扩1~2 cm形成CTV，CTV基础上外扩3~5 mm形成计划靶区（planning target volume，PTV），并建议每天进行图像验证，尤其是PTV外扩≤3 mm者。如首程放疗靶区包括水肿区，二程计划时照射区可仅包括残余肿瘤或瘤腔［15］。HGG放疗靶区争议焦点主要是最初的CTV是否需要包括瘤周水肿区。临床试验证实，靶区是否包括水肿区，在肿瘤控制和生存期上差异没有统计学意义［16］。 专家共识9：在CT或CT/MRI融合图像上勾画靶区和危及器官；建议高级别胶质瘤GTV为术腔和残存肿瘤，GTV外扩形成CTV，是否包括瘤周相关水肿区给予二程放疗，需个体化对待；GTV外扩1~2 cm形成CTV，CTV外扩3~5 mm形成PTV［证据级别：Ⅲ~Ⅳ级；推荐级别：强］。 4. GBM（IDH野生型）的治疗模式：替莫唑胺同步放化疗（75 mg/m2）联合辅助化疗（150~200 mg/m2）是GBM患者的标准治疗［17］。替莫唑胺同步放化疗联合辅助化疗和电场治疗也作为一类证据的标准治疗被国内外指南推荐［18］。另外，可选择的化疗方案包括洛莫司汀和替莫唑胺联合同步放化疗后继续两药联合辅助化疗［19］。化疗方案的选择，主要根据患者卡诺夫斯凯计分（Kanofsky performance score，KPS）及MGMT甲基化等进行综合评判。KPS≥60分者，若存在MGMT启动子区甲基化，推荐标准放疗加替莫唑胺同步和辅助化疗加或不加电场治疗，还可推荐标准放疗加替莫唑胺同步和辅助化疗并联合洛莫司汀化疗；对于MGMT启动子区非甲基化或甲基化情况不明确者，推荐放疗加替莫唑胺同步和辅助化疗加或不加电场治疗［20］。KPS<60分者，推荐短程放疗，加或不加替莫唑胺同步和辅助化疗；MGMT启动子区甲基化者，也可单独替莫唑胺化疗［21］。此外，目前没有可靠的证据显示超过6个周期的替莫唑胺辅助化疗或更改替莫唑胺化疗方案，如75~100 mg/m2的21 d方案和50 mg/m2的每天方案等能显著延长患者生存期［22-23］。医生在临床实践中可根据患者病情、化疗耐受及经济情况等，采用个体化化疗方案。 专家共识10：强烈推荐成人新诊断GBM采用放疗联合替莫唑胺（75 mg/m2）同步放化疗，并随后进行6个周期的替莫唑胺辅助化疗。在放疗中和放疗后应用替莫唑胺，显著延长患者生存期［证据级别：Ⅰ级；推荐级别：强］。这一协同作用在MGMT启动子区甲基化者中最为明显。MGMT启动子甲基化者还可选择替莫唑胺联合洛莫司汀同步和辅助放化疗［证据级别：Ⅱ级；推荐级别：强］。KPS≥60分的幕上GBM患者，还可在以上治疗模式基础上，加入电场治疗［证据级别：Ⅰ级；推荐级别：强］。 5. 3级少突胶质瘤的治疗模式：2021版WHO分类定义的3级少突胶质瘤分子特征为IDH突变伴1p/19q共缺失，属于高级别胶质瘤，相比星形细胞瘤对放化疗敏感。RTOG 9813试验中，3级胶质瘤单次剂量为1.8 Gy，50.4 Gy后缩野至总剂量59.4 Gy［24］。对于体积较大或累及重要功能区的3级少突胶质瘤总剂量可降低至54 Gy。EORTC 26951和RTOG 9402这2个研究的放疗单次量均为1.8 Gy，总剂量59.4 Gy［25-26］。尽管替莫唑胺的不良反应较小，但CODEL研究证实替莫唑胺单独化疗在此类患者中无效［27］。 专家共识11：存在1p/19q联合缺失的患者对化疗和放疗更敏感，放疗联合PCV化疗是一线治疗方案［证据级别：Ⅲ~Ⅳ级；推荐级别：强］。目前放疗联合替莫唑胺治疗3级胶质瘤显示初步疗效，且不良反应更少［证据级别：Ⅱ级；推荐级别：强］。研究替莫唑胺、放疗、1p/19q共缺失三者关系的试验正在进行，初步结果显示单独替莫唑胺化疗无效，替莫唑胺化疗联合放疗能够改善生存。 6. 3级星形细胞瘤的治疗模式：2021版WHO分类定义的3级星形细胞瘤的分子特征为IDH突变、无1p/19q共缺失。此类患者预后一般，放疗联合化疗的中位生存期为6~7年。放疗剂量为59.4~60 Gy，常规分割1.8~2.0 Gy/次。推荐在此类患者进行12个周期的替莫唑胺辅助化疗。临床实践中应综合考虑患者的身体状况、病理和分子病理及其他临床因素，积极探索个体化治疗方案。 专家共识12：放疗联合12个周期的辅助替莫唑胺化疗，显著延长3级星形细胞瘤患者的生存期［证据级别：Ⅲ~Ⅳ级；推荐级别：中等］，根据患者具体情况推荐同步替莫唑胺化疗。 7. 4级星形细胞瘤的治疗模式：2021版WHO分类重新定义了IDH野生型的较低级别胶质瘤。此类胶质瘤分子病理中只要有下列之一：TERT突变、EGFR扩增或+7/-10染色体异常，即使组织病理为2~3级，也被定义为4级星形。