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Journal articles on the topic 'Brain cancer'

Author: Grafiati

Published: 4 June 2021

Last updated: 29 July 2024

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1

Lucke-Wold, Brandon. "Principles of Lung Cancer Metastasis to Brain." Journal of Skeleton System 1, no. 1 (December 18, 2022): 01–04. http://dx.doi.org/10.58489/2836-2284/003.

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Lung cancer is a disease associated with significant morbidity and mortality on a global setting. This form of cancer commonly gives raise to metastatic lesions the brain, which can further worsen outcomes. In this focused review, we discuss an overview of lung cancers that metastasize to the brain: known risk factors; means of detection and diagnosis; and options for treatment including a comparison between surgical resection, stereotactic radiosurgery, and whole-brain radiation therapy. These interventions are still being assessed by clinical trials and continue to be modified through evidence-based practice.

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2

Agrawal, Madhav, and Arham Jain. "Deep Learning Techniques in Brain Cancer Detection." International Journal of Science and Research (IJSR) 12, no. 11 (November 5, 2023): 41–49. http://dx.doi.org/10.21275/sr231029151256.

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3

Lucke-Wold, Brandon, Elizabeth Klaas, Shahd Mohamed, Jordan Poe, Ramya Reddy, and Abeer Dagra. "Innovative Approaches for Breast Cancer Metastasis to the Brain." Archives of Medical Case Reports and Case Study 6, no. 4 (October 31, 2022): 01–09. http://dx.doi.org/10.31579/2692-9392/147.

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Breast cancer metastasis is a continued concern for patients with recent development in our understanding of disease progression. In this paper, we highlight the pathophysiology behind breast cancer metastasis. Blood brain barrier disruption plays a critical component in progression. We then investigate the current treatment strategies and recommended guidelines. This focuses on radiation and medical management. Finally, we address the role of surgical intervention. The data is organized into tables and figures to highlight key components. Finally, we address emerging treatments and pre-clinical data. The paper will serve as a user-friendly guide for clinicians and researchers to help formulate a strategy to manage breast cancer metastasis patients sufficiently.

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4

Christy, Pat, and Melinda Granger Oberleitner. "Brain Cancer." American Journal of Nursing 100, no. 4 (April 2000): 4. http://dx.doi.org/10.2307/3521927.

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5

Brody, Herb. "Brain cancer." Nature 561, no. 7724 (September 2018): S39. http://dx.doi.org/10.1038/d41586-018-06703-8.

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6

Christy, Pat, and Melinda Granger Oberleitner. "Brain Cancer." AJN, American Journal of Nursing &NA;, Supplement (April 2000): 4–8. http://dx.doi.org/10.1097/01.naj.0000370629.09937.4a.

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7

Bredel, Markus. "Brain Cancer." Lancet Oncology 4, no. 4 (April 2003): 257–58. http://dx.doi.org/10.1016/s1470-2045(03)01040-4.

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8

Friedman, Henry. "Brain cancer." Cancer 94, no. 11 (May 23, 2002): 3071. http://dx.doi.org/10.1002/cncr.10569.

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9

Joshi, Vaibhavi, Kate Beecher, Malcolm Lim, Andrew Stacey, Yufan Feng, Parmjit S. Jat, Pascal H. G. Duijf, Peter T. Simpson, Sunil R. Lakhani, and Amy E. McCart Reed. "B7-H3 Expression in Breast Cancer and Brain Metastasis." International Journal of Molecular Sciences 25, no. 7 (April 3, 2024): 3976. http://dx.doi.org/10.3390/ijms25073976.

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Brain metastasis is a significant challenge for some breast cancer patients, marked by its aggressive nature, limited treatment options, and poor clinical outcomes. Immunotherapies have emerged as a promising avenue for brain metastasis treatment. B7-H3 (CD276) is an immune checkpoint molecule involved in T cell suppression, which is associated with poor survival in cancer patients. Given the increasing number of clinical trials using B7-H3 targeting CAR T cell therapies, we examined B7-H3 expression across breast cancer subtypes and in breast cancer brain metastases to assess its potential as an interventional target. B7-H3 expression was investigated using immunohistochemistry on tissue microarrays of three clinical cohorts: (i) unselected primary breast cancers (n = 347); (ii) brain metastatic breast cancers (n = 61) and breast cancer brain metastases (n = 80, including a subset of 53 patient-matched breast and brain metastasis cases); and (iii) mixed brain metastases from a range of primary tumours (n = 137). In primary breast cancers, B7-H3 expression significantly correlated with higher tumour grades and aggressive breast cancer subtypes, as well as poorer 5-year survival outcomes. Subcellular localisation of B7-H3 impacted breast cancer-specific survival, with cytoplasmic staining also correlating with a poorer outcome. Its expression was frequently detected in brain metastases from breast cancers, with up to 90% expressing B7-H3. However, not all brain metastases showed high levels of expression, with those from colorectal and renal tumours showing a low frequency of B7-H3 expression (0/14 and 2/16, respectively). The prevalence of B7-H3 expression in breast cancers and breast cancer brain metastases indicates potential opportunities for B7-H3 targeted therapies in breast cancer management.

