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The analysis of Medical Images (MI), particularly the detection and classification of anomalies in 3D MRI (Magnetic Resonance Imaging) scans, plays a critical part in timely intervention and personalized therapy plans. In our paper, a comprehensive methodology for anomaly detection in 3D MRI scans of the brain is proposed that combines advanced Deep Learning (DL) techniques, including Convolutional Long Short-Term Memory (ConvLSTM) model, with efficient statistical feature extraction from segmented anomaly regions. The data collection phase utilizes three main datasets namely the Brain Tumor Segmentation Challenge (BRATS), the Federated Tumor Segmentation Challenge (FETS), and the Medical Segmentation Decathlon (MSD). The research begins with preprocessing steps including image resizing, intensity normalization, and alignment of anomaly region segmentation masks. The targeted anomaly regions within the samples are segmented using U-Net architecture and then follow statistical feature extraction procedure. Dimensionality reduction methods such as Principal Component Analysis (PCA) and Recursive Feature Elimination (RFE) are utilized to streamline the feature space. The ConvLSTM is then used to classify the anomalies using both convolution and recurrent layers to capture spatiotemporal patterns in MRI data. The model is fine-tuned and iterated for better classification performance using Adam optimizer. The statistical evaluation results with accuracy of 98.9 % showed that the designed ConvLSTM method is more suitable for clinical diagnosis and treatment design in detecting anomalies in 3D MRI images. • Advanced Anomaly Detection in 3D MRI. • Deep Learning Integration. • Crucial for ensuring data quality and consistency. • This optimizes feature space while preserving discriminative information. [ABSTRACT FROM AUTHOR]

Background: Glioblastoma is the most common and aggressive primary tumor in adults. A narrative review of all the relevant papers known was conducted. Materials and methods: Reviews, clinical trials, and randomized controlled trials published from 1981 through September 2021 and written, or at least abstracted, in English were analyzed. Results: The standard of care for glioblastoma is the maximum safe resection possible, followed by radiation therapy and concurrent temozolomide (TMZ) and daily TMZ and tumor treatment fields (TTFields) after irradiation. There is no evidence to date of the benefit of brachytherapy, radiosurgery (SRS), fractional stereotactic radiotherapy (FSRT), and hyperfractionated radiotherapy over conventional external beam radiation therapy (EBRT) for the primary tumor. The assessment of age and performance status before treatment in the elderly enables hypofractionated radiotherapy. The research of tumor molecular signatures contributes to the choice of the best-targeted drug therapy. In recurrent glioblastoma, it is necessary to balance the risks and benefits of re-radiation and association with bevacizumab. Solid data confirming the role of immunotherapy in the treatment of malignant glioma are still lacking. Conclusions: Although the treatment of glioblastoma has evolved in terms of local control, mortality remains close to 12 months after diagnosis. To obtain better results and reduce recurrence, future research needs to investigate the frontiers of knowledge, such as the elucidation of the molecular mechanisms related to the tumor, the optimization of drugs to overcome the blood-brain barrier effectively, and the discovery of new therapies aimed at the heterogeneous profile of this neoplasm. [ABSTRACT FROM AUTHOR]

Glioblastoma (GBM) is the most common aggressive malignant tumor in brain neuroepithelial tumors and remains incurable. A variety of treatment options are currently being explored to improve patient survival, including small molecule inhibitors, viral therapies, cancer vaccines, and monoclonal antibodies. Among them, the unique advantages of small molecule inhibitors have made them a focus of attention in the drug discovery of glioblastoma. Currently, the most used chemotherapeutic agents are small molecule inhibitors that target key dysregulated signaling pathways in glioblastoma, including receptor tyrosine kinase, PI3K/AKT/mTOR pathway, DNA damage response, TP53 and cell cycle inhibitors. This review analyzes the therapeutic benefit and clinical development of novel small molecule inhibitors discovered as promising anti-glioblastoma agents by the related targets of these major pathways. Meanwhile, the recent advances in temozolomide resistance and drug combination are also reviewed. In the last part, due to the constant clinical failure of targeted therapies, this paper reviewed the research progress of other therapeutic methods for glioblastoma, to provide patients and readers with a more comprehensive understanding of the treatment landscape of glioblastoma. The dominating targets of glioblastoma (GBM) and corresponding clinical small molecule inhibitors. Synergistic theoretical basis of representative small molecule PARP inhibitors in combination with temozolomide. [Display omitted] [ABSTRACT FROM AUTHOR]