美国国家综合癌症网（National Comprehensive Cancer Network，NCCN）指南指出，鉴于此类胶质瘤恶性度高，建议放疗剂量为59.4~60 Gy。最新的2项回顾和前瞻性临床研究也证实。较好的生存期与更高的放疗剂量（54~60 Gy）有关［28］，且高剂量放疗联合化疗（Stupp方案）能够进一步延长生存期［29］。此外，IDH突变的2~3级胶质瘤如同时伴CDKN2A/B缺失，同样被WHO定义为4级星形细胞瘤［30］。回顾性数据显示此类患者生存期较差，没有标准治疗方案。此类胶质瘤的标准治疗方案仍需更多的临床试验证实。 专家共识13：分子病理定义的4级星形细胞瘤的治疗目前无统一标准。鉴于该类肿瘤恶性程度较高，临床多给予更积极的治疗策略，59.4~60 Gy的放疗联合替莫唑胺同步和辅助化疗可能是有效方法［证据级别：Ⅱ级；推荐级别：强］。目前回顾性和小型前瞻性临床研究初步证实了高剂量放疗和积极化疗（Stupp方案）能够进一步延长生存期。 三、儿童型弥漫性高级别胶质瘤（弥漫性中线胶质瘤） 发生于儿童和青少年（<19岁）的弥漫性高级别胶质瘤发病率较低，5年生存率小于20%，所有患者需要由具有中枢神经系统肿瘤治疗经验的多学科团队进行诊疗。 1.儿童型弥漫性高级别胶质瘤的临床表现及病理分类：儿童弥漫性高级别胶质瘤的临床表现主要包括颅内压增高、癫痫发作和神经功能损伤三大类。幕上肿瘤患者通常表现为癫痫发作或颅内压升高。颅后窝肿瘤通常表现为头痛、恶心、呕吐、步态异常和协调异常。 儿童型弥漫性高级别胶质瘤分类包括：①弥漫性中线胶质瘤，组蛋白H3第27位赖氨酸（H3 K27）改变（包括由于p.K27M突变、EZHIP过表达或EGFR突变导致H3 K27‐三甲基化缺失的肿瘤），WHO 4级。②弥漫性半球形胶质瘤、组蛋白H3第34位甘氨酸突变（H3 G34R）突变型。这类肿瘤在H3‐3A（H3F3A）基因中有一个错义突变，导致组蛋白变体上的p.G34R或p.G34V被取代。③弥漫性儿童型高级别胶质癌、H3野生型和IDH野生型，是一组主要发生在儿童或年轻人中的恶性胶质瘤，可能出现在幕上或幕下的任何地方。肿瘤细胞有丝分裂活性增加，常见TP53突变，MYCN扩增，PDGFRA改变（突变或扩增），ID2、NF1改变和EGFR扩增。④婴儿型半球形胶质瘤，由多个亚型组成，大多数有RTK融合，涉及NTRK、ROS1、ALK和MET基因［31］。 专家共识14：儿童型弥漫性高级别胶质瘤常见临床症状与成人相似，临床表现主要包括颅内压增高、癫痫发作和神经功能损伤三大类［证据级别：Ⅱ~Ⅲ级；推荐级别：强］。病理分类结合组织病理学和分子病理学，强调整合诊断和分子特征改变的重要性。儿童型弥漫性高级别胶质瘤分为4类：弥漫性中线胶质瘤，H3 K27改变，WHO 4级；弥漫性半球形胶质瘤、H3 G34R突变型；弥漫性儿童型高级别胶质癌、H3野生型和IDH野生型；婴儿型半球形胶质瘤［证据级别：Ⅰ~Ⅱ级；推荐级别：强］。 2.儿童型弥漫性高级别胶质瘤的治疗策略：儿童型弥漫性高级别胶质瘤的治疗要根据患儿的年龄、一般状态、病变部位和范围、病理诊断结果等，进行综合判断，制订合理的治疗方案。 对于可手术切除的病变，推荐最大范围地安全切除肿瘤。对于发生梗阻性脑积水的患儿，推荐应用脑室镜做第三脑室底部引流手术，以改善脑积水的症状［32］。放疗在≥3岁儿童弥漫性高级别胶质瘤患者的治疗中起着重要作用，放疗开始时间尚有争议。儿童脑胶质瘤诊疗规范强烈推荐术后尽早（术后2~6周）开始放疗，NCCN指南推荐术后4~8周开始放疗。对于<3岁的患儿，考虑到射线照射对患儿大脑发育的影响，通常选择延迟放疗，推荐术后化疗［33-34］。 首选的化疗药物包括替莫唑胺和洛莫司汀［35］。<3岁患儿中，推荐给予单纯化疗者，可采用的化疗药物包括环磷酰胺、长春新碱、顺铂和依托泊苷［36］或者长春新碱、卡铂和替莫唑胺［37］。近年来，靶向治疗和免疫治疗尚处于临床探索阶段，目前研究的药物包括表皮生长因子受体（epidermal growth factor receptor，EGFR）单克隆抗体尼妥珠单抗、周期依赖性蛋白激酶（cyclin‐dependent kinases 4，CDK）4/6抑制剂瑞博西尼、多巴胺D2受体（dopamine receptor D2，DRD2）拮抗剂ONC201、H3.3K27M特异性疫苗等。一项回顾性研究提示纳武利尤单抗联合再程放疗，对复发的弥漫性脑桥胶质瘤具有较好的安全性，并且有望带来生存获益［38］。此外，也有个案病例尝试电场治疗，显示安全性良好［39］。 专家共识15：儿童型弥漫性高级别胶质瘤推荐临床试验。手术治疗目标是最大范围安全切除肿瘤，并获得足够的组织进行组织学和分子分类［证据级别：Ⅰ~Ⅱ级；推荐级别：强］。