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10

Saeed, Soobia, Afnizanfaizal Abdullah, and NZ Jhanjhi. "Implementation of Fourier Transformation with Brain Cancer and CSF Images." Indian Journal of Science and Technology 12, no. 37 (October 10, 2019): 1–9. http://dx.doi.org/10.17485/ijst/2019/v12i37/146151.

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11

Agung Bagus Bramardipa, Anak. "Squamous Cell Lung Cancer with Brain Metastasis: A Case Report." International Journal of Science and Research (IJSR) 12, no. 4 (April 5, 2023): 1599–602. http://dx.doi.org/10.21275/sr23426102646.

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12

Farajirad, Mohammad. "The Gut-Brain Axis: How the Microbiome may Influence Brain Tumors, A Narrative Review." International Journal of Surgery & Surgical Techniques 7, no. 2 (2023): 1–6. http://dx.doi.org/10.23880/ijsst-16000192.

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Aim: To review the current literature and demonstrate the potential relationship between gut microbiome and brain tumor. Methods: A comprehensive search of the available literature was conducted using the PubMed, Google Scholar, OVID, Embase and other database to identify studies investigating the relationship between the gut microbiome and brain cancer. The search was limited to articles published in English between 2010 and 2022. Conclusion: While the research on the relationship between the gut microbiome and brain cancer is limited, the studies that have been conducted suggest that there may be a connection. The gut microbiome has been shown to play roles in a number of diseases, and some evidence suggests that it may also be involved in the development and progression of brain cancer. The gut microbiome may suggest a new method for the prevention, diagnosis, and treatment of brain cancer and further research in this area has the potential to lead to new and innovative strategies for managing this disease.

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13

Mastrangelo, Stefano. "Special Issue: Childhood Brain Cancer Treatment." Cancers 15, no. 21 (November 3, 2023): 5278. http://dx.doi.org/10.3390/cancers15215278.

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14

Tyagi, Abhishek, Shih-Ying Wu, Ravindra Deshpande, Kerui Wu, Liang Liu, and Kounosuke Watabe. "Abstract 5515: Low body mass index (BMI) induces neuronal NPY and promotes brain metastasis of lung cancer." Cancer Research 84, no. 6_Supplement (March 22, 2024): 5515. http://dx.doi.org/10.1158/1538-7445.am2024-5515.

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Abstract Brain metastases (BrMs) are a common occurrence in lung cancer with a dismal outcome. To develop a more effective therapeutic strategy, it is crucial to understand the underlying pathological mechanism of brain metastasis. Recent clinical data has unveiled a significant association between low body mass index (BMI) and an increased risk of brain metastasis in lung cancer patients, leading to reduced survival rates compared to other primary tumors. However, the molecular mechanism underlying this paradoxical relationship, often referred to as the "obesity paradox," in the context of lung cancer mortality presents a complex and intriguing puzzle and warrants in-depth investigation. Here, we examined biological mechanism of how low BMI promotes lung cancer brain metastasis. In this study, we conducted a retrospective pan-analysis of 5,516 patient cohorts with brain metastasis originating from lung, breast, melanoma, and renal cancers with their BMI status. We found that lung cancer patients with low BMI have significantly higher brain metastatic incidence compared to the high BMI patients, in contrast to breast, melanoma, and renal cancers. Furthermore, we found that low BMI plays a pivotal role in mediating neuron activation within the brain and that the secretion of neuronal neuropeptide Y (NPY), a protein involved in appetite and energy homeostasis via GHSR-receptor manner, promotes metabolic switching through NPY/NPY5R axis in the tumor cells in the brain thereby enabling metastasis. Elevated levels of neuronal NPY in the brains of cancer-free subjects with low BMI suggest its potential utility as a promising prognostic biomarker for identifying the increased risk of metastatic disease in lung cancer patients with low BMI. We also demonstrated that reversing low BMI or blocking the NPY/Y5R interactions effectively abrogated brain metastasis in our animal model. Our findings suggest a novel pro-metastatic role of low BMI-induced NPY in the progression of brain metastasis. We emphasize the importance of elucidating the clinical implications of this relationship to develop an updated intervention strategy for the clinical care of patients with lung cancer and low BMI. Citation Format: Abhishek Tyagi, Shih-Ying Wu, Ravindra Deshpande, Kerui Wu, Liang Liu, Kounosuke Watabe. Low body mass index (BMI) induces neuronal NPY and promotes brain metastasis of lung cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 5515.

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15

Reddel, Roger, and Adel Aref. "Targeting brain cancer." Science 377, no. 6605 (July 29, 2022): 467–68. http://dx.doi.org/10.1126/science.add4839.

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16

Saste, Akshay, Shubham Sethiya, and Prof Pavan Kulkarni. "Brain Cancer Detection." IJARCCE 7, no. 11 (November 30, 2018): 68–70. http://dx.doi.org/10.17148/ijarcce.2018.71115.

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17

Chong, Lisa D. "Brain cancer therapy." Science 355, no. 6322 (January 19, 2017): 258.1–258. http://dx.doi.org/10.1126/science.355.6322.258-a.

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18

Haas, Michael J. "LAMbasting brain cancer." Science-Business eXchange 3, no. 43 (November 2010): 1282. http://dx.doi.org/10.1038/scibx.2010.1282.

