Epidemiology of primary tumours of the brain and spinal cord: a regional survey in southern England.

This survey is based upon 894 patients presenting with primary tumours of the brain, spinal cord, and meninges, over a nine year period in the Wessex population of about 1 1/2 million. All patients were 15 years of age or over. Each tumour type is characterized by age, sex, district, social class, and by rural or urban distribution. Standardized morbidity ratios for each tumour type are calculated for each health district. Gliomas are the commonest tumour with an average annual incidence of 3.94 per 100,000; they occur with a lower frequency in large urban areas. Grade 3-4 astrocytomas (glioblastoma multiforme) have a peak annual incidence of 7.53 per 100,000 in the 50-59 years age group and are more common in males. The peak incidence for oligodendrogliomas is also 50-59 years but for grade 1-2 astrocytomas it is 30-39 years. Meningiomas have an average annual incidence of 1.23 per 100,000 with a peak incidence of 2.48 per 100,000 at 60-69 years; they have a female predominance (female 1.76 per 100,000; male of 0.64 per 100,000). Rural districts have a lower incidence of meningiomas than urban areas. There is some variation in the distribution of gliomas, meningiomas, and Schwannomas throughout the Wessex region and there is a suggestion of geographical clustering of ependymomas, acoustic neuromas, and meningiomas. An excess of patients with grade 1-2 astrocytomas and oligodendrogliomas is seen in social classes 1 and 2 and a deficit in classes 4-5; a similar, but less marked, preponderance is seen with meningiomas.     

Estrogen receptors in brain tumors

We examined the cytosolic estrogen receptor (ER) level in tumor tissue from 77 patients: 36 meningiomas, 20 gliomas (12 glioblastomas, 2 cerebellar astrocytomas, 2 ependymomas, and 4 medulloblastomas), 8 neurinomas, 7 pituitary adenomas (2 prolactin-producing adenomas, 1 growth hormone-producing adenoma, and 4 nonfunctioning adenomas), and 6 metastatic brain tumors (1 from breast cancer, 4 from lung cancers, and 1 from colon cancer). Nuclear ER levels were assayed in 11 meningiomas and 2 glioblastomas. ER was determined by the dextran-coated charcoal method and calculated by Scatchard analysis. Cytosolic ER was detected in 100% of the pituitary adenomas, 50% of the meningiomas, 50% of the metastatic brain tumors, 25% of the neurinomas, and 15% of the gliomas. In gliomas, only medulloblastomas had ER activity. Nuclear ER was found in three premenopausal women with meningioma. The dissociation constant of the ER complex was, in each case, less than 10(-9) M. These observations suggest that some brain tumors may be responsive to estrogen via the cellular ER.     

Analysis of the IDH1 codon 132 mutation in brain tumors

A recent study reported on mutations in the active site of the isocitrate dehydrogenase (IDH1) gene in 12% of glioblastomas. All mutations detected resulted in an amino acid exchange in position 132. We analyzed the genomic region spanning wild type R132 of IDH1 by direct sequencing in 685 brain tumors including 41 pilocytic astrocytomas, 12 subependymal giant cell astrocytomas, 7 pleomorphic xanthoastrocytomas, 93 diffuse astrocytomas, 120 adult glioblastomas, 14 pediatric glioblastomas, 105 oligodendrogliomas, 83 oligoastrocytomas, 31 ependymomas, 58 medulloblastomas, 9 supratentorial primitive neuroectodermal tumors, 17 schwannomas, 72 meningiomas and 23 pituitary adenomas. A total of 221 somatic IDH1 mutations were detected and the highest frequencies occurred in diffuse astrocytomas (68%), oligodendrogliomas (69%), oligoastrocytomas (78%) and secondary glioblastomas (88%). Primary glioblastomas and other entities were characterized by a low frequency or absence of mutations in amino acid position 132 of IDH1. The very high frequency of IDH1 mutations in WHO grade II astrocytic and oligodendroglial gliomas suggests a role in early tumor development.     