推荐≥3岁儿童弥漫性高级别胶质瘤患者术后放疗［证据级别：Ⅱ~Ⅲ级；推荐级别：强］，但术后放疗时机有争议，建议术后恢复良好后尽量在4~8周内开始放疗，<3岁患者考虑延迟放疗［证据级别：Ⅳ~Ⅴ级；推荐级别：中等］。化疗常用药物包括替莫唑胺和洛莫司汀等［证据级别：Ⅲ~Ⅳ级；推荐级别：中等］。 3.儿童型弥漫性高级别胶质瘤的靶区勾画及剂量选择：推荐采用调强放疗技术，常规分割方案，每次1.8~2 Gy，每周5次，总剂量50.4~54 Gy，残余肿瘤局部加量至59.4~60 Gy。对于年龄较小，需要镇静才能接受放疗的患儿，也可以采用低分割的放疗方案，总剂量39~44.8 Gy，分13~16次［40-41］。 术后放疗靶区通常根据术前和术后磁共振成像来确定，使用T1增强像和T2/FLAIR序列来确定GTV。GTV1通常包括术后T1增强像的强化区域和手术术腔，并结合术前影像和T2/FLAIR序列来确定。GTV2包括术后残余肿瘤及瘤床区。CTV1由GTV1各方向外扩1~2 cm（沿白质束方向外扩2 cm）形成，CTV2由GTV2各方向外扩0.5~1 cm形成，根据解剖屏障进行修订。根据固定技术的不同，外扩0.3~0.5 cm得到PTV，给予PTV1 50.4~54 Gy，PTV2 59.4~60 Gy［41］。弥漫性中线胶质瘤建议诊断后尽早开始放疗，结合MRI的T1增强像和T2/FLAIR序列勾画GTV，各方向外扩1 cm形成CTV，推荐总剂量54 Gy，单次剂量1.8 Gy。 对于无法手术的儿童，目前有病例报道立体定向放疗可以达到缩瘤减症的效果。质子放疗在儿童低级别胶质瘤的治疗中与传统放疗疗效相当，但不良反应发生率大大降低，有望成为无法手术高级别胶质瘤儿童在降低脑损伤的同时改善预后的新模式治疗［42］。 专家共识16：推荐采用调强放疗技术。靶区勾画需结合MRI T1增强像和T2/FLAIR序列勾画GTV，CTV建议外扩1~2 cm，总剂量50.4~54 Gy，单次1.8~2 Gy，残余肿瘤局部推量至59.4~60 Gy ［证据级别：Ⅱ~Ⅲ级；推荐级别：强］。弥漫性中线胶质瘤建议诊断后尽早开始放疗，推荐总剂量54 Gy，单次剂量1.8 Gy ［证据级别：Ⅱ~Ⅲ级；推荐级别：强］。有条件的患儿可考虑质子治疗［证据级别：Ⅳ~Ⅴ级；推荐级别：中等］。 四、老年胶质瘤 本共识推荐和定义的老年胶质瘤为≥70周岁的胶质瘤患者［43］。临床特征方面，除了神经肿瘤常见的颅内压升高及神经功能缺失等症状之外，老年胶质瘤患者常常以人格改变、记忆力下降等非典型症状起病，同时癫痫发生率比年轻患者低［44］。参照WHO CNS‐5神经系统肿瘤病理诊断标准，老年胶质瘤患者中除2%伴IDH突变的低级别胶质瘤之外，其余均为胶质母细胞瘤，IDH野生型［45］。 1.老年胶质瘤的术后辅助治疗策略：老年胶质瘤患者目前仍缺乏统一的标准，主要因为患者个体之间体能状况及神经系统外合并症等因素差异较大，并且缺乏高级别循证医学证据等［46］。建议根据每位患者的情况，在多学科诊疗（multidisciplinary team，MDT）模式下根据以下原则选择个体化的治疗方案［47］：对于不伴手术禁忌且术前评估可以实现最大限度安全切除的患者，建议首先最大限度地安全切除。对于手术风险较高的患者，建议立体定向活检明确病理诊断［48］。 专家共识17：临床工作中建议根据每个患者的术后病理分级、KPS评分情况，在MDT模式下选择个体化治疗方案。低级别胶质瘤（WHO 2级）：常规分割放疗或常规分割放疗+辅助化疗［证据级别：Ⅰ级；推荐级别：强］［20，49］。高级别胶质瘤（WHO 3~4级）：KPS≥70分，常规分割/大分割同步放化+辅助化疗［证据级别：Ⅰ级；推荐级别：强］［50］或常规分割/大分割同步放化+辅助化疗+电场治疗［证据级别：Ⅲ~Ⅳ级；推荐级别：中等］［51］。KPS<70分，常规分割/大分割放疗、替莫唑胺单药化疗或替莫唑胺+贝伐珠单抗［证据级别：Ⅲ~Ⅳ级；推荐级别：中等］［52-54］或支持治疗/姑息对症处理［证据级别：Ⅲ~Ⅳ级；推荐级别：中等］［55］。 2.老年胶质瘤的放疗时机、放疗剂量及分割模式选择：老年胶质瘤患者的放疗策略，包括治疗时机、剂量及分割模式的选择，需综合考虑患者的整体状况和疾病特点。需要辅助放疗的老年胶质瘤患者，建议术后2~6周内启动放疗。手术切除不完全或病情快速进展的患者，应考虑伤口愈合情况，并可能需要提前开始放疗［56］。 分割模式和放疗剂量选择方面，近年来，大分割短程放疗已逐渐成为老年或身体状态较差（KPS<60分）的3~4级胶质瘤患者的主流治疗选择［57］。该治疗模式在联合替莫唑胺同步化疗后，能够带来更好的疗效［58］。