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19

Ferrarelli, Leslie K. "Channeling brain cancer." Science Signaling 8, no. 392 (September 1, 2015): ec245-ec245. http://dx.doi.org/10.1126/scisignal.aad3213.

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20

Perryman, Lara, and Janine T. Erler. "Brain Cancer Spreads." Science Translational Medicine 6, no. 247 (July 30, 2014): 247fs28. http://dx.doi.org/10.1126/scitranslmed.3009920.

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The discovery that ~20% of patients with brain cancer have circulating tumor cells breaks the dogma that these cells are confined to the brain and has important clinical implications (Müller et al., this issue).

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21

Müller, Volkmar, Elena Laakmann, Astrid Grottke, Kerstin Riecke, and Isabell Witzel. "Cerebral metastasis in breast cancer." Senologie - Zeitschrift für Mammadiagnostik und -therapie 15, no. 04 (December 2018): 213–18. http://dx.doi.org/10.1055/a-0753-3504.

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AbstractThe incidence of breast cancer brain metastases has risen steadily in recent years. Brain metastases are often the limiting factor of the disease, as survival is usually only a few months after brain metastasis occurs. Apart from the poor prognosis, cognitive and neurological deficits lead to a massive impairment of quality of life. HER2-positive or triple-negative cancers develop brain metastases more often. Studies on the subject of brain metastases were conducted mainly in cohorts with different primary tumours. To improve the available data on patients with breast cancer, the “Brain Metastases in Breast Cancer (BMBC)” registry was initiated to record the German care reality. Because of the lack of specific systemic treatment options, the main primary therapy of brain metastases is local (surgery, stereotactic radiation, whole-brain radiation). Local therapy is supplemented by systemic therapy. The choice of systemic therapy is guided especially by the extracranial disease situation, as there are practically no study data currently on the subject of systemic therapy of brain metastases specifically. Only very recently have drugs been investigated explicitly in women with breast cancer brain metastases.

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22

Nizam, Amanda, Donald L. Trump, and Jeanny B. Aragon-Ching. "Molecular characterization of brain metastases in patients with metastatic urothelial cancer." Journal of Clinical Oncology 36, no. 6_suppl (February 20, 2018): 509. http://dx.doi.org/10.1200/jco.2018.36.6_suppl.509.

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509 Background: Urothelial cancers are the 6th most common cause of all new cancer cases in 2017. Metastatic disease to the brain is rare but has a poor prognosis. There is little information regarding the phenotypic and molecular characteristics of urothelial cancers involving the brain. We sought to evaluate the clinical and tumor molecular characteristics in patients with metastatic urothelial cancer to the brain. Methods: In a single institution retrospective chart review, 48 patients were found to have metastatic bladder cancer from 2006 to 2015, 4 had brain metastases. The demographics, stage, phenotypic characteristics and molecular characteristics using Oncomine, a cancer microarray platform targeting 143 cancer genes, was determined. Results: Of the 4 patients identified with metastatic brain urothelial cancer, 3 were men. 2 had both upper tract and bladder urothelial cancers and 2 had bladder cancer alone. 3 had prior nephroureterectomy and/or radical cystectomy initially and had subsequent development of initial distant metastases at a median of 7.9 months, and time between the first to brain metastases at a median onset of 11.8 months. Median overall survival (OS) was short upon diagnosis of brain metastasis with a median OS of 119 days (range: 96 – 391 days) from the time of brain metastasis diagnosis. All received surgical resection followed by radiation for brain metastases. Three patients had brain tumor examined for comprehensive somatic tumor profiling using the Oncomine panel. Results showed APC mutation in patient 1, loss of TP53, BRCA-2 loss of function mutation with MSH2 deletion in patient 2, as well as FGFR3 gene mutation and TP53 mutation in patient 3. All patients received prior platinum-based systemic therapy with additional FGFR3-therapy for patient 3 and atezolizumab for patient 4. Conclusions: Metastatic brain urothelial cancers are rare events with a uniformly poor prognosis. The role for targeted therapy and immunotherapy is still evolving.

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23

Grebstad Tune, Benedicte, Heena Sareen, Branka Powter, Smadar Kahana-Edwin, Adam Cooper, Eng-Siew Koh, Cheok S. Lee, et al. "From Pediatric to Adult Brain Cancer: Exploring Histone H3 Mutations in Australian Brain Cancer Patients." Biomedicines 11, no. 11 (October 27, 2023): 2907. http://dx.doi.org/10.3390/biomedicines11112907.

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Genetic histone variants have been implicated in cancer development and progression. Mutations affecting the histone 3 (H3) family, H3.1 (encoded by HIST1H3B and HIST1H3C) and H3.3 (encoded by H3F3A), are mainly associated with pediatric brain cancers. While considered poor prognostic brain cancer biomarkers in children, more recent studies have reported H3 alterations in adult brain cancer as well. Here, we established reliable droplet digital PCR based assays to detect three histone mutations (H3.3-K27M, H3.3-G34R, and H3.1-K27M) primarily linked to childhood brain cancer. We demonstrate the utility of our assays for sensitively detecting these mutations in cell-free DNA released from cultured diffuse intrinsic pontine glioma (DIPG) cells and in the cerebral spinal fluid of a pediatric patient with DIPG. We further screened tumor tissue DNA from 89 adult patients with glioma and 1 with diffuse hemispheric glioma from Southwestern Sydney, Australia, an ethnically diverse region, for these three mutations. No histone mutations were detected in adult glioma tissue, while H3.3-G34R presence was confirmed in the diffuse hemispheric glioma patient.

