Relevant bibliographies by topics / Brain cancer

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Brain cancer'

Author: Grafiati
Published: 4 June 2021
Last updated: 29 July 2024

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Journal articles on the topic "Brain cancer"

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

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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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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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Dissertations / Theses on the topic "Brain cancer"

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Shelton, Laura Marie. "Targeting Energy Metabolism in Brain Cancer." Thesis, Boston College, 2010. http://hdl.handle.net/2345/1183.

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Thesis advisor: Thomas N. Seyfried
It has long been posited that all cancer cells are dependent on glucose for energy, termed the "Warburg Effect". As a result of an irreversible injury to the mitochondria, cancer cells are less efficient in aerobic respiration. Therefore, calorie restriction was thought to be a natural way to attenuate tumor growth. Calorie restriction lowers blood glucose, while increasing the circulation of ketone bodies. Ketone bodies are metabolized via oxidative phosphorylation in the mitochondria. Only cells that are metabolically capable of aerobic respiration will thus be able to acquire energy from ketone bodies. To date, calorie restriction has been shown to greatly reduce tumor growth and angiogenesis in the murine CT2A, EPEN, and human U87 brain tumor models. Using the novel VM-M3 model for invasive brain cancer and systemic metastatic cancer, I found that though calorie restriction had some efficacy in reducing brain tumor invasion and primary tumor size, metastatic spread was unaffected. Using a bioluminescent-based ATP assay, I determined the viability of metastatic mouse VM-M3 tumor cells grown in vitro in serum free medium in the presence of glucose alone (25 mM), glutamine alone (4 mM), or in glucose + glutamine. The VM-M3 cells could not survive on glucose alone, but could survive in glutamine alone indicating an absolute requirement for glutamine in these metastatic tumor cells. Glutamine could also maintain viability in the absence of glucose and in the presence of the F1 ATPase inhibitor oligomycin. Glutamine could not maintain viability in the presence of the Krebs (TCA) cycle enzyme inhibitor, 3-nitropropionic acid. The data indicate that glutamine can provide ATP for viability in the metastatic VM-M3 cells through Krebs cycle substrate level phosphorylation in the absence of energy from either glycolysis or oxidative phosphorylation. I therefore developed a metabolic therapy that targeted both glucose and glutamine metabolism using calorie restriction and 6-diazo-5-oxo-L-norleucine (DON), a glutamine analog. Primary tumor growth was about 20-fold less in DON treated mice than in untreated control mice. I also found that DON treatment administered alone or in combination with CR inhibited metastasis to liver, lung, and kidney as detected by bioluminescence imaging and histology. Although DON treatment alone did not reduce the incidence of tumor metastasis to spleen compared to the controls, DON administered together with CR significantly reduced the incidence of metastasis to the spleen, indicating a diet/drug synergy. In addition, the phagocytic capabilities of the VM-M3 tumor cells were enhanced during times of energy stress. This allowed for the digestion of engulfed material to be used in energy production. My data provide proof of concept that metabolic therapies targeting both glucose and glutamine metabolism can manage systemic metastatic cancer. Additionally, due to the phagocytic properties of the VM-M3 cell line also seen in a number of human metastatic cancers, I suggest that a unique therapy targeting metabolism and phagocytosis will be required for effective management of metastatic cancer
Thesis (PhD) — Boston College, 2010
Submitted to: Boston College. Graduate School of Arts and Sciences
Discipline: Biology
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Oosterhout, Anselmus Gerardus Maria van. "Small cell lung cancer and brain metastasis." Maastricht : Maastricht : Rijksuniversiteit Limburg ; University Library, Maastricht University [Host], 1995. http://arno.unimaas.nl/show.cgi?fid=6643.

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Boltman, Taahirah. "Liposomal drug delivery to brain cancer cells." University of the Western Cape, 2015. http://hdl.handle.net/11394/4706.