低级别胶质瘤，常规分割放疗45~54 Gy分25~30次［58］；高级别胶质瘤，采用大分割短程放疗40 Gy分15次［36-37］、52.5 Gy分15次［58］、34 Gy分10次［21］、25 Gy分5次［57］。 专家共识18：建议术后2~6周开始放疗，对于手术切除程度不佳或疾病进展迅速的患者可考虑伤口愈合后尽早开始放疗［证据级别：Ⅲ~Ⅳ级；推荐级别：强］。低级别胶质瘤，常规分割放疗45~54 Gy分25~30次［证据级别：Ⅰ~Ⅱ级；推荐级别：强］。高级别胶质瘤，大分割短程放疗40 Gy分15次、34 Gy分10次、25 Gy分5次［证据级别：Ⅰ~Ⅱ级；推荐级别：强］。 3. MGMT启动子甲基化对于在老年GBM患者的指导意义：根据NOA‐08研究的结果，MGMT启动子甲基化状态可作为评估患者预后的潜在生物标志物［48］。MGMT启动子甲基化状态可作为预测替莫唑胺治疗效果的一种生物标志物［50，59-60］。对于MGMT启动子甲基化的老年患者，推荐考虑使用替莫唑胺单药治疗或联合其他治疗手段，以期获得更佳的治疗效果。对于MGMT启动子未甲基化的患者，单纯放疗可能是更安全且有效的治疗选择。 专家共识19：临床工作中MGMT启动子甲基化状态可作为老年GBM患者选择辅助治疗方案的重要参考指标。KPS≥70分的高级别老年胶质瘤患者，无论是否伴有MGMT启动子甲基化，均推荐在放疗的基础上联合替莫唑胺进行同步及序贯化疗［证据级别：Ⅰ级；推荐级别：强］。KPS<70分的高级别老年胶质瘤患者，如果伴MGMT启动子甲基化，建议综合评估化疗风险后决定是否采用替莫唑胺化疗［证据级别：Ⅲ~Ⅳ级；推荐级别：强］；不伴甲基化的患者，建议单纯常规或大分割放疗［证据级别：Ⅰ级；推荐级别：强］。 4.老年胶质瘤患者放疗的靶区勾画特点：目前尚缺乏专门针对老年胶质瘤患者靶区勾画的高级别循证医学临床研究。因此，现阶段老年患者主要参照相应成人胶质瘤靶区勾画原则进行靶区勾画［16，61-63］。 专家共识20：老年患者主要参照相应成人胶质瘤靶区勾画原则进行靶区勾画［证据级别：Ⅲ~Ⅳ级；推荐级别：强］。 五、复发胶质瘤 局部复发是胶质瘤主要的失败模式。病理结果是重要的诊断依据，无法获得病理结果者需根据临床表现、影像学及其动态变化，结合神经肿瘤疗效评估标准（response assessment in neuro‐oncology，RANO）2.0标准判断［64-65］。胶质瘤复发须与假性进展、放射性坏死鉴别。准确诊断胶质瘤复发是后续治疗的基础。 1.复发胶质瘤的治疗原则：复发胶质瘤的治疗应充分考虑再次手术的可行性。再次手术可减少肿瘤负荷并获得病理，有利于后续的治疗选择。复发低级别胶质瘤，既往未行放疗者，可按初治高危低级别胶质瘤治疗；既往已行放疗者，应充分平衡预期疗效与风险，考虑是否行再程放疗。复发高级别胶质瘤，需根据患者年龄、神经功能状态、KPS、复发模式、既往治疗、疗效及不良反应、与初次放疗间隔时间、初次放疗剂量等因素选择治疗方案，常用治疗选择包括：参与临床试验、再次手术、再程放疗、药物治疗、肿瘤电场治疗及对症支持治疗等。 专家共识21：目前尚无复发胶质瘤的标准治疗方案，建议采用MDT诊疗模式，综合考虑个体化因素合理制订治疗策略［证据级别：Ⅱ~Ⅳ级；推荐级别：强］。 2.复发胶质瘤的再程放疗原则：再程放疗前应充分评估患者获益和风险。部分经选择患者可从再程放疗中获益。有学者认为再程放疗更适用于年龄<70岁、KPS>60分、无进展生存（progression free survival，PFS）期>1年、认知功能受损较轻、无其他有效治疗、复发肿瘤位于原照射靶区外、复发病灶体积较小、疾病进展较缓慢、地塞米松用量<4 mg/d的患者［66］。再程放疗应尽可能降低正常脑组织放射损伤风险，推荐采用图像引导放疗、立体定向放射治疗（stereotactic radiotherapy，SRT）、立体定向放射外科（stereotactic radiosurgery，SRS）、质子重离子放疗等技术。 专家共识22：复发胶质瘤须充分平衡再程放疗的获益和风险；再程放疗推荐采用精确放疗技术［证据级别：Ⅲ~Ⅳ级；推荐级别：强］。 3.复发胶质瘤的再程放疗技术、靶区和剂量：较小病灶的再程放疗，既往研究多采用SRS或SRT；较大病灶常选择常规分割放疗。再程放疗的靶区勾画尚无标准，功能影像可能有助于靶区勾画［66-67］。GTV范围应包括T1增强像异常强化区域，多数研究中CTV范围同GTV；部分研究将T2/FLAIR序列像异常信号区域也纳入CTV。二次术后再程放疗，CTV一般包含手术残腔。PTV外放控制在3~5 mm内。 不同再程放疗技术所致脑坏死发生率明显上升的2 Gy等效剂量（equivalent dose in 2 Gy，EQD2）累积剂量阈值分别为100 Gy（常规分割放疗）、105 Gy（SRT）和135 Gy（SRS）［68］。