• The present management of HGGs is described as surgery,EBRT, and chemotherapy. • The GKRS is a feasible modality for local control and survival outcomes of HGGs. • The boost GKRS can increase the PFS and OS in HGG patients following GTR. High-grade gliomas (HGGs) are presently managed via surgical resection, external beam radiation therapy (EBRT), and chemotherapy. Although Gamma Knife radiosurgery (GKRS) is currently used to manage HGGs, it has not been considered standard care. This paper aims to compare the contribution of GKRS to clinical outcomes in patients in which gross total resection (GTR) cannot be achieved. We retrospectively reviewed the data of 99 patients with HGG (World Health Organization (WHO) grade III and IV) from two groups: group 1 consisted of 68 patients for which only EBRT was administered, and group 2 consisted of 31 patients for which EBRT and GKRS were administered. Patient demographic data, the extent of resection, IDH mutation, radiation dosage, progression-free survival (PFS), overall survival (OS), and follow-up time were recorded and compared across groups. The grade III/IV tumor ratio was 10/58 and 10/21 in groups 1 and 2, respectively. In group 2, PFS and OS were higher than in group 1 (P = 0.030 and 0.021). The mean follow–up time was 15.02 ± 11.8 (3–52) and 18.9 ± 98.6 (7–43) months in groups 1 and 2, respectively. In addition to the standard management of HGGs in patients without GTR, boost GKRS during the early postoperative period is beneficial for increasing PFS and OS. [ABSTRACT FROM AUTHOR]

• Proposed approach DAF2 enhances the baseline U-Net outcome by approximately 10.47% • Introducing a novel Convolution Block 2 for effective integration of multi-scale information. • Design model parameter to address resource constraints, inference time and prevent overfitting. • Highlight the significance of Focal Tversky loss during the training process. Precise delineation of brain glioblastoma or tumor through segmentation is pivotal in the diagnosis, formulating treatment strategies, and evaluating therapeutic progress in patients. Precisely identifying brain glioblastoma within multimodal MRI scans poses a significant challenge in the field of medical image analysis as different intensity profiles are observed across the sub-regions, reflecting diverse tumor biological properties. For segmenting glioblastoma areas, convolutional neural networks have displayed astounding performance in recent years. This paper introduces an innovative methodology for brain glioblastoma segmentation by combining the Dense-Attention 3D U-Net network with a fusion strategy and the focal tversky loss function. By fusing information from multiple resolution segmentation maps, our model enhances its ability to discern intricate tumor boundaries. Incorporating the focal tversky loss function, we effectively emphasize critical regions and mitigate class imbalance. Recursive Convolution Block 2 is proposed after fusion to ensure efficient utilization of all accessible features while maintaining rapid convergence. The network's effectiveness is assessed using diverse datasets BraTS 2020 and BraTS 2021. Results show comparable dice similarity coefficient compared to other methods with increased efficiency and segmentation performance. Additionally, the architecture achieved an average dice similarity coefficient of 82.4% and an average hausdorff distance (HD95) of 10.426, which demonstrated consistent performance improvement compared to baseline models like U-Net, Attention U-Net, V-Net and Res U-Net and indicating the effectiveness of proposed architecture. [ABSTRACT FROM AUTHOR]

• Patients explore meaning of their crisis in light of self-identity and quality of life. • Providers evaluate treatment decisions relative to patients' values and identity. • Patients describe sources of strength and resilience, new insights, and hope for the future. • Narrative Medicine sessions encourage rapport, patient trust, and mutual understanding. We explore the applications of Narrative Medicine (NM) in the clinical care of brain cancer patients whose self-identity and quality of life are challenged by their disease and treatment. This paper considers how NM may help patients retain and rediscover self-identity during treatment. We performed a retrospective review of NM sessions at our institution in 2016 with focus on life perspectives and priorities along with outlook or attitude and any changes in their symptoms and possible impact on their lives. The narratives shared by four brain cancer patients provided examples of loss of self-identity during illness and treatment, along with ways that NM sessions encouraged patient resilience and discovery of meaning. NM sessions made visible contributions for the patients mentioned in these case studies. Understanding the patient's story is critical for evaluating the significance of impairments due to brain cancer and treatment relative to the patient's unique sense of self and quality of life. NM is at the nexus of clinical management and quality of life concerns for brain cancer patients. Insights from NM sessions may also help the treatment team as they assess patient needs, attitudes, and abilities. [ABSTRACT FROM AUTHOR]