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Dirks, Peter B. "Brain Tumor Stem Cells: Bringing Order to the Chaos of Brain Cancer." Journal of Clinical Oncology 26, no. 17 (June 10, 2008): 2916–24. http://dx.doi.org/10.1200/jco.2008.17.6792.

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Brain tumors are generally incurable cancers. Work from a number of laboratories strongly suggests that they are organized as a hierarchy based on a subset of cancer cells that have stem-cell properties. These cells have now been shown to be resistant to conventional therapy and responsive to differentiation therapy. New in vitro and in vivo models for interrogating brain tumor cells in stem-cell conditions have been developed that provide important new opportunities for elucidating the key pathways responsible for driving the proliferation of these cells. Continued application of the principles of stem-cell biology to the study of brain cancers is likely to continue to bring further important insight into these aggressive cancers, bringing new treatments and understanding of the origins.

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Kuroiwa, Yuka, Jun Nakayama, Chihiro Adachi, Takafumi Inoue, Shinya Watanabe, and Kentaro Semba. "Proliferative Classification of Intracranially Injected HER2-positive Breast Cancer Cell Lines." Cancers 12, no. 7 (July 6, 2020): 1811. http://dx.doi.org/10.3390/cancers12071811.

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HER2 is overexpressed in 25–30% of breast cancers, and approximately 30% of HER2-positive breast cancers metastasize to the brain. Although the incidence of brain metastasis in HER2-positive breast cancer is high, previous studies have been mainly based on cell lines of the triple-negative subtype, and the molecular mechanisms of brain metastasis in HER2-positive breast cancer are unclear. In the present study, we performed intracranial injection using nine HER2-positive breast cancer cell lines to evaluate their proliferative activity in brain tissue. Our results show that UACC-893 and MDA-MB-453 cells rapidly proliferated in the brain parenchyma, while the other seven cell lines moderately or slowly proliferated. Among these nine cell lines, the proliferative activity in brain tissue was not correlated with either the HER2 level or the HER2 phosphorylation status. To extract signature genes associated with brain colonization, we conducted microarray analysis and found that these two cell lines shared 138 gene expression patterns. Moreover, some of these genes were correlated with poor prognosis in HER2-positive breast cancer patients. Our findings might be helpful for further studying brain metastasis in HER2-positive breast cancer.

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Morotti, Annamaria, Francesco Gentile, Gianluca Lopez, Giulia Passignani, Luca Valenti, Marco Locatelli, Manuela Caroli, Claudia Fanizzi, Stefano Ferrero, and Valentina Vaira. "Epigenetic Rewiring of Metastatic Cancer to the Brain: Focus on Lung and Colon Cancers." Cancers 15, no. 7 (April 4, 2023): 2145. http://dx.doi.org/10.3390/cancers15072145.

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Distant metastasis occurs when cancer cells adapt to a tissue microenvironment that is different from the primary organ. This process requires genetic and epigenetic changes in cancer cells and the concomitant modification of the tumor stroma to facilitate invasion by metastatic cells. In this study, we analyzed differences in the epigenome of brain metastasis from the colon (n = 4) and lung (n = 14) cancer and we compared these signatures with those found in primary tumors. Results show that CRC tumors showed a high degree of genome-wide methylation compared to lung cancers. Further, brain metastasis from lung cancer deeply activates neural signatures able to modify the brain microenvironment favoring tumor cells adaptation. At the protein level, brain metastases from lung cancer show expression of the neural/glial marker Nestin. On the other hand, colon brain metastases show activation of metabolic signaling. These signatures are specific for metastatic tumors since primary cancers did not show such epigenetic derangements. In conclusion, our data shed light on the epi/molecular mechanisms that colon and lung cancers adopt to thrive in the brain environment.

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B. Subudhi, Bharat, and Vijay K. Singh. "Brain Delivery of Chemotherapeutics in Brain Cancer." Anti-Cancer Agents in Medicinal Chemistry 16, no. 2 (November 17, 2015): 212–20. http://dx.doi.org/10.2174/1871520615666150611110354.

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28

Zaytseva, Olga, Nan-hee Kim, and Leonie M. Quinn. "MYC in Brain Development and Cancer." International Journal of Molecular Sciences 21, no. 20 (October 20, 2020): 7742. http://dx.doi.org/10.3390/ijms21207742.

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The MYC family of transcriptional regulators play significant roles in animal development, including the renewal and maintenance of stem cells. Not surprisingly, given MYC’s capacity to promote programs of proliferative cell growth, MYC is frequently upregulated in cancer. Although members of the MYC family are upregulated in nervous system tumours, the mechanisms of how elevated MYC promotes stem cell-driven brain cancers is unknown. If we are to determine how increased MYC might contribute to brain cancer progression, we will require a more complete understanding of MYC’s roles during normal brain development. Here, we evaluate evidence for MYC family functions in neural stem cell fate and brain development, with a view to better understand mechanisms of MYC-driven neural malignancies.