Scoccianti等［69］综合文献建议：小体积肿瘤（≤12.5 ml）采用SRS（单次12~15 Gy），EQD2<65 Gy；中体积肿瘤（12.5~35 ml）采用SRT（25 Gy分5次），EQD2<50 Gy；大体积肿瘤（35~50 ml）采用常规分割放疗（36 Gy分20次），EQD2<36 Gy。 专家共识23：复发胶质瘤的再程放疗技术、靶区和剂量需充分平衡预期获益与风险。体积较小病灶再程放疗可选择SRS或SRT，较大者常选择常规分割放疗［证据级别：Ⅳ~Ⅴ级；推荐级别：强］。 4.复发胶质瘤再程放疗新技术的应用：质子和重离子射线的布拉格峰效应有利于降低正常脑组织损伤。重离子射线较光子射线具有更强的肿瘤杀伤生物学效应，如碳离子照射不同胶质瘤细胞的相对生物效应为2.10~3.44。复发胶质瘤质子再程放疗耐受性较好［70］。多中心研究提示复发GBM质子再程放疗疗效与光子相当［中位总生存（overall survival，OS）期14.2个月，中位PFS期13.9个月］，不良反应发生率低［71］。目前关于碳离子治疗复发胶质瘤的临床研究（ChiCTR1800017918）正在进行中。硼中子俘获治疗（boron neutron capture therapy，BNCT）是放射与药物相结合的靶向肿瘤细胞的放疗。多中心Ⅱ期研究显示，BNCT较历史对照组延长复发GBM的中位OS期（18.7比10.5个月），主要不良反应是放射性脑水肿［72］。 专家共识24：初步临床结果显示，质子放疗可减轻复发胶质瘤再程放疗的不良反应［证据级别：Ⅳ级；推荐级别：中等］，BNCT可能有助于延长复发胶质瘤生存期［证据级别：Ⅳ级；推荐级别：中等］。 5.儿童弥漫性内生型脑桥胶质瘤（pediatric diffuse intrinsic pontine glioma，DIPG）再程放疗建议：DIPG复发后缺乏有效治疗方案，再程放疗得到重视。回顾性研究显示，复发DIPG再程放疗（总剂量21.6~36 Gy）中位OS优于历史对照未再程放疗，可延长DIPG复发后生存期［73-74］。 专家共识25：再程放疗是儿童复发DIPG重要的姑息性治疗方案，有助于缓解症状和延长生存期［证据级别：Ⅲ~Ⅳ级；推荐级别：中等］，再程放疗的剂量和照射靶区需个体化考虑。 六、室管膜瘤 室管膜瘤是一种胶质细胞肿瘤，起源于室管膜细胞，即脑和脊髓中的一种放射状胶质细胞，最常见于小脑附近的第四脑室或脊髓内，极少发生在中枢神经系统之外。室管膜瘤占所有中枢神经系统肿瘤的不到10%，在儿童和年轻人中发病率更高，占脊髓肿瘤的40%~60%，按照发病部位分为幕上室管膜瘤、幕下室管膜瘤和脊髓室管膜瘤。根据WHO中枢神经系统病理分型，室管膜瘤分为典型室管膜瘤（WHO 2级）、间变性室管膜瘤（WHO 3级）、RELA融合基因阳性室管膜瘤（WHO 2级或3级）、室管膜瘤下室管膜瘤（WHO 1级）、黏液乳头状室管膜瘤（WHO 1级）［75］。 1.室管膜瘤的主要预后因素：室管膜瘤预后因素包括临床因素及分子病理学因素。临床因素包括是否达到肿瘤完整切除、肿瘤分级、KPS、肿瘤位置及术后辅助放疗情况等。病理分级为3级（间变性）、肿瘤位于幕上、肿瘤部分切除（subtotal resection，STR）都是不良预后因素［75-78］。与室管膜瘤预后相关的分子标志物包括ZFTA融合、YAP1融合、H3 K27 me3状态、MYCN扩增状态等［79-81］。 专家共识26：室管膜瘤预后临床因素包括肿瘤是否完整切除、肿瘤分级、KPS、肿瘤位置及术后辅助放疗情况等。分子标志物包括ZFTA融合、YAP1融合、组蛋白H3第27位赖氨酸三甲基化（H3K27 me3）状态、MYCN扩增状态。推荐在初诊时完善相应的临床、病理及分子病理学资料。［证据级别：Ⅲ~Ⅳ级；推荐级别：强］。 2.颅内室管膜瘤的放疗适应证及剂量推荐：WHO 3级间变性室管膜瘤无论是否手术全切，均需行59.4~60 Gy（1.8~2.0 Gy/次）的术后放疗［82］。成人WHO 1级、2级室管膜瘤未能手术全切者，需行术后放疗。对于手术完全切除的成人WHO 2级室管膜瘤是否行术后放疗仍有争议［82-83］。如无禁忌，有高危因素的成人WHO 2级室管膜瘤患者（肿瘤位于颅后窝，黏液乳头状室管膜瘤伴有包膜破坏等），完整切除术后也建议接受54 Gy（1.8~2.0 Gy/次）的术后放疗。儿童WHO 2级、3级室管膜瘤需行术后放疗［78，82，84］，18月龄以上推荐术后放疗剂量为59.4 Gy（1.8 Gy/次），12~18月龄患儿建议术后放疗剂量为54 Gy（1.6~1.8 Gy/次）。有条件的患儿可考虑质子治疗［85］。