• The Inferior Fronto-Occipital fascicle is a multitasking White Matter bundle bridging frontal, temporal, parietal and occipital lobe. • Dissecting the specimens from lateral to medial we can describe 3 segments: vertical; horizontal segment running along frontal lobe; horizontal segment running from the limen insulae to the parietal and occipital lobes. • The IFOF role seems to be associated with semantic language processing and transmission, executive control network, goal-oriented behavior. • At subcortical stimulation, 9 responses were obtained.: alteration at the PPT Test at third segment of the IFOF (22.2%); paraphasias on the first segment of the IFOF (11.1%). • Overall we experienced a slight early post-operative impairment on on main cognitive domains with a complete recovery at 30 days after surgery for all of these, except for memory. The Inferior Fronto-Occipital fascicle (IFOF) is a multitasking white matter (WM) bundle bridging frontal, temporal, parietal and occipital lobe. Many papers describe its role in the physiology of language, attention and affective behavior but its anatomical components and cortical terminations remain unclear. We analyze the surgical anatomy of the IFOF in the light of our experience with awake surgery, anatomical dissection on 10 human adult hemispheres (Klingler method) and literature review. Dissecting the specimens from lateral to medial we can describe 3 segments: a vertical segment that runs along the frontal lobe; an horizontal segment that runs along frontal lobe; an horizontal segment that runs from the limen insulae, passes into to the temporal stem and arrives at the parietal and occipital lobes. We retrospectively analyzed also 23 awake surgeries. 2 responses were elicited at subcortical stimulation at the third segment of the IFOF; stimulation gave paraphasias on the first segment of the IFOF in one case. All IFOF responses were founded in the left hemisphere. Anatomical knowledge is the cornerstone of surgical orientation, it allows eloquent structures to be reached quickly and it is of primary importance in awake surgery to avoid patient fatigue with lack of concentration. [ABSTRACT FROM AUTHOR]

As a noncanonical inflammatory kinase, IKBKE is frequently overexpressed and activated and has been identified as an oncogenic protein in glioblastoma. However, the potential function and underlying mechanism of IKBKE contributing to tumor angiogenesis remain elusive. First, we analyzed the correlation between IKBKE and VEGF expression in glioma samples by immunohistochemistry (IHC). Second, HUVEC-related assays and Western blot were used to detect the regulatory effect of IKBKE on angiogenesis by modulating VEGF expression. Third, IKBKE depletion could alleviate the influence of VEGF expression on IHC of intracranial glioma model. We demonstrate that depletion of IKBKE markedly inhibits tumor growth and angiogenesis in glioblastoma. Mechanistically, IKBKE induces VEGF expression and secretion by regulating AKT/FOXO3a in glioblastoma. This study reveals that IKBKE is a novel oncogenic molecule that induces angiogenesis through the promotion of VEGF expression and highlights the potential of targeting IKBKE for glioblastoma therapy. • In this paper, we first demonstrate that IKBKE is a novel oncogenic molecule that induces angiogenesis through the promotion of VEGF expression in glioblastoma. • Mechanistically, IKBKE induces VEGF expression and secretion by regulating AKT/FOXO3a in glioblastoma. • The studies suggest that IKBKE is a promising therapeutic target for glioblastoma therapy. [ABSTRACT FROM AUTHOR]

In recent years, nano-based drug delivery systems have gradually been regarded as a promising approach to improve the current glioblastoma treatment, attracting many researchers to engage in this field. To gain comprehensive insights into the advancements in the field of nano-based drug delivery systems for glioblastoma treatment over the past 24 years (1999–2022), we have undertaken a systematic scientometric analysis. This analysis aims to explore the development of the field, identify prominent research themes, and examine key trends in terms of annual publications and citations, as well as the involvement of countries, institutions, subject categories, journals, authors, and references. It was found that papers and their citations gradually grew in the past two decades. China and the United States had the most significant publications related to this field. Keywords analysis provided the research trends and hot spots or foci of this field, establishing the foundation for further discussions. The common therapies and corresponding drugs, and four main requests or tasks for nanocarriers used for drug delivery in glioma treatment were discussed. Moreover, the nine main types of nanocarriers used in this field were recognized, along with the up-to-date review of the related studies in recent three years. We hope this review will inspire novel ideas for researchers in related areas and facilitate the development of a nano-based drug delivery system for effective glioblastoma therapy. [Display omitted] • This is the first comprehensive scientometric analysis of nano-based drug delivery systems in GBM treatment. • The scientometric analysis provided a good detection of research hotspots and trends of this field. • An up-to-date review for the applications of nine types of nanocarriers in GBM treatment was made based on the bibliometric analysis. • Nanocarriers with dual targeting abilities plus combined therapies or novel therapies (e.g., immunotherapy, gene therapy) were stressed. [ABSTRACT FROM AUTHOR]