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Silva, Arnaldo Neves Da, Kazuki Nagayama, David J. Schlesinger, and Jason P. Sheehan. "Gamma Knife surgery for brain metastases from gastrointestinal cancer." Journal of Neurosurgery 111, no. 3 (September 2009): 423–30. http://dx.doi.org/10.3171/2008.9.jns08281.

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Object Brain metastases from gastrointestinal cancers are rare. However, the incidence is increasing because patients with gastrointestinal carcinoma tend to live longer due to earlier diagnosis and more effective treatment of systemic disease. The purpose of this study was to evaluate the efficacy of Gamma Knife surgery (GKS) for the treatment of brain metastases from gastrointestinal cancers. Methods The authors performed a retrospective review of 40 patients (18 women and 22 men) who had undergone GKS to treat a total of 118 metastases from gastrointestinal cancers between January 1996 and December 2006. The mean patient age was 58.7 years, and the mean Karnofsky Performance Scale (KPS) score was 70. There were 7 patients with esophageal cancer, 25 with colon cancer, 5 with rectal cancer, 2 with pancreatic cancer, and 1 with gastric cancer. Nineteen patients were treated with whole-brain radiotherapy and/or local brain radiotherapy before GKS. Twenty-four patients had extracranial metastases, and 3 had an additional primary cancer. The mean metastatic brain tumor volume was 4.3 cm3, and the mean maximum tumor dose varied from 17.1 to 76.7 Gy (mean 41.8 Gy). Results Follow-up imaging studies were available in 25 patients with a total of 90 treated metastases. The results demonstrate a tumor control rate of 91%. The median survival time was 6.7 months, and the 6-month and 1-year survival rates were 55 and 25%, respectively. A univariate analysis revealed that the KPS score (≤ 70 vs ≥ 80) was significant (p = 0.018) for improved survival. Conclusions Results in this series suggest that GKS can be an effective tool for the treatment of brain metastases from gastrointestinal cancer.

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Kanodia, Avinash Kumar. "An Update on Current and Emerging Therapies for Brain Metastases." Neurology & Neurotherapy Open Access Journal 5, no. 2 (2020): 1–6. http://dx.doi.org/10.23880/nnoaj-16000154.

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Brain metastases (BMs) are the most common cause of brain malignancy, occurring 10 times more often than intracranial neoplasms. BMs most frequently arise from non-small cell lung cancer, melanoma, renal cell carcinoma and breast carcinoma. The overall survival after BM diagnosis remains poor, but depends on patient age, performance status, type of primary tumour, time of diagnosis from the primary, as well as many other factors. The incidence of BMs may be due to the fact that some therapies control growth of the primary tumour, but such agents has a limited role in BM treatment, as they cannot or only partially penetrate the BBB. The brain therefore acts as a ‘sanctuary site’ for cancers which have successfully invaded the brain and escaped the effects of systemic cancer therapies. A reduced effect of classical systemic therapies on BMs can also be explained by other resistance mechanisms that only occur in the brain such as the astrocytic protection of extravagated cancer cells. Alternative approaches include surgery, stereotactic radiosurgery or whole brain radiotherapy. This review looks at the benefits and risks of different approaches to treatment of BMs and highlights areas of research in both current and prospective BM therapies.

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Kanodia, Avinash Kumar. "An Update on Current and Emerging Therapies for Brain Metastases." Neurology & Neurotherapy Open Access Journal 5, no. 2 (2020): 1–6. http://dx.doi.org/10.23880/nnoaj-16000154.

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Brain metastases (BMs) are the most common cause of brain malignancy, occurring 10 times more often than intracranial neoplasms. BMs most frequently arise from non-small cell lung cancer, melanoma, renal cell carcinoma and breast carcinoma. The overall survival after BM diagnosis remains poor, but depends on patient age, performance status, type of primary tumour, time of diagnosis from the primary, as well as many other factors. The incidence of BMs may be due to the fact that some therapies control growth of the primary tumour, but such agents has a limited role in BM treatment, as they cannot or only partially penetrate the BBB. The brain therefore acts as a ‘sanctuary site’ for cancers which have successfully invaded the brain and escaped the effects of systemic cancer therapies. A reduced effect of classical systemic therapies on BMs can also be explained by other resistance mechanisms that only occur in the brain such as the astrocytic protection of extravagated cancer cells. Alternative approaches include surgery, stereotactic radiosurgery or whole brain radiotherapy. This review looks at the benefits and risks of different approaches to treatment of BMs and highlights areas of research in both current and prospective BM therapies.

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Madzudzo, Michelle, Godwin Musosi, and Ivan Muzvondiwa. "PAEDIATRIC-16 ADVANCING IN PAEDEATRIC BRAIN CANCER CARE." Neuro-Oncology Advances 5, Supplement_4 (October 31, 2023): iv11. http://dx.doi.org/10.1093/noajnl/vdad121.047.