12月龄以下患儿可考虑仅行化疗［86］。若合并脑脊液或脊髓播散，建议全脑全脊髓照射36 Gy（1.8 Gy/次）后，局部病灶加量至45~54 Gy（1.8~2.0 Gy/次）。 术后放疗靶区需参考术前、术后的影像资料。GTV指术后残留肿瘤及手术残腔，同时参考手术前、后MRI图像判断肿瘤是否有残留及瘤床范围。GTV外扩1 cm形成CTV，需要针对骨性结构及小脑幕进行修正。CTV通常应包括整个瘤床区，剂量通常为54~59.4 Gy，若采用59.4 Gy剂量，CTV在枕骨大孔下方区域可适当减少以保护颈段脊髓。CTV均匀外扩3~5 mm形成PTV，在采用图像引导调强放疗的前提下可采用3 mm的外扩边界。 专家共识27：WHO 3级间变性室管膜瘤无论是否手术全切，均需行术后放疗［证据级别：Ⅱ~Ⅲ级；推荐级别：强］。有高危因素的成人WHO 2级室管膜瘤患者（肿瘤位于颅后窝，黏液乳头状室管膜瘤伴有包膜破坏等），肿瘤完整切除术后建议接受辅助放疗［证据级别：Ⅲ~Ⅳ级；推荐级别：强］。儿童WHO 2级、3级室管膜瘤需行术后放疗，12月龄以下患儿可考虑仅行化疗［证据级别：Ⅳ级；推荐级别：中等］。颅内室管膜瘤术后放疗靶区包括残留肿瘤及瘤床区，术后放疗剂量54~59.4 Gy，具体根据年龄、肿瘤分级及手术切除程度而定。［证据级别：Ⅲ~Ⅳ级；推荐级别：强］。有条件的患儿可考虑质子治疗［证据级别：Ⅳ~Ⅴ级；推荐级别：中等］。 3.脊髓室管膜瘤的治疗推荐和放疗策略：脊髓室管膜瘤在成人中比在儿童中更常见，包括WHO 1级室管膜下瘤，WHO 2、3级（间变性）室管膜瘤。手术是脊髓室管膜瘤的重要治疗手段。对于WHO 2、3级脊髓室管膜瘤患者，STR术后辅助放疗显著延长患者PFS期［87］。原发于脊髓的成人室管膜瘤（WHO 2级）手术全切后不需要补充放疗，未完全切除者建议接受45~54 Gy（1.8 Gy/次）术后辅助放疗。原发于脊髓黏液乳头型室管膜瘤被归类入WHO 2级。未完全切除者建议接受50 Gy以上（1.8~2.0 Gy/次）的术后放疗［88-91］。WHO 3级（间变性）室管膜瘤无论手术切除状况如何，均建议接受45~54 Gy（1.8~2.0 Gy/次）术后放疗。脊髓圆锥下的肿瘤，最高可局部加量至60 Gy（1.8~2.0 Gy/次）［87］。儿童WHO 2、3级脊髓室管膜瘤STR术后接受辅助放疗也可获益［88，91］。 专家共识28：原发于脊髓的室管膜瘤首选手术完全切除［证据级别：Ⅲ级；推荐级别：强］。WHO 2、3级室管膜瘤STR术后，以及WHO 3级脊髓室管膜瘤术后，推荐接受45~54 Gy（1.8 Gy/次）辅助放疗［证据级别：Ⅲ~Ⅳ级；推荐级别：强］。脊髓黏液乳头型室管膜瘤未完整切除者，术后推荐50 Gy以上的辅助放疗［证据级别：Ⅲ~Ⅳ级；推荐级别：强］。 七、放射性脑损伤 放射性脑损伤发生率为3%~24%［92-93］。从广义上来说，放射性脑损伤是放疗后神经细胞和颅内血管受损后出现的一系列病理生理改变，可有影像学可见的脑部病灶，依据发生的时间和临床表现，分为3种类型：急性（放疗中或放疗后6周内）、亚急性（放疗后6周~6个月）和晚期（放疗后数月至数年）。恶性胶质瘤在常规放疗后生存期超过1年的患者中，放射性脑损伤的发病率为10%~15%［94-95］。 1.放射性脑损伤的危险因素。①治疗相关因素：放疗总剂量、分次剂量、照射体积、同步化疗、辅助化疗、再程放疗等增加放射性脑损伤的发生［5，95］。②非治疗相关因素：如糖尿病、高血压、高血脂、高龄及吸烟等，可使放射性脑损伤的发生率增加［45，96］。 专家共识29：减轻正常脑组织的放疗剂量是降低放射性脑损伤发生的关键［证据级别Ⅱ~Ⅲ级；推荐级别：强］，非剂量相关因素也可能与放射性脑损伤发生相关［证据级别Ⅲ~Ⅳ级；推荐级别：中等］。 2.放射性脑损伤的预防策略：有条件的单位首选调强放疗，尽量减少正常脑组织受照射的剂量及体积［97］。此外，质子重离子治疗的应用提高了肿瘤的治疗效果，但放射性脑损伤的发生需要更大样本的评估和随访。 随着放疗剂量的增加，放射性脑损伤的发生明显增加，脑组织在>60 Gy剂量照射后，脑损伤的发生增加。基于对放疗时正常组织可耐受的剂量体积限量的分析，形成三维放疗的推荐意见：全脑Dmax<60 Gy，V12 Gy<10%；颞叶Dmax<60 Gy，V65 Gy<1%；脑干Dmax<54 Gy，V65 Gy<3 ml。基于调强放疗时代的研究数据，预防放射性颞叶损伤的剂量限制建议：Dmax<68 Gy，D0.5 cm3<69 Gy，V45 Gy>15.1 cm3， D2 cm3<60.3 Gy［98-101］。预防放射性脑干损伤的剂量限制建议：Dmax<67.4 Gy， D1%<60.13 Gy， D0.1 cm3<60.75 Gy，D1 cm3<54.58 Gy［102-104］。