Abstract Background Glioblastoma is one of the most malignant brain cancer, thus, establishing an effective therapy is paramount. Our previous results indicate that dendritic cell-derived factor (DCF1) is an attractive candidate for therapy against Glioblastoma, since its overexpression in Glioblastoma U251 cells leads to apoptosis. However, the delivery approach limits its clinical application, in this paper, we expressed TAT-DCF1 fusion protein in E.coli in order to surmount its current delivery problems. Methods The coding sequences of the different domains of DCF1 (full length, cytoplasmic, extracellular, 19-amino acid), together with the N-terminal transactivator of transcription (TAT) sequence, were amplified and subcloned into the bacterial expression vector pET30a(+) in order to produce (His) 6 -tagged fusion proteins. Coomassie blue-stained SDS-PAGE and Western blotting identification showed that purity of the fusion proteins. Results Immunofluorescence and flow cytometry show that U251 cells were efficiently transduced with the fusion proteins. Cell viability, proliferation, and migration assays suggest that the complete TAT-DCF1 fusion protein significantly decreased U251 proliferation and migration. Flow cytometry further reveals that TAT-DCF1 triggered cellular apoptosis. Conclusions In conclusion, these findings suggest that the TAT-DCF1 fusion protein was efficiently transduced into Glioblastoma U251 cells and induced the antitumor effect and support further investigation into specific targeting and side effects of TAT-DCF1 during drug delivery. Highlights • U251 cells were efficiently transduced with TAT- DCF1 fusion proteins. • TAT-DCF1 fusion protein inhibits proliferation and induces apoptosis of U251 cells. • The full length TAT-DCF1 significantly reduces the migration rate of U251 cells. [ABSTRACT FROM AUTHOR]

Abstract: There is increasing evidence that glioblastoma possess ‘stem-like’ cells, low concentrations of which can initiate a tumour. It has been proposed that these cells are radioresistant, and that this property contributes to the poor treatment outcomes of these tumours. In this paper we propose that radioresistance is not simply an intrinsic characteristic of glioma stem cells but a result of interactions between these cells and microenvironmental factors, i.e. the ‘microenvironment – stem cell unit’. The critical role of the microenvironment, along with glioma stem cells, is supported directly or indirectly by the following observations: glioma stem cells have been shown to reside preferentially in specific niches, the characteristics of which are known to influence cellular responses to radiation; radiation modifies environmental factors; and, contrarily to the consistency of clinical data, in vitro experiments have reported a wide variety in the radiation response of these cells. The paper, therefore, focuses on the interaction between tumour stem cells and the microenvironment, analyzing how its various elements (endothelial cells, extracellular matrix, cytokines, nitric oxide, oxygen levels) are affected by radiation and how these might influence the response of tumour stem cells to radiation. Finally, we summarize the ongoing debate on the optimal culture conditions for glioma stem cells and the difficulties in designing assays that reliably characterize their radiation response. [Copyright &y& Elsevier]

Over the last decade, the knowledge on the molecular genetic background of gliomas has dramatically increased. This information provides the basis for the molecular target therapies and molecular tests serve to complement the subjective nature of histopathologic criteria and add useful data regarding response to treatments and prognosis. In particular, the use of loss of heterozygosity (LOH) and methylation specific polymerase chain reaction (PCR) (MSP) based testing of gliomas is already in place and used clinically in several centers. This paper provides a brief overview of these molecular genetic aberrations and discusses the clinical utility, as well as the advantages and disadvantages of such approach. Newly developed molecular techniques, such as LOH testing, fluorescence in situ hybridization (FISH), DNA sequencing and MSP, are currently being employed in assessment of gliomas in some laboratories. However, the clinical use of some markers and the context in which the information obtained should be used are still not entirely understood. Therefore, this paper will focus on validation and implementation of molecular testing in gliomas, with emphasis on LOH on chromosomes 1p, 19q, 17p and 10q and O6-methylguanine-DNA methyltransferase (MGMT) methylation status. [ABSTRACT FROM AUTHOR]