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Master of Science (Nanoscience)
Neuroblastomas (NBs) are the most common solid extra-cranial tumours diagnosed in childhood and characterized by a high risk of tumour relapse. Like in other tumour types, there are major concerns about the specificity and safety of available drugs used for the treatment of NBs, especially because of potential damage to the developing brain. Many plant-derived bioactive compounds have proved effective for cancer treatment but are not delivered to tumour sites in sufficient amounts due to compromised tumour vasculature characterized by leaky capillary walls. Betulinic acid (BetA) is one such naturally-occurring anti-tumour compound with minimum to no cytotoxic effects in healthy cells and rodents. BetA is however insoluble in water and most aqueous solutions, thereby limiting its therapeutic potential as a pharmaceutical product. Liposomes are self-assembling closed colloidal structures composed of one or more concentric lipid bilayers surrounding a central aqueous core. The unique ability of liposomes to entrap hydrophilic molecules into the core and hydrophobic molecules into the bilayers renders them attractive for drug delivery systems. Cyclodextrins (CDs) are non-reducing cyclic oligosaccharides which proximate a truncated core, with features of a hydrophophilic outer surface and hydrophobic inner cavity for forming host-guest inclusion complexes with poorly water soluble molecules. CDs and liposomes have recently gained interest as novel drug delivery vehicles by allowing lipophilic/non-polar molecules into the aqueous core of liposomes, hence improving the therapeutic load, bioavailability and efficacy of many poorly water-soluble drugs. The aim of the study was to develop nano-drug delivery systems for BetA in order to treat human neuroblastoma (NB) cancer cell lines. This was achieved through the preparation of BetA liposomes (BetAL) and improving the percent entrapment efficiency (% EE) of BetA in liposomes through double entrapment of BetA and gamma cyclodextrin BetA inclusion complex (γ-CD-BetA) into liposomes (γ-CD-BetAL). We hypothesized that the γ-CD-BetAL would produce an increased % EE compared to BetAL, hence higher cytotoxic effects. Empty liposomes (EL), BetAL and γ-CD-BetAL were synthesized using the thin film hydration method followed by manual extrusion. Spectroscopic and electron microscopic characterization of these liposome formulations showed size distributions of 1-4 μm (before extrusion) and less than 200 nm (after extrusion). As the liposome size decreased, the zeta-potential (measurement of liposome stability) decreased contributing to a less stable liposomal formulation. Low starting BetA concentrations were found to be more effective in entrapping higher amounts of BetA in liposomes while the incorporation of γ-CD-BetA into liposomes enhanced the % EE when compared to BetAL, although this was not statistically significant. Cell viability studies using the WST-1 assay showed a time-and concentration-dependent decrease in SK-N-BE(2) and Kelly NB cell lines exposed to free BetA, BetAL and γ-CD-BetAL at concentrations of 5-20 ug/ml for 24, 48 and 72 hours treatment durations. The observed cytotoxicity of liposomes was dependant on the % EE of BetA. The γ-CD-BetAL was more effective in reducing cell viability in SK-N-BE(2) cells than BetAL whereas BetAL was more effective in KELLY cells at 48-72 hours. Exposure of all cells to EL showed no toxicity while free BetA was more effective overall than the respective liposomal formulations. The estimated IC₅₀ values following exposure to free BetA and BetAL were similar and both showed remarkable statistically significant decrease in NB cell viability, thus providing a basis for new hope in the effective treatment of NBs.
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Isham, L. "Quality of life in paediatric brain cancer." Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1445605/.

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This paper reviews the recent literature on quality of life (QOL) in survivors of paediatric brain tumours. QOL is defined as comprising three domains (physical, emotional and social), and studies investigating single or multiple domains are included. A psychological perspective is taken on QOL whereby it is the degree to which circumstances relating to these domains are distressing or problematic for the individual that is considered key, rather than the circumstances themselves. A total of 23 studies are reviewed and findings are presented in terms of overall QOL, physical QOL, emotional QOL and social QOL. Overall, paediatric brain-tumour survivors appear to be at risk of reduced QOL both when compared to population norms and to other paediatric cancer-populations. Possible risk factors are discussed but fiirther research is needed before definitive conclusions can be reached. Methodological limitations observed in the literature are considered and directions for future research are proposed. In particular, the need for more theory-driven studies is highlighted.
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Kiebish, Michael Andrew. "Mitochondrial lipidome and genome alterations in mouse brain and experimental brain tumors." Thesis, Boston College, 2008. http://hdl.handle.net/2345/27.