有研究证实，有效控制患者糖尿病、高血压等基础疾病，可在一定程度上降低放射性脑损伤的发生［93］。 专家共识30：精确放疗技术的选择和糖尿病、高血压等基础疾病的控制可降低放射性脑损伤的发生，改善患者的生活质量。建议尽量减少正常脑组织接受>60 Gy剂量照射体积（即减少V60 Gy）。颞叶D2 cm3<60.3 Gy；脑干Dmax<67.4 Gy，D1 cm3<54.58 Gy［证据级别：Ⅲ~Ⅳ级；推荐级别：强］。 3.放射性脑损伤的治疗策略：推荐确诊后3个月内启动早期治疗。急性和亚急性损伤短暂可逆，建议予糖皮质激素治疗，并密切随访脑损伤的后续转归；急性期轻症患者可予观察。对于晚期放射性脑损伤，贝伐珠单抗的应用可以减轻MRI上脑损伤的强化病灶，减少脑水肿的发生，改善临床症状［105-106］。推荐新确诊的晚期放射性脑损伤患者行贝伐珠单抗分子靶向治疗，部分患者也可考虑用小分子抗血管生成药物如阿帕替尼［107］。放射性脑损伤患者出现病情急速进展，且影像学证实放射性脑损伤病灶存在急性占位效应时，推荐短期应用糖皮质激素和脱水治疗。 高压氧、神经营养（神经节苷脂、注射用鼠神经生长因子、维生素B12）、脑保护治疗（如胞磷胆碱）和自由基清除剂（如艾地苯醌、超氧化物歧化酶、维生素E）治疗可延缓脑损伤的进程和降低其严重程度等。经积极内科保守治疗无效、囊性变或者脑水肿等占位效应明显、颅内高压症状或者相应神经功能障碍进行性加重的患者，推荐行外科手术［108］。 专家共识31：放射性脑损伤宜早期启动治疗［证据级别：Ⅱ~Ⅲ级；推荐级别：强］。治疗方案上优选贝伐珠单抗分子靶向治疗，其他内科治疗手段是放射性脑损伤治疗的重要补充，外科手术是重要的非药物治疗手段，建议开展多学科联合治疗［证据级别：Ⅲ~Ⅳ级；推荐级别：强］。 1. Ostrom QT, Price M, Neff C, et al. 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DOI: 10.47363/JNRRR/2023(5)181. 共识专家组组长 郎锦义 四川省肿瘤医院 二级教授/ 一级主任医师，医学博士，博士/博士后导师 四川省人民政府参事（2021—2024） 四川省肿瘤医院原院长/书记，放疗中心首席专家/指导主任，罕见病/头颈肿瘤MDT专家组长，肿瘤精准放疗四川省重点实验室主任，放射肿瘤学/肿瘤学/头颈肿瘤综合治疗（国家临床重点专科 ）学科带头人 电子科技大学肿瘤医工研究院/成都中医药大学肿瘤中西医结合研究院院长 国家卫生计生突出贡献中青年专家，国务院特殊津贴专家，全国卫生计生系统先进工作者，全国优秀科技工作者，四川省学术技术带头人/天府名医，荣获四川省第二届杰出贡献人才奖 中华医学会放射肿瘤治疗学分会第八届主委，中华医学会肿瘤学分会常务委员，中国抗癌协会鼻咽癌专委会第五届主委，泛珠江放射肿瘤学协作组(PPRO-RTOG) 主席，西部放射治疗协会(CSWOG-RTOG)/四川省抗癌协会理事长，国家科技部“十三五”国家重点研发计划首席专家 李   光 中国医科大学附属第一医院 中国医科大学附属第一医院放疗科主任，中国医科大学肿瘤所放射生物学研究室主任，辽宁省放射治疗临床医学研究中心主任 中国医师协会放射肿瘤治疗医师分会副会长，中华医学会放射肿瘤治疗学分会常委，中国抗癌协会肿瘤放射治疗专业委员会常委，国家肿瘤质控中心放射治疗质控委员会委员，辽宁省医学会第六、七届放射肿瘤治疗学分会主委，辽宁省医师协会放射肿瘤治疗医师分会会长，《中华放射肿瘤学杂志》等杂志编委 共识执笔人 （以姓氏汉语拼音为序） 冯   梅 四川省第三人民医院 主任医师，二级教授，博士，博士生导师 四川省第三人民医院党委书记，放射肿瘤学四川省重点实验室副主任（四川省肿瘤医院特聘教授） 美国威斯康辛医学院访问学者，意大利CNAO中心高级访问学者 国家医学高层次人才首届优秀青年医师，四川省学术技术带头人，四川省卫生计生委学术技术带头人，海外高层次人才 中华医学会放射肿瘤治疗学分会常委，中国临床肿瘤学会鼻咽癌专委会副主委，四川省医师协会副会长，四川省医学会肿瘤专委会主委，四川省医学会放射肿瘤专委会候任主委，四川省抗癌协会鼻咽癌专委会候任主委 主持和参与多项国家级及省级科研课题，获四川省科技进步二等奖、四川省医学科技奖一等奖 发表论著50余篇，参编多部肿瘤专业著作 姜   炜 天津市第一中心医院 天津市第一中心医院肿瘤放射治疗科主任，天津市高压氧质量控制中心（2015—2023）主任 