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Abstract OBJECTIVE To empower health workers in the cancer care continuum to nationally reduce the disease burden from brain cancer through active engagement, advocacy , collaboration and education -to introduce theories and concepts including current trends, issues , challenges and debates in brain cancer. METHOD The talk cancer zim trust organised a hybrid national webinar on paedeatric brain cancer on 26 May 2023 under the mantra "advancing in brain cancer care , where are we? The objectives were to be met through presantations from the neurosurgeon , oncologist, psychiatrist, palliative care specialist , Kidzcan and the GICC focal person for the country.Thematic areas covered were palliative care,radiation oncology, neurosurgery, advocacy and psychooncology. RESULTS a total of 193 health proffessionals attended the meeting online while 24 health proffessionals attended the meeting in.person.The targeted audience consisted of radiographers, oncology nurses, pharmacists, rehabilitation specialists, medical physicists and specialist doctors such as oncologists, neurosurgeons and psychiatriasts. CONCLUSION There is need for a holistic approach to paedatric brain cancers throughout the cancer trajectory from awareness, diagnosis, screening through treatment and palliative care and research

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Khamis, Zahraa I., Drishty B. Sarker, Yu Xue, Nancy Al-Akkary, Viviana D. James, Changchun Zeng, Yan Li, and Qing-Xiang Amy Sang. "Modeling Human Brain Tumors and the Microenvironment Using Induced Pluripotent Stem Cells." Cancers 15, no. 4 (February 16, 2023): 1253. http://dx.doi.org/10.3390/cancers15041253.

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Brain cancer is a group of diverse and rapidly growing malignancies that originate in the central nervous system (CNS) and have a poor prognosis. The complexity of brain structure and function makes brain cancer modeling extremely difficult, limiting pathological studies and therapeutic developments. Advancements in human pluripotent stem cell technology have opened a window of opportunity for brain cancer modeling, providing a wealth of customizable methods to simulate the disease in vitro. This is achieved with the advent of genome editing and genetic engineering technologies that can simulate germline and somatic mutations found in human brain tumors. This review investigates induced pluripotent stem cell (iPSC)-based approaches to model human brain cancer. The applications of iPSCs as renewable sources of individual brain cell types, brain organoids, blood–brain barrier (BBB), and brain tumor models are discussed. The brain tumor models reviewed are glioblastoma and medulloblastoma. The iPSC-derived isogenic cells and three-dimensional (3D) brain cancer organoids combined with patient-derived xenografts will enhance future compound screening and drug development for these deadly human brain cancers.

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Lai Wu, Alex Man, Selamawit Gossa, Ramakrishna Samala, Monika Chung, Brunilde Gril, Howard Yang, Helen Thorsheim, et al. "29. ROLE OF AGE AND CNS MYELOID CELLS ON BREAST CANCER BRAIN METASTASIS." Neuro-Oncology Advances 2, Supplement_2 (August 2020): ii5. http://dx.doi.org/10.1093/noajnl/vdaa073.017.

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Abstract Women diagnosed with breast cancer at a younger age (typically defined as < 40 years old) often have a poorer prognosis and an increased risk of brain metastasis compared to their older counterparts. Multivariate analyses accounting for differences in tumor characteristics have shown that age is an independent predictor of worse outcome. We therefore hypothesized that rather than intrinsic tumor properties, extrinsic microenvironmental factors contribute to age-related differences in aggressiveness. The effect of age was examined by injecting brain-selected breast cancer cells into young (2 – 6 months) and older (>12 months) mice. In four brain metastasis models examined, young mice developed 2- to 16-fold (p < 0.05) more brain metastases compared to older mice. The effect of age was not observed in mouse breast cancer models that metastasize to liver and lungs, suggesting that this is an organ-specific phenomenon. Flow cytometry-based immune-profiling of mouse brains showed that T-cells (CD4+, CD8+, and FOXP3+CD25+ regulatory T-cells), monocytes and neutrophils were elevated in brains with metastases, but the abundance of these populations did not vary dramatically with age. Furthermore, antibody-based depletion of T-cells, monocytes and neutrophils did not significantly alter brain metastasis development. Microglia, which are resident CNS myeloid cells, were 1.5-fold more abundant in young brains compared to older brains. Depletion of CNS myeloid cells using the colony stimulating factor-1-receptor inhibitor PLX3397 reduced brain metastatic tumor burden in young mice by 2.1-fold (p < 0.001). Importantly, loss of CNS myeloid cells/microglia, which are normally more activated in aged mice and thus may protect the older brain against metastasis, did not augment brain metastasis formation in older mice. These results suggest that the younger brain is more permissive for breast cancer metastasis and that targeting resident CNS myeloid cells may be an effective strategy to prevent brain metastasis development in younger patients.

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Tsapakidis, Konstantinos. "Prostate cancer presented with de novo brain metastases as initial manifestation: A case report with review of the literature." Cancer Research and Cellular Therapeutics 5, no. 1 (February 12, 2021): 01–04. http://dx.doi.org/10.31579/2640-1053/073.

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Prostate cancer is the most common cancer and among the leading causes of cancer death in men and its clinical symptoms vary a lot. The most common metastatic site is the bones, but rarely prostate cancer can metastasize to brain in very advanced stages of the disease. However, brain metastases giving neurological symptoms as first manifestation of prostate cancers have been reported. Research of international literature revealed only seventeen patients (including our own) that were diagnosed with prostate cancer presented with neurological symptoms.