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Thesis advisor: Thomas N. Seyfried
Mitochondria are the key regulators of the bioenergetic state of the cell. Damage to mitochondrial protein, DNA, or membrane lipids can result as the cause or affect of disease pathology. Regardless, this damage can impair mitochondrial function resulting in a decreased ability to produce ATP to support cellular viability. This thesis research examined the mitochondrial lipidome by shotgun lipidomics in different populations of C57BL/6J (B6) brain mitochondria (non-synaptic and synaptic) and correlated lipid changes to differences in electron transport chain (ETC) activities. Furthermore, a comparison was made for non-synaptic mitochondria between the B6 and the VM mouse strain. The VM strain has a 1.5% incidence of spontaneous brain tumors, which is 210 fold greater than the B6 strain. I determined that differences in the brain mitochondrial lipidome existed in the VM strain compared to the B6 strain, likely corresponding to an increased rate of spontaneous brain tumor formation. Analysis of the mitochondrial genome in the CT-2A, EPEN, VM-NM1, and VM-M3 brain tumors compared to their syngeneic controls mouse strains, C57BL/6J (B6) and VM mice, was examined to determine if mutations existed in experimental brain cancer models. No pathogenic mtDNA mutations were discovered that would likely cause a decrease in the mitochondrial functionality. A novel hypothesis was devised to examine the tumor mitochondrial lipidome to determine if quantitative or molecular species differences existed that could potentially alter the functionality of the ETC. Brain tumor mitochondria were examined from tumors grown in vivo as well as in vitro. Numerous lipid differences were found in the mitochondria of brain tumors, of which the most interesting involved the unique molecular speciation of cardiolipin. ETC activities were significantly decreased in the primary ETC complexes which contribute protons to the gradient as well as the linked complexes of brain tumor mitochondria compared to controls. Taken together, it is likely that differences in the mitochondrial lipidome of brain tumors results in severe impairment of the mitochondria’s ability to produce ATP through the ETC. This research has provided a new understanding of the role of mitochondrial lipids in brain as well as brain cancer and offers an alternative explanation for metabolic dysfunction in cancer
Thesis (PhD) — Boston College, 2008
Submitted to: Boston College. Graduate School of Arts and Sciences
Discipline: Biology
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Rivera, Maricruz. "MOLECULAR MECHANISMS OF STRESS RESPONSE IN BRAIN CANCER." Case Western Reserve University School of Graduate Studies / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=case1445956088.

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Dudley, Alix. "DRR regulates the activation of AKT kinase in brain cancer." Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=110452.

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Brain cancer invasion is a leading cause of treatment failure yet there are no therapies to prevent invasion. In developing therapeutic strategies, we must first identify the molecular mechanisms that regulate this event. We previously identified downregulated in renal cell carcinoma (DRR) as a promoter of invasion that augments focal adhesion turnover in malignant glial cells. We continued to investigate the molecular mechanisms that underlie this invasion by examining cell signaling in the context of DRR. We found that AKT phosphorylation (Ser473, Thr308) is elevated in DRR-over-expressing cells compared to control. Through a series of molecular and pharmacologic techniques, we selectively targeted AKT inputs in order to identify how DRR regulates its activation. We demonstrated that phospho-AKT is recruited to focal adhesions and is activated in an adhesion, SRC-family kinase (SFK), phosphoinositide-3-kinase (PI3K)-dependent and epidermal growth factor receptor (EGFR)-independent manner. We concluded our work by testing the relevance of our model in a 3D invasion assay. Our results demonstrated that SFK but not EGFR inhibition significantly prevents DRR-induced invasion. Together, these findings support a model by which DRR regulates AKT activity to drive malignant glial cell invasion.
L'invasion des cellules cancéreuses est la principale cause d'échec des traitements des gliomes car il n'existe actuellement aucune thérapie permettant de bloquer ce processus. Afin de développer des stratégies thérapeutiques efficaces, il apparaît donc essentiel d'identifier les mécanismes moléculaires régulant la migration de ces cellules. Nous avons précédemment montré que la protéine 'downregulated in renal cell carcinoma' (DRR) contribue à l'invasion des cellules gliales malignes en augmentant le renouvellement de leurs complexes d'adhésion focaux. Nous avons poursuivi cette étude par l'analyse des voies de signalisation impliquées dans ce processus et nous avons tout d'abord mis en évidence une augmentation de la phosphorylation d'AKT (Ser473, Thr308) dans les cellules surexprimant DRR. Par une combinaison d'approches moléculaires et pharmacologiques, nous avons alors étudié spécifiquement le rôle de DRR dans l'activation d'AKT et avons démontré que la forme phosphorylée d'AKT est localisée au sein des complexes d'adhésion focaux. Nous avons également mis en évidence que son activation est régulée par SRC, membre de la famille des protéines tyrosine kinase (PTK), et par phosphatidylinositol-3-kinase (PI3K), indépendamment du récepteur à l'EGF. Enfin, nous avons validé notre modèle dans un système d'invasion en trois dimensions ou nous avons montré que l'inhibition spécifique de SRC bloque significativement l'invasion des cellules induite par DRR.L'ensemble de ces résultats nous permet finalement de proposer un modèle selon lequel l'invasion des cellules malignes gliales est régulée par l'activation de la protéine AKT par DRR.
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Walker, William Harry II. "Effects of Breast Cancer and Chemotherapy on Brain and Behavior." The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu1541942974196214.