Cerebral blood volume mapping by MR imaging in the initial evaluation of brain tumors

PURPOSE: To assess the contribution of magnetic resonance (MR) cerebral blood volume (CBV) mapping in the initial evaluation of brain tumors. METHODS: 63 patients presenting a brain tumor underwent dynamic susceptibility-contrast MR imaging before surgery or biopsy: 28 high grade gliomas, 8 low grade gliomas, 2 pilocytic astrocytomas, 4 lymphomas, 12 metastases, 9 meningiomas. The CBV maps were obtained for each patient and the relative CBV (rCBV) in different areas was calculated using the ratio between the CBV in the pathological area (CBVp) and in the contralateral normal tissue(CBVn). The maximum rCBV (rCBVmax) for each tumor was determined and the mean values of rCBVmax in each group of tumors were compared using an unpaired Student t test (p=0.05). RESULTS: The rCBVmax for high grade gliomas (mean +/- SD: 2.6 +/- 1,2) was statistically different from low grade gliomas (0.9 +/- 0.4) (p<0.001), lymphomas (0.7 +/- 0.2) (p=0.002), meningiomas (9.1 +/- 4.4) (p<0.001) and kidney metastases (8.9 +/- 2.1) (p<0.001). The two pilocytic astrocytomas had a much lower rCBVmax than high grade gliomas. No statistically significant difference was found between high grade gliomas and lung metastases (2.4 +/- 0.9) (p=0.72). CONCLUSION: CBV mapping provides additional information on the vascularity of the lesions, which is not available with conventional MR imaging. It might be useful for differentiating certain lesions showing contrast enhancement, mainly high grade gliomas from kidney metastases, meningiomas, lymphomas or pilocytic astrocytomas.     

Neuropeptide Y receptors in primary human brain tumors: overexpression in high-grade tumors

Peptide receptors are often overexpressed in tumors, and they may be targeted in vivo. We evaluated neuropeptide Y (NPY) receptor expression in 131 primary human brain tumors, including gliomas, embryonal tumors, meningiomas, and pituitary adenomas, by in vitro receptor autoradiography using the 125I-labeled NPY receptor ligand peptide YY in competition with NPY receptor subtype-selective analogs. Receptor functionality was investigated in selected cases using [35S]GTPgammaS-binding autoradiography. World Health Organization Grade IV glioblastomas showed a remarkably high expression of the NPY receptor subtype Y2 with respect to both incidence (83%) and density (mean, 4,886 dpm/mg tissue); astrocytomas World Health Organization Grades I to III and oligodendrogliomas also exhibited high Y2 incidences but low Y2 densities. In glioblastomas, Y2 agonists specifically stimulated [35S]GTPgammaS binding, suggesting that tumoral Y2 receptors were functional. Furthermore, nonneoplastic nerve fibers containing NPY peptide were identified in glioblastomas by immunohistochemistry. Medulloblastomas, primitive neuroectodermal tumors of the CNS, and meningiomas expressed Y1 and Y2 receptor subtypes in moderate incidence and density. In conclusion, Y2 receptors in glioblastomas that are activated by NPY originating from intratumoral nerve fibers might mediate functional effects on the tumor cells. Moreover, identification of the high expression of NPY receptors in high-grade gliomas and embryonal brain tumors provides the basis for in vivo targeting.     

Mutations and immunohistochemistry ofp53 and proliferation markers in astrocytic tumors of childhood

Thirty cases of hemispheric astrocytic tumors of childhood, consisting of 11 pilocytic astrocytomas, 2 fibrillary astrocytomas, 9 anaplastic astrocytomas, and 8 glioblastomas, were studied for the presence ofp53 mutations and for immunohistochemical demonstrations ofp53 and proliferation markers PCNA and Ki-67 MIB-1. The study was performed using polymerase chain reaction (PCR)-as-sisted single-strand conformation polymorphism analysis of exons 5–8 and direct sequence analysis of PCR products. For immunohistochemistry, DO1 and PAb 1801 were used. No mutation and no positivity forp53 protein were found in pilocytic astrocytomas. Mutations (at codons 144, 202, and 245) were found in 2 out of 8 glioblastomas and in 1 out of 9 anaplastic astrocytomas, whereas positive staining was found in 11 out of 17 malignant gliomas. Cases with mutations showed the highestp53 labeling index and also PCNA and MIB-1 labeling indices. The negative results in pilocytic astrocytomas are in line with the benign course of these tumors, whereas for malignant gliomas no difference seems to exist in comparison with adult cases.     