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Andersen, Klaus Kaae, Anne Julie Tybjerg, Alejandro Daniel Babore, and Tom Skyhøj Olsen. "Occult primary brain cancers manifesting in the aftermath of ischaemic and haemorrhagic stroke." European Stroke Journal 5, no. 3 (April 15, 2020): 237–44. http://dx.doi.org/10.1177/2396987320920101.

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Introduction Symptoms of occult brain cancer may mimic stroke. Misdiagnosis may lead to improper treatment and delayed diagnosis. We characterised strokes associated with occult primary brain cancer and determined risk that ischaemic and haemorrhagic strokes are associated with occult primary brain cancer. Patients and methods All patients with incident stroke in Denmark 2003–2015 were identified through the Danish Stroke Registry (n = 85,893) and matched 1:10 on age and sex to the Danish background population without a stroke history (n = 858,740). This cohort was linked to the Danish Cancer Registry and prevalence of occult primary brain cancer defined as the event of previously unknown primary brain cancer during a one-year follow-up was estimated. We used Cox regression models to study risk of occult primary brain cancer in comparison to the background population. Results Of 77,484 patients with ischaemic strokes, 39 (1 in 2000) were associated with primary brain cancer; of 8409 with haemorrhagic strokes, it was 126 (1 in 66). In the background cohort, 205 (1 in 4000) had occult primary brain cancer. The multivariate stroke risk factor analysis showed that patients with occult primary brain cancer differed significantly from those without occult primary brain cancer indicating they might have stroke mimics rather than true strokes. Discussion and conclusions: Strokes associated with occult primary brain cancer tend to be stroke mimics rather than true strokes. Primary brain cancer is rare in patients with ischaemic stroke (1 in 2000); risk that misdiagnosis results in maltreatment is, therefore, very low. Occult primary brain cancers are mainly found among patients with haemorrhagic stroke; they are not uncommon (1 in 66) and should always be kept in mind.

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Sevyan, N. V., V. B. Karakhan, D. R. Naskhletashvili, A. Kh Bekyashev, E. V. Prozorenko, D. M. Belov, A. A. Mitrofanov, A. A. Pogosova, and B. I. Polyakov. "Brain metastases from gynaecological cancers." Voprosy ginekologii, akušerstva i perinatologii 19, no. 4 (2020): 172–77. http://dx.doi.org/10.20953/1726-1678-2020-4-172-177.

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The spread of female genital tract tumours to the brain is a rare and insufficiently studied pathology. The problems of diagnosis and treatment of this group of patients still remain. The article gives a detail account of the clinical picture, radiological and morphological diagnosis, and the principles of treating patients with brain metastases from gynaecological cancers. Conclusion. A probable cause of a rare occurrence of brain metastases from gynaecological malignancies might be a high resistance of nervous tissue to various kinds of tumours. When local control over a brain tumour is achieved, this might improve the patient’s survival and quality of life in some particular cases. Key words: ovarian cancer, endometrial cancer, cervical cancer, brain metastases

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McCann, Brendan, Kiran Bhatti, and Vivienne MacLaren. "Incidence of brain metastasis in esophageal cancer." Journal of Clinical Oncology 33, no. 3_suppl (January 20, 2015): 46. http://dx.doi.org/10.1200/jco.2015.33.3_suppl.46.

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46 Background: Brain metastasis in oesophageal cancer is a rare but often fatal complication. In previous studies the incidence has ranged from 1.4% - 13% with the largest studies from China and Japan that have been retrospectively based over fifteen to twenty years. (Ogawa K, Toita T, Sueyama H. Brain metastases from esophageal carcinoma: natural history, prognostic factors, and outcome. Cancer. 2002 Feb 1;94(3):759-64.) With improving diagnostic techniques and differing histology of oesophageal cancer from Eastern countries we undertook a study to determine the incidence of brain metastases in oesophageal cancers in the West of Scotland. Methods: Data from all the new patients diagnosed with oesophageal cancer was obtained with permission from the Regional Managed Clinical Network from the years 2011 and 2012 yielding a total of 701 patients. The individual clinical records were examined to ascertain if the patient developed brain metastases on CT/MRI scan, their tumour type and management. Results: Of the 701 patients diagnosed with oesophageal cancer, 19 developed brain metastasis demonstrating an incidence of 2.7%. 12 of these patients primary diagnosis was adenocarcinoma. The others were small cell (3), neuroendocrine (2), squamous (1) and no histology (1). At the time of writing 17 out of 19 patients had died from their oesophageal cancer. The 2 surviving patients had a single brain metastasis that was resected and treated with adjuvant radiotherapy. 6 other patients had whole brain radiotherapy, 1 patient had partial brain radiotherapy and 10 were managed with best supportive care. Mean survival from diagnosis of brain metastasis for best supportive care was 26 +/- 14 days versus mean survival for radiotherapy treatment from 100+/- 57 days (p = 0.003) demonstrating a difference between the groups. Conclusions: The incidence of brain metastasis in oesophageal cancer in the West of Scotland was 2.7% with the prognosis generally poor unless resected.