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Paglia, Simona <1989&gt. "Development and characterisation of a neurogenic model of brain cancer." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2021. http://amsdottorato.unibo.it/9936/2/Simona%20Paglia%20PhD%20thesis.pdf.

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Primary glioblastoma (GB), the most common and aggressive adult brain tumour, is refractory to conventional therapies and characterised by poor prognosis. GB displays striking cellular heterogeneity, with a sub-population, called Glioblastoma Stem Cells (GSCs), intrinsically resistant to therapy, hence the high rate of recurrence. Alterations of the tumour suppressor gene PTEN are prevalent in primary GBM, resulting in the inhibition of the polarity protein Lgl1 due to aPKC hyperactivation. Dysregulation of this molecular axis is one of the mechanisms involved in GSC maintenance. After demonstrating that the PTEN/aPKC/Lgl axis is conserved in Drosophila, I deregulated it in different cells populations of the nervous system in order to individuate the cells at the root of neurogenic brain cancers. This analysis identified the type II neuroblasts (NBs) as the most sensitive to alterations of this molecular axis. Type II NBs are a sub-population of Drosophila stem cells displaying a lineage similar to that of the mammalian neural stem cells. Following aPKC activation in these stem cells, I obtained an adult brain cancer model in Drosophila that summarises many phenotypic traits of human brain tumours. Fly tumours are indeed characterised by accumulation of highly proliferative immature cells and keep growing in the adult leading the affected animals to premature death. With the aim to understand the role of cell polarity disruption in this tumorigenic process I carried out a molecular characterisation and transcriptome analysis of brain cancers from our fly model. In summary, the model I built and partially characterised in this thesis work may help deepen our knowledge on human brain cancers by investigating many different aspects of this complicate disease.
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Khong, Pek-Lan. "Diffusion tensor MR imaging in the evaluation of treatment-induced white matter injury in childhood cancer survivors." Click to view the E-thesis via HKUTO, 2006. http://sunzi.lib.hku.hk/hkuto/record/B38320666.

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Books on the topic "Brain cancer"

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Michael, Prados, and American Cancer Society, eds. Brain cancer. Hamilton, Ont: B.C. Decker, 2002.

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H, Goldfarb Ronald, ed. Brain tumor invasiveness. Dordrecht: Kluwer Academic, 1994.

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Hayat, M. A. Methods of Cancer Diagnosis, Therapy, and Prognosis: Brain Cancer. Dordrecht: Springer Science+Business Media B.V., 2010.

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1930-, Nagai M., and Japanese Conference on Brain Tumor Research and Therapy (3rd : 1994 : Nasu-machi, Japan), eds. Brain tumor: Research and therapy. Tokyo: Springer, 1996.

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R, Kleinberg Lawrence, ed. Brain metastasis: A multidisciplinary approach. New York, NY: Demos, 2009.

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1959-, Mikkelsen Tom, ed. Brain tumor invasion: Biological, clinical, and therapeutic considerations. New York: Wiley-Liss, 1998.

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Peter, Chambers, and BACUP, eds. Understanding brain tumours. London: BACUP, 1994.

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Ebrahimi, Meysam. Nano Drug Delivery to Brain Cancer: Medicine to help treat cancer. Saarbrücken: LAP LAMBERT Academic Publishing, 2017.

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Alessandro, Olivi, ed. Johns Hopkins patients' guide to brain cancer. Sudbury, Mass: Jones & Bartlett Learning, 2012.

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Freedman, Jeri. Brain cancer: Current and emerging trends in detection and treatment. New York: Rosen, 2008.

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Book chapters on the topic "Brain cancer"

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Zhong, Yi. "Brain Cancer." In Alternative and Complementary Therapies for Cancer, 351–67. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-1-4419-0020-3_14.

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Dunn, William D., and Rivka R. Colen. "Brain cancer." In Radiomics and Radiogenomics, 203–27. Boca Raton, FL : CRC Press, Taylor & Francis Group, [2019] |: Chapman and Hall/CRC, 2019. http://dx