Epidemiology of brain tumors: the national survey of intracranial neoplasms

A national survey, based on a probability sample of patients admitted to short-term hospitals in the United States during 1973 to 1974 with a discharge diagnosis of an intracranial neoplasm, was conducted in 157 hospitals. The annual incidence was estimated at 17,000 for primary intracranial neoplasms and 17,400 for secondary intracranial neoplasms--8.2 and 8.3 per 100,000 US population, respectively. Rates of primary intracranial neoplasms increased steadily with advancing age. The age-adjusted rates were higher among men than among women (8.5 versus 7.9 per 100,000). However, although men were more susceptible to gliomas and neuronomas, incidence rates for meningiomas and pituitary adenomas were higher among women.     

Expression of Bax and bcl-2 proteins,regulators of programmed cell death,in human brain tumors

Abstract

Expression of Bcl-2, a programmed cell death (PCD)-suppressing molecule, and Bax, the Bcl-2 related PCDaccelerating protein was investigated in varied human brain tumors. Thirty-six cases ofhuman brain tumors comprising 4 astrocytomas, 3 anaplastic astrocytomas, 4 glioblastomas multiforme, 5 medulloblastomas, 1 ependymoma, 2 choroid plexus papilloma, 1 ganglioglioma, 1 central neurocytoma, 4 meningotheliomatous meningiomas, 3 transitional meningiomas, 4 fibroblastic meningiomas, 3 acoustic neurinomas and. 1 craniopharyngioma were analyzed for the localization of Bax and Bcl-2 proteins. No relationship between the degree of the histological malignancy and the presence of Bax or Bcl-2 proteins was found in varied human brain tumors. However, it is suggested that reduced expression of Bax protein is necessary for the malignant transformation and progression of the brain tumors, since no histologically malignant brain tumors with positive Bax protein were present. Our findings indicate that the expression pattern of Bax and Bcl-2 may reflect histogenetic difference of each type of brain tumors. [Neural Res 1997; 19: 623-628]     

Epidemiology and etiology of gliomas

Gliomas of astrocytic, oligodendroglial and ependymal origin account for more than 70% of all brain tumors. The most frequent (65%) and most malignant histological type is the glioblastoma. Since the introduction of computerized tomography and magnetic resonance imaging, the incidence rates of brain tumors have been rather stable, with a tendency of higher rates in highly developed, industrialized countries. Some reports indicate that Caucasians have higher incidence than black or Asian populations, but to some extent, this may reflect socio-economic differences and under-ascertainment in some regions, rather than a significant difference in genetic susceptibility. With the exception of pilocytic astrocytomas, the prognosis of glioma patients is still poor. Less than 3% of glioblastoma patients are still alive at 5 years after diagnosis, higher age being the most significant predictor of poor outcome. Brain tumors are a component of several inherited tumor syndromes, but the prevalence of these syndromes is very low. Several occupations, environmental carcinogens, and diet (N-nitroso compounds) have been reported to be associated with an elevated glioma risk, but the only environmental factor unequivocally associated with an increased risk of brain tumors, including gliomas, is therapeutic X-irradiation. In particular, children treated with X-irradiation for acute lymphoblastic leukemia show a significantly elevated risk of developing gliomas and primitive neuroectodermal tumor (PNET), often within 10 years after therapy. TP53 mutations are frequent in low-grade gliomas and secondary glioblastomas derived therefrom. Approximately 60% of mutations are located in the hot spot codons 248 and 273, and the majority of these are G:CA:T transitions at CpG sites. TP53 mutations are significantly more frequent in low-grade astrocytomas with promoter methylation of the O⁶-methylguanine-DNA methyltransferase repair gene, suggesting that, in addition to deamination of 5-methylcytosine, exogenous or endogenous alkylation in the O⁶ position of guanine may contribute to the formation of these mutations.     