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Kuo, Min-Hsun, Wen-Wei Chang, Bi-Wen Yeh, Yeh-Shiu Chu, Yueh-Chun Lee, and Hsueh-Te Lee. "Glucose Transporter 3 Is Essential for the Survival of Breast Cancer Cells in the Brain." Cells 8, no. 12 (December 4, 2019): 1568. http://dx.doi.org/10.3390/cells8121568.

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Breast cancer brain metastasis commonly occurs in one-fourth of breast cancer patients and is associated with poor prognosis. Abnormal glucose metabolism is found to promote cancer metastasis. Moreover, the tumor microenvironment is crucial and plays an active role in the metabolic adaptations and survival of cancer cells. Glucose transporters are overexpressed in cancer cells to increase glucose uptake. The glucose transporter 3 (GLUT3) is a high-affinity glucose transporter that is highly expressed in mammalian neurons. GLUT3 is also overexpressed in several malignant brain tumors. However, the role of GLUT3 in breast cancer brain metastasis remains unknown. The results of the present study demonstrated that GLUT3 is highly overexpressed in brain metastatic breast cancers and mediates glucose metabolic reprogramming. Furthermore, knockdown of cAMP-response element binding protein (CREB) could directly regulate GLUT3 expression in brain metastatic breast cancer cells. Notably, we verified and provided a novel role of GLUT3 in mediating glucose metabolism and assisting breast cancer cells to survive in the brain to promote brain metastasis.

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Eldesouki, Salma, Kamel A. Samara, Rama Qadri, Anas A. Obaideen, Ahmad H. Otour, Omar Habbal, and Samrein BM Ahmed. "XIST in Brain Cancer." Clinica Chimica Acta 531 (June 2022): 283–90. http://dx.doi.org/10.1016/j.cca.2022.04.993.

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41

Quader, Sabina, Kazunori Kataoka, and Horacio Cabral. "Nanomedicine for brain cancer." Advanced Drug Delivery Reviews 182 (March 2022): 114115. http://dx.doi.org/10.1016/j.addr.2022.114115.

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Marie, Suely Kazue Nagahashi, and Sueli Mieko Oba Shinjo. "Metabolism and brain cancer." Clinics 66 (2011): 33–43. http://dx.doi.org/10.1590/s1807-59322011001300005.

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43

Milker-Zabel, Stefanie. "Radiosensitizers in Brain Cancer." American Journal of Cancer 5, no. 6 (2006): 363–70. http://dx.doi.org/10.2165/00024669-200605060-00003.

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44

Osborne, Joseph R., Jessica D. Kondraciuk, Samuel L. Rice, Xiaosun Zhou, Andrea Knezevic, Daniel E. Spratt, Mona Sabra, Steven M. Larson, and Ravinder K. Grewal. "Thyroid Cancer Brain Metastasis." Clinical Nuclear Medicine 44, no. 7 (July 2019): 544–49. http://dx.doi.org/10.1097/rlu.0000000000002618.

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45

Grisold, Wolfgang, and Anna Grisold. "Cancer around the brain." Neuro-Oncology Practice 1, no. 1 (March 1, 2014): 13–21. http://dx.doi.org/10.1093/nop/npt002.

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Abstract Background Neuro-oncologists are familiar with primary brain tumors, intracerebral metastases meningeal carcinomatosis and extracerebral intracranial tumors as meningeoma. For these conditions, and also some other rare tumor entities several treatment options exist. Cancer can also involve structures around the brain as the dura, the base of the skull, the cavities of the skull and tissue around the bony skull, the skin, the tissue of the neck. and either compress, invade or spread in the central or peripheral nervous system. Methods A systematic literature research was conducted determining symptoms and signs, tumor sites of nerve invasion, tumor types, diagnostic techniques, mechanisms of nerve invasion, and important differential diagnosis. Additional cases from own experience were added for illustration. Results The mechanisms of tumor invasion of cranial nerves is heterogenous and not only involves several types of invasion, but also spread along the cranial nerves in antero- and retrograde fashion and even spread into different nerve territories via anastomosis. In addition the concept of angiosomas may have an influence on the spread of metastases. Conclusion In addition to the well described tumor spread in meningeal carcinomatosis and base of the skull metastases, dural spread, lesions of the bony skull, the cavities of the skull and skin of the face and tissue of the neck region need to be considered, and have an impact on therapeutic decisions.

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Glatzel, Markus, and Ronald L. Hamilton. "Standardizing Brain Cancer Reporting." Brain Pathology 29, no. 4 (July 2019): 465. http://dx.doi.org/10.1111/bpa.12727.

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Miura, Grant. "Brain cancer: Staying alive." Nature Chemical Biology 11, no. 6 (May 15, 2015): 381. http://dx.doi.org/10.1038/nchembio.1824.

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McCrone, John. "The brain-cancer puzzle." Lancet Neurology 3, no. 4 (April 2004): 256. http://dx.doi.org/10.1016/s1474-4422(04)00716-1.

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Levi, F., and C. La Vecchia. "TRENDS IN BRAIN CANCER." Lancet 334, no. 8668 (October 1989): 917. http://dx.doi.org/10.1016/s0140-6736(89)91573-0.

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Roberts, HJ. "Aspartame and brain cancer." Lancet 349, no. 9048 (February 1997): 362. http://dx.doi.org/10.1016/s0140-6736(05)62868-1.

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