Purpose In recent years, the reaction-diffusion (Fisher-Kolmogorov) equation has received much attention from the oncology research community due to its ability to describe the infiltrating nature of glioblastoma multiforme and its extraordinary resistance to any type of therapy. However, in a number of previous papers in the literature on applications of this equation, the term (R) expressing the ‘External Radiotherapy effect’ was incorrectly derived. In this note we derive an analytical expression for this term in the correct form to be included in the reaction-diffusion equation. Methods The R term has been derived starting from the Linear-Quadratic theory of cell killing by ionizing radiation. The correct definition of R was adopted and the basic principles of differential calculus applied. Results The compatibility of the R term derived here with the reaction-diffusion equation was demonstrated. Referring to a typical glioblastoma tumour, we have compared the results obtained using our expression for the R term with the ‘incorrect’ expression proposed by other authors. [ABSTRACT FROM AUTHOR]

Glioblastoma multiforme (GBM) has a poor prognosis despite maximal multimodal therapy. Biomarkers of relevance to prognosis which may also identify treatment targets are needed. A few hundred genetic and molecular predictors have been implicated in the literature, however with the exception of IDH1 and O6-MGMT, there is uncertainty regarding their true prognostic relevance. This study analyses reported genetic and molecular predictors of prognosis in GBM. For each, its relationship with univariate overall survival in adults with GBM is described. A systematic search of MEDLINE (1998–July 2010) was performed. Eligible papers studied the effect of any genetic or molecular marker on univariate overall survival in adult patients with histologically diagnosed GBM. Primary outcomes were median survival difference in months and univariate hazard ratios. Analyses included converting 126 Kaplan–Meier curves and 27 raw data sets into primary outcomes. Seventy-four random effects meta-analyses were performed on 39 unique genetic or molecular factors. Objective criteria were designed to classify factors into the categories of clearly prognostic, weakly prognostic, non-prognostic and promising. Included were 304 publications and 174 studies involving 14,678 unique patients from 33 countries. We identified 422 reported genetic and molecular predictors, of which 52 had ⩾2 studies. IDH1 mutation and O6-MGMT were classified as clearly prognostic, validating the methodology. High Ki-67/MIB-1 and loss of heterozygosity of chromosome 10/10q were classified as weakly prognostic. Four factors were classified as non-prognostic and 13 factors were classified as promising and worthy of additional investigation. Funnel plot analysis did not identify any evidence of publication bias. This study demonstrates a novel literature and meta-analytical based approach to maximise the value that can be derived from the plethora of literature reports of molecular and genetic factors in GBM. Caution is advised in over-interpreting the results due to study limitations. Further research to develop this methodology and improvements in study reporting are suggested. [ABSTRACT FROM AUTHOR]

This paper presents an atypical case of a patient with brain tumor of the glioblastoma multiforme (GBM) type who achieved a 5-year survival. Some general information is provided including epidemiology, diagnostic and treatment procedures (surgery and radio-chemo-therapy), and prognosis of survival related to GBM. The course of the disease, including its main symptoms, individual reasons for the delay of adjuvant treatment, after the primary surgical treatment, 37-month period of the decease free survival, as well as comprehensive management after the tumor recurrence are also presented. Histopathology confirming the clinical diagnosis is discussed in a separate chapter. [ABSTRACT FROM AUTHOR]

Abstract: Glioblastoma multiforme is a malignant tumour with a universally fatal diagnosis. We report two patients with glioblastoma with symptomatic metastasis to the spinal cord and perform a systematic review all 35 reports of symptomatic glioblastoma dissemination to the spinal leptomeninges and/or intramedullary spinal axis. Our analysis of the data shows a median time to spinal metastasis of 10months and a median time of three months from spinal metastasis to death. Treatments described include palliative laminectomies, radiotherapy and chemotherapy. No treatment strategy offered a therapeutic advantage as patients deteriorated rapidly regardless of intervention. Patients who underwent only a biopsy for intracranial glioblastoma had a shorter time to development of spinal metastasis. In addition, there may be an association between intramedullary metastasis and shorter survival. This paper highlights the importance of considering symptomatic spinal dissemination in glioblastoma multiforme. We also review the incidence and postulate mechanisms of tumour dissemination in the central nervous system. Clearly, further research into radiotherapeutic and chemotherapeutic options in this clinical setting is required. [Copyright &y& Elsevier]