中国医师协会脑胶质瘤专业委员会常委，中华医学会高压氧医学分会副主委，天津市医学会高压氧医学分会主委，天津市医学会放射肿瘤学分会第三届委员会副主委，天津市医疗健康学会放射治疗专委会主委，天津市医学会理事，天津市抗癌协会神经肿瘤专业委员会常委，美国放射肿瘤学会（ASTRO）会员，美国临床肿瘤学会（ASCO）会员，中国罕见病联盟脑胶质瘤分会委员，中国脑胶质瘤协作组（CGCG）成员 《国际放射医学核医学杂志》编委、《中华航海医学与高气压医学杂志》编委 乔   俏 中国医科大学附属第一医院 中国医科大学附属第一医院放射治疗科副主任，教授，博导 兴辽英才青年医学名家，中华预防医学会放射卫生专业委员会委员，中华医学会放射肿瘤治疗学分会青年学组副组长，中国抗癌协会胶质瘤专委会常务委员，中国临床肿瘤学会鼻咽癌专委会常务委员，中国抗癌协会放射肿瘤治疗学分会委员，中国抗癌协会鼻咽癌专委会委员，辽宁省医学会放射肿瘤治疗学分会候任主委，辽宁省抗癌协会放射肿瘤治疗专业委员会副主委 《中华肿瘤防治杂志》青年编委，《辽宁医学杂志》编委 邱晓光 北京天坛医院 主任医师，教授，博导 首都医科大学附属北京天坛医院放疗科主任，首都医科大学首都医科大学脑胶质瘤临床诊疗与研究中心副主任 中国医师协会脑胶质瘤专业委员会副主委，中国抗癌协会神经肿瘤专业委员会副主委，中国临床肿瘤学会（CSCO）神经肿瘤专家委员会副主委 石   梅 空军军医大学西京医院 西京医院放射治疗科教授、主任医师，空军军医大学博士研究生导师，美国斯坦福大学访问学者 中华医学会放射肿瘤治疗学分会第六至十届常委，中国临床肿瘤学会放射肿瘤治疗专业委员会第一、二届副主委，全军肿瘤放射治疗专业委员会第八、九届主委，西部肿瘤放射治疗协会副理事长，陕西省放射肿瘤治疗专业委员会前任主委 汪   洋 复旦大学附属附属华山医院 复旦大学附属华山医院放疗中心副主任，党支部书记；射波刀中心主任医师，主任医师，医学博士 中华医学会放射肿瘤治疗学分会中枢神经肿瘤筹备学组副组长，中国抗癌协会脑胶质瘤专业委员会副主委，中国抗癌协会小儿神经肿瘤专委会副主委，中国医师协会胶质瘤放疗专委会副主委，中国生物医学工程学会肿瘤电场治疗专委会主委，中国医师协会放射肿瘤学专委会中枢神经系统肿瘤学组副组长，中国研究型医院学会放射肿瘤学专委会神经肿瘤学组副组长，中国临床肿瘤学会神经肿瘤专家委员会常委，中国抗癌协会神经肿瘤专业委员会常委，中国抗癌协会神经肿瘤病学专委会常委，北京医学基金会脑转移瘤专委会副主委，上海抗癌协会儿童肿瘤专委会常委，上海抗癌协会神经肿瘤专委会常委，上海抗癌协会脑转移瘤专委会常委，国家肿瘤微创治疗产业技术创新战略联盟立体定向放疗专委会常委 获得2006年国家教育部科技进步一等奖（第四完成人）、2016年上海市科技进步一等奖（第四完成人） 共识秘书 黄叶才：四川省肿瘤医院 共识专家组成员 （以姓氏汉语拼音为序） 蔡林波：广东三九脑科医院 陈媛媛：中山大学附属肿瘤医院 范   铭：四川省肿瘤医院 冯   梅：四川省第三人民医院 高   劲：中国科学技术大学附属第一医院 顾   浩：郑州大学第一附属医院 贺   政：中国医科大学附属第一医院 洪金省：福建医科大学附属第一医院 胡   漫：山东省肿瘤医院 胡广原：华中科技大学同济医学院附属同济医院 黄叶才：四川省肿瘤医院 惠周光：中国医学科学院肿瘤医院 姜   炜：天津市第一中心医院 金   风：贵州医科大学附属肿瘤医院 孔   琳：上海质子和重离子医院 郎锦义：四川省肿瘤医院 李   光：中国医科大学附属第一医院 刘   峰：湖南省肿瘤医院 刘彦伟：北京天坛医院 陆雪官：复旦大学附属肿瘤医院 欧   丹：复旦大学附属肿瘤医院 乔   俏：中国医科大学附属第一医院 邱献新：复旦大学附属华山医院 邱晓光：北京天坛医院 石   梅：空军军医大学西京医院 苏   宁：空军军医大学西京医院 汪   洋：复旦大学附属附属华山医院 王   颖：重庆大学附属肿瘤医院 王   政：天津市第一中心医院 王若峥：新疆医科大学附属肿瘤医院 魏启春：浙江大学附属第二医院 吴君心：福建省肿瘤医院 薛晓英：河北医科大学第二医院 阎   英：北部战区总医院 严森祥：浙江大学附属第一医院 杨坤禹：华中科技大学同济医学院附属协和医院 杨治花：宁夏医科大学总医院 阴   骏：四川省第三人民医院 殷   麟：青海大学附属肿瘤医院 张   静：北京天坛医院 张俊平：首都医科大学附属三博脑科医院 周   鹏：四川省肿瘤医院 责编  吕媛媛 审阅  崔敬璐 终审  何海青 -The End- 投稿网址：medpress.yiigle.com 编辑部电话： 010-87788294 邮箱：cjron@cmaph.org 谨防诈骗 任何以“某编辑”名义用个人邮箱 与您联系者均为假冒！ 任何收费相关的疑似假冒行为， 请拨打电话确认！ 点击“阅读原文”，查看全文