Normal or non-diagnostic neuroimaging studies prior to the detection of malignant primary brain tumors

We aimed to describe a single institution experience of neuroimaging failure to demonstrate malignant primary brain tumors. We retrospectively reviewed case histories for all newly diagnosed adult patients with malignant primary brain tumors treated at a single institution between 1 July 2006 and 30 June 2008. We specifically looked at patients in whom neuroimaging was normal or non-diagnostic at initial presentation. Among 193 patients with malignant primary brain tumors, there were 102 with World Health Organization (WHO) grade IV gliomas (glioblastoma multiforme, GBM), 54 with anaplastic gliomas, 18 with low grade gliomas, and 19 with primary central nervous system lymphomas (PCNSL). Initial imaging was normal in nine patients and abnormal but non-diagnostic in an additional eight patients with primary brain cancer. Normal or non-diagnostic neuroimaging was not uncommon among patients with GBM. Dramatic, rapid tumor growth is possible. Close interval clinical and radiographic follow-up can be important especially in the management of elderly patients presenting with seizures and non-diagnostic neuroimaging studies.     

Descriptive epidemiology of primary tumors of the brain, cranial nerves and cranial meninges in Los Angeles County

This report presents data on the distribution of 8,612 cases of primary tumors of the brain, cranial nerves and cranial meninges (both benign and malignant) diagnosed among residents of Los Angeles County from 1972 to 1985. Incidence rates of gliomas, meningiomas, nerve sheath tumors and all histologic types combined are presented for specific age, sex and ethnic groups. At all ages, the highest incidence is seen for gliomas among men. Meningioma rates are higher among women than men in every ethnic group. In both sexes, glioma rates are highest among whites, and meningioma rates are highest among blacks. Asians have the lowest rates of both types of tumors. Proportional incidence ratios are elevated among those born in Eastern Europe, Southern Europe and the Middle East and among Jewish residents of Los Angeles County. A clear trend of increasing glioma incidence with increasing social class is seen among males. An analysis among white men aged 25-64 by occupation and industry at the time of diagnosis supports several previously published findings. A glioma excess is evident among workers in the aircraft industry. Workers in the petroleum industry and the rubber and plastics industry have an excess of meningiomas. Occupational groups at excess risk include dentists who have an increased risk of all types of brain tumors and electricians whose excess risk is limited to gliomas.     

人脑肿瘤已糖激酶的活性测定

测定10例良性胶质瘤、18例恶性胶质瘤、12例良性脑膜瘤和1例恶性脑膜瘤的溶解性和总体己糖激酶(Hexokinase,HK)活性,以18例正常脑组织作对照.结果表明:良性与恶性脑瘤的HK活性明显低于正常脑组织(P<0.01).良性脑瘤的总体HK活性明显低于恶性脑瘤(P<0.05),脑膜瘤的HK活性明显低于良性及恶性胶质瘤(P<0.05,P相似文献   

Localization of basic fibroblast growth factor,a mitogen and angiogenic factor,in human brain tumors

Summary Fibroblast growth factor (FGF) is a potent angiogenic factor and a mitogen for a variety of mesoderm-and neuroectoderm-derived cell types (e.g., fibroblasts, endothelial cells, astrocytes, oligodendrocytes). After application of a monospecific polyclonal antiserum, we localized basic FGF on frozen sections of 73 human brain tumors using immunohisto-chemistry. FGF was present in a variable number of tumor cells (16/16 astrocytomas, 5/5 ependymomas, 0/3 benign and 4/7 anaplastic oligodendrogliomas, 11/12 glioblastomas, 11/11 meningiomas, 6/6 neurilemmomas, 0/3 pituitary adenomas, 2/2 choroid plexus papillomas, 0/1 neurocytoma, 2/2 benign fibrous histiocytomas, 2/5 metastatic carcinomas). FGF was detected in vascular cells of 59 tumors and in fibroblasts of connective tissue stroma from all papillomas and metastases. These results tend to indicate FGF involvement in the malignant progression of gliomas due to an autocrine or paracrine action. Histopathological aspects of malignant gliomas (e.g., pseudopalisading or pathological vessels) could be related to FGF activity.     

Expression of Rac3 in human brain tumors.

Rac3 may play an important role in tumor growth but little is known about its expression and mutation in human tumor tissues. We examined the expression of Rac3 using RT-PCR and mutation of the Rac3 gene by DNA sequencing. Overexpression of the Rac3 gene occurred in 19% (5/26) of brain tumors; 3 of 9 (33%) meningiomas, 1 of 11 (9%) astrocytomas and 1 of 6 (17%) pituitary adenomas. Two of the 3 meningiomas with Rac3 overexpression were recurrent meningiomas. The only astrocytoma with Rac3 overexpression was a glioblastoma multiforme. Mutation of the Rac3 gene occurred in 63% (12/19) of brain tumours; 4 of 7 (57.1%) meningiomas, 4 of 5 (80%) pituitary adenomas and 4 of 7 (57.1%) astrocytomas. Except in one astrocytoma, the other four tumors with Rac3 overexpression (3 meningiomas and one pituitary adenoma) did not have Rac3 mutations. Our data is the first report of the frequency of Rac3 overexpression and mutation in human brain tumors. Overexpression may be associated with aggressive tumor behavior. The relationship between Rac3 expression and mutation requires further investigation.     

Frequent ATRX mutations and loss of expression in adult diffuse astrocytic tumors carrying IDH1/IDH2 and TP53 mutations

Gliomas are the most common primary brain tumors in children and adults. We recently identified frequent alterations in chromatin remodelling pathways including recurrent mutations in H3F3A and mutations in ATRX (α-thalassemia/mental-retardation-syndrome-X-linked) in pediatric and young adult glioblastoma (GBM, WHO grade IV astrocytoma). H3F3A mutations were specific to pediatric high-grade gliomas and identified in only 3.4?% of adult GBM. Using sequencing and/or immunohistochemical analyses, we investigated ATRX alterations (mutation/loss of expression) and their association with TP53 and IDH1 or IDH2 mutations in 140 adult WHO grade II, III and IV gliomas, 17 pediatric WHO grade II and III astrocytomas and 34 pilocytic astrocytomas. In adults, ATRX aberrations were detected in 33?% of grade II and 46?% of grade III gliomas, as well as in 80?% of secondary and 7?% of primary GBMs. They were absent in the 17 grade II and III astrocytomas in children, and the 34 pilocytic astrocytomas. ATRX alterations closely overlapped with mutations in IDH1/2 (p?<?0.0001) and TP53 (p?<?0.0001) in samples across all WHO grades. They were prevalent in astrocytomas and oligoastrocytomas, but were absent in oligodendrogliomas (p?<?0.0001). No significant association of ATRX mutation/loss of expression and alternative lengthening of telomeres was identified in our cohort. In summary, our data show that ATRX alterations are frequent in adult diffuse gliomas and are specific to astrocytic tumors carrying IDH1/2 and TP53 mutations. Combined alteration of these genes may contribute to drive the neoplastic growth in a major subset of diffuse astrocytomas in adults.     

Frequency of seizures in patients with newly diagnosed brain tumors: a retrospective review

Brain tumors may lead to symptomatic epilepsy. A retrospective analysis was undertaken to evaluate the frequency of seizure as the presenting symptom leading to brain tumor diagnosis in adults. One hundred and forty-seven consecutive patients with newly diagnosed brain tumors were analyzed regarding the frequency of seizures as the initial presenting symptoms and those subsequently developing seizures. One hundred twelve patients had primary central nervous system tumors (CNS) and 35 had metastatic lesions. Statistical evaluation was carried out using the Chi-square test with p values of <0.05 considered to be statistically significant. Astrocytomas and meningiomas were the most common primary CNS tumors in this study. Of these, oligodendrogliomas and grade 2 astrocytomas were significantly more likely to present with seizures (p<0.001). Seizures were a frequent presenting symptom, occurring in over 38% of those with primary brain neoplasms and 20% of those with cerebral metastases. Primary location of tumor also correlated amongst primary CNS tumors and was associated with a trend in seizure risk: parietal (80%); temporal (74%); frontal (62%); and occipital (0%) (p<0.5). The findings highlight the importance of obtaining appropriate evaluation for underlying malignancy in adults with new-onset seizures as well as provide more information to the patient for prognosis and counseling.     

Positron emission tomography and perfusion weighted imaging in the detection of brain tumors recurrence: A meta-analysis

Objectives:To assess and compare the diagnostic accuracy, sensitivity and specificity of perfusion-weighted imaging (PWI) and positron emission tomography (PET) in distinguishing between treatment-related changes and tumor recurrence.Methods:We carried out a systematic review of PubMed, Embase, Web of Science, the Cochrane Library, and CINAHL databases from database inception until August 2021 for pertinent articles. Particular inclusion and exclusion criteria were applied to select the eligible studies. The Quality Assessment of Diagnostic Accuracy tool was used to assess the risk of bias and methodological quality of the eligible studies. From the included studies, the rate ratio (RR) of pooled accuracy, sensitivity, specificity and their corresponding confidence intervals (CIs) were estimated for both PWI and PET.Results:The systematic review and meta-analysis comprised 14 research studies, with a total of 542 patients. Although PET revealed a moderately higher accuracy and sensitivity when compared to PWI (RR: 0.94, 95% CI 0.86-1.02 and RR: 0.95 95% CI 0.85-1.06, respectively), the difference was not statistically significant (p>0.05). Similarly, while PWI demonstrated a moderately higher specificity when compared to PET (RR:1.10, 95% CI 0.98-1.23) but. However, no statistically significant difference between the 2 modalities was detected (p>0.05). Interestingly, we revealed that 18F-FET-PET was significantly more efficient than PWI in terms of accuracy (RR: 0.82, 95% CI 0.72-0.93) and sensitivity (RR: 0.72, 95% CI 0.62-0.83) (p>0.05).Conclusion:Both PET and PWI yielded good diagnostic performance in distinguishing treatment-related changes from tumor recurrence, and neither modality seemed to be superior. PROSPERO ID: CRD42021288160

Brain tumors occur when abnormal and uncontrolled cell division appears in the brain. Nowadays, non-cancerous (benign) tumors and cancerous (malignant) tumors are the 2 groups of tumors recognized worldwide. ¹ Brain tumors can also be categorized as primary tumors, starting in the brain, and secondary tumors, also known as brain metastasis tumors, which most frequently have spread to the brain from primary tumors in other organs. ² The Central Brain Tumor Registry of the United States reported that primary brain tumors account for around 2% of all cancers, while metastases occur approximately in 10-20% of people with cancerous tumors and are 10 times more frequent than primary brain tumors. ³ The annual frequency of primary brain tumors can reach 19 cases per 100,000 people. The incidence is 3 cases per 100,000 people at less than 4 years of age. The prevalence decreases between 15 and 24 years of age and then increases regularly to a peak of 19 cases per 100,000 people between 65 and 79 years of age. ⁴ The World Health Organization (WHO) classifies brain tumors into different types, and each of them may be classified into diverse grades, including neuroepithelial and non-neuroepithelial tumors. ⁵ The majority of primary tumors of the brain in adulthood are gliomas, with a prevalence of 45% among all brain tumors and 90% of primary brain tumors in elderly patients. ⁶ Gliomas are classified into 4 grades (I, II, III, and IV) based on the WHO classification. Low-grade gliomas include grades I and II, while high-grade gliomas include grades III and IV. The grade IV glioma is also known as glioblastoma multiforme. ⁷ Many studies have demonstrated a higher prevalence of brain cancer in developed countries. Furthermore, the prevalence of brain cancer depends on many factors, such as age, gender, and race. Meningioma and glioblastoma are mostly detected at approximately 65 years of age. However, the other types of brain tumors, such as pilocytic astrocytoma, germ cell, and pineal region tumors are detected at an early age. ⁸ The prevalence of brain tumors is moderately greater in men as compared to that in women, but meningeal tumors seem to be 2 times as frequent among women. Regarding gliomas, their incidence is higher in men (7.7/100,000) as compared to that in women (5.61/100,000). ⁹ The prevalence of primary brain tumors is higher in Asian, white, and black populations with regard to American and Indian Native race groups. Brain cancers have a 5-year survival rate of approximately 33%. In general, high performance status, young age, and low histopathological grade are positive prognostic characteristics for primary brain tumors. ¹⁰ Therapeutic options are dependent upon the kind of brain tumor, as well as its location and size. Treatments for brain tumors include surgical resection of solitary lesions, stereotactic brain surgery and radiation with or without chemotherapy. ¹¹ Treatment-induced necrosis is a frequent treatment-related condition occurring during the treatment of gliomas, which is usually detected 3 to 12 months post-treatment. ¹² Indeed, after high radiation doses, patients usually develop constant or continuous enhancement detected with recurrent tumors (pseudoprogression), radionecrosis and inflammation. These conditions mimic tumor progression or recurrence after remission. ¹³ Pseudoprogression appears as an increase in the size of the primary tumor or the appearance of a new lesion, thus resembling early progressive tumors. ¹⁴ It is evident that misdiagnosis of recurrent brain tumors changes the treatment strategy, which leads potentially to unnecessary repeat surgery or non-effective second-line treatment. ¹⁵ Histopathologic technique is the current gold standard to confirm the diagnosis of recurrent brain tumors, but biopsy is dangerous, with many adverse impacts (such as inflammation and hemorrhage). ¹⁶ Hence, differentiating tumor recurrence from other types of treatment-related changes is challenging. Consequently, valid, effective and non-invasive imaging techniques are required to improve the post-treatment surveillance of patients.Due to the disadvantages of histopathology, diverse neuroimaging techniques have been developed for the distinction of recurrent tumors from treatment-related changes. Magnetic resonance imaging (MRI) modalities, such as diffusion-weighted imaging (DWI) and perfusion-weighted imaging (PWI), and nuclear modalities, including positron emission tomography (PET), which can be associated with computed tomography (PET-CT) or magnetic resonance imaging (PET-MRI), are usually used for this purpose. ¹⁴ Nowadays, MRI is the standard neuroimaging modality for follow-up after treatment. ¹⁵ Standard MRI is based on the magnetization properties of atomic nuclei. The most common MRI sequences are T1-weighted and T2-weighted scans. ¹⁷ Even with the perfect ability to diagnosis brain tumors, the conventional MRI presents some limitations regarding the distinction between tumor recurrence and non-specific changes, which is especially relevant after therapy.To surmount these deficiencies, PET based on radioactive amino acids and PWI are suggested as alternative modalities that may supply supplementary pathophysiological evidence to standard MRI. Perfusion-weighted imaging is one of the most broadly used clinical techniques. It is accurate, reliable, and safe, as well as radiation-free. There are 3 types of PWI-dynamic magnetic contrast-enhanced, dynamic contrast-enhanced, and arterial spin labeling. ¹⁸ In recent years, PET using radioactive amino acids has been considered a very pertinent modality and is described as clinically helpful for managing patients with brain tumors. ¹⁹ Different types of radioactively labeled tracers (such as, 11C-MET, ¹⁸ F-FDG [fluorine18-fluorodeoxyglucose], ¹⁸ F-FLT [fluorothymidine], or ¹⁸ F-FET [fluorine-fluoro-ethyl-tyrosine]) are injected with PET to improve the detection of recurrent brain tumors. ²⁰ The first radiopharmaceutical tracer to be developed was ¹¹ C-methyl-L-methionine (MET), and ¹⁸ F-FDG is the most broadly applied tracer. ²¹ Nowadays, both of them are considered the best tracers for PET imaging of brain tumors. ²² In summary, imaging findings from PWI and PET may contribute, in addition to MRI, to improve both diagnostic and therapeutic planning, particularly in clinically challenging situations. However, each of these modalities has its disadvantages. Standard MRI does not produce reliable data to distinguish radiation-related changes from true tumor progression, while Magnetic resonance (MR) spectroscopy and PET can provide false positive results regarding recurrent tumors. ²³ Despite their significant contribution to better differentiate recurrent tumors from treatment-related conditions, research comparing the effectiveness of PET and PWI is limited.Therefore, this systematic review and meta-analysis was carried out to evaluate the diagnostic performance of PWI compared to PET for distinction between tumor recurrence and treatment-related changes. Then, we performed a subgroup analysis to investigate the effectiveness of each PET modality and tracer in comparison with PWI.