Abstract: CD133+ cells in glioblastoma (GBM) display cancer stem cell-like properties and have been considered as the culprit of tumor recurrence, justifying exploration of potential therapeutic modalities targeting CD133+ cancer stem-like cells (CSCs). For photothermolysis studies, GBM-CD133+ and GBM-CD133– cells mixed with various ratios were challenged with single-walled carbon nanotubes (SWNTs) conjugated with CD133 monoclonal antibody (anti-CD133) and then irradiated with near-infrared laser light. Results show that GBM-CD133+ cells were selectively targeted and eradicated, whereas GBM-CD133– cells remained viable. In addition, in vitro tumorigenic and self-renewal capability of GBM-CD133+ treated with localized hyperthermia was significantly blocked. Furthermore, GBM-CD133+ cells pretreated with anti-CD133-SWNTs and irradiated by near-infrared laser 2 days after xenotransplantation in nude mice did not exhibit sustainability of CSC features for tumor growth. Taken altogether, our studies demonstrated that anti-CD133-SWNTs have the potential to be utilized as a thermal-coupling agent to effectively target and destroy GBM CSCs in vitro and in vivo. From the Clinical Editor: Glioblastoma remains one of the most notorious cancer from the standpoint of recurrence and overall resistance to therapy. CD133+ stem cells occur among GBM cells, and may be responsible for the huge recurrence risk. This paper discusses a targeted elimination method of these cells, which may enable more efficient therapy in an effort to minimize or prevent recurrence. [ABSTRACT FROM AUTHOR]

Abstract: Background: Glioblastoma multiform (GBM) is the most common and most aggressive type of primary brain tumour in humans. It has a very poor prognosis despite multi-modality treatments consisting of open craniotomy with surgical resection, followed by chemotherapy and/or radiotherapy. Recently, a new treatment has been proposed – Boron Neutron Capture Therapy (BNCT) – which exploits the interaction between Boron-10 atoms (introduced by vector molecules) and low energy neutrons produced by giant accelerators or nuclear reactors. Methods: The objective of the present study is to compute the deposited dose using a natural source of neutrons (atmospheric neutrons). For this purpose, Monte Carlo computer simulations were carried out to estimate the dosimetric effects of a natural source of neutrons in the matter, to establish if atmospheric neutrons interact with vector molecules containing Boron-10. Results: The doses produced (an average of 1μGy in a 1g tumour) are not sufficient for therapeutic treatment of in situ tumours. However, the non-localised yet specific dosimetric properties of 10B vector molecules could prove interesting for the treatment of micro-metastases or as (neo)adjuvant treatment. On a cellular scale, the deposited dose is approximately 0.5Gy/neutron impact. Conclusion: It has been shown that BNCT may be used with a natural source of neutrons, and may potentially be useful for the treatment of micro-metastases. The atmospheric neutron flux is much lower than that utilized during standard NBCT. However the purpose of the proposed study is not to replace the ordinary NBCT but to test if naturally occurring atmospheric neutrons, considered to be an ionizing pollution at the Earth''s surface, can be used in the treatment of a disease such as cancer. To finalize this study, it is necessary to quantify the biological effects of the physically deposited dose, taking into account the characteristics of the incident particles (alpha particle and Lithium atom) and radio-induced effects (by-stander and low dose effect). One of the aims of the presented paper is to propose to experimental teams (which would be interested in studying the phenomena) a simple way to calculate the dose deposition (allometric fit of free path, transmission factor of brain). [Copyright &y& Elsevier]

Introduction: The increased incidence of Glioblastoma Multiforme, the most aggressive and most common primary brain tumour, is evident worldwide. Survival rates are reaching only 15 months due to its high recurrence and resistance to current combination therapies including oncotomy, radiotherapy and chemotherapy. Light has been shed in the recent years on the anticancer properties of cannabinoids from Cannabis sativa.Objective: To determine whether cannabinoids alone or in combination with radiotherapy and/or chemotherapy inhibit tumour progression, induce cancer cell death, inhibit metastasis and invasiveness and the mechanisms that underlie these actions.Method: PubMed and Web of Science were used for a systemic search to find studies on the anticancer effects of natural cannabinoids on glioma cancer cells in vitro and/or in vivo.Results: A total of 302 papers were identified, of which 14 studies were found to fit the inclusion criteria. 5 studies were conducted in vitro, 2 in vivo and 7 were both in vivo and in vitro. 3 studies examined the efficacy of CBD, THC and TMZ, 1 study examined CBD and radiation, 2 studies examined efficacy of THC only and 3 studies examined the efficacy of CBD only. 1 study examined the efficacy of CBD, THC and radiotherapy, 2 studies examined the combination of CBD and THC and 2 more studies examined the efficacy of CBD and TMZ.Conclusion: The evidence in this systematic review leads to the conclusion that cannabinoids possess anticancer potencies against glioma cells, however this effect varies with the combinations and dosages used. Studies so far were conducted on cells in culture and on mice as well as a small number of studies that were conducted on humans. Hence in order to have more accurate results, higher quality studies mainly including human clinical trials with larger sample sizes are necessitated urgently for GBM treatment. [ABSTRACT FROM AUTHOR]

Background. Stroke-like syndrome is defined as a rare, delayed complication of brain oncotherapy. Cases with more favorable brain cancer diagnoses and longer life expectancy have been previously reported, but here we present, for the first time, three long-term survivors of glioblastoma with stroke-like syndromes. Methods and Results. Three young or middle-aged patients underwent tumor resection and chemoradiotherapy. They received regular clinical and imaging follow-up with stable neurological status and no signs of tumor recurrence. They exhibited varied signs and symptoms (motor and sensory deficits, aphasia, memory and cognitive disorders, seizures, and headache) accompanied by imaging abnormalities. Stroke-like syndromes developed within 2-5 days and resolved in 2-6 weeks. Diffusion-weighted MRI and T2 brain perfusion abnormalities were demonstrated in all patients. In addition, there was focal T1 MRI contrast enhancement due to blood-brain barrier disruption. In addition to tumor recurrence, classic stroke, encephalitis, metabolic and mitochondrial disorders, and post-seizure swelling should be excluded. The imaging indicated intensive MRI scanning and symptomatic medication (steroids supplemented by antiepileptics, vasoactive agents, etc.) for judicious management. With respect to the course, an invasive procedure was still considered an option. Conclusion. All stroke-like syndromes are diagnoses of exclusion. To avoid misinterpretation of imaging findings as glioblastoma recurrence and avert recall oncotherapy or redundant interventions, better understanding of delayed complications of brain tumor therapy is crucial. [ABSTRACT FROM AUTHOR]

Background and Aim. Oncologists play a vital role in the interpretation of radiographic results in glioblastoma patients. Molecular pathology and information on radiation treatment protocols among others are all important for accurate interpretation of radiology images. One important issue that may arise in interpreting such images is the phenomenon of tumor "pseudoprogression"; oncologists need to be able to distinguish this effect from true disease progression. Exact knowledge about the location of high-dose radiotherapy region is needed for valid determination of pseudoprogression according to RANO (Response Assessment in Neuro-Oncology) criteria in neurooncology. The aim of the present study was to evaluate the radiologists' understanding of a radiotherapy high-dose region in routine clinical practice since radiation oncologists do not always report 3-dimensional isodoses when ordering follow up imaging. Methods. Eight glioblastoma patients who underwent postresection radiotherapy were included in this study. Four radiologists worked with their pre-radiotherapy planning MR, however, they were blinded to RT target volumes which were defined by radiation oncologists according to current guidelines. The aim was to draw target volume for high dose RT fields (that is the region, where they would consider that there may be a pseudoprogression in future MRI scans). Many different indices describing structure differences were analyzed in comparison with original per-protocol RT target volumes. Results. The median volume for RT high dose field was 277 ccm (range 218 to 401 ccm) as defined per protocol by radiation oncologist and 87 ccm (range 32-338) as defined by radiologists (median difference of paired difference 31%, range 15-112%). The Median Dice index of similarity was 0.46 (range 0.14 - 0.78), the median Hausdorff distance 25 mm. Conclusion. Continuing effort to improve education on specific procedures in RT and in radiology as well as automatic tools for exporting RT targets is needed in order to increase specificity and sensitivity in response evaluation. [ABSTRACT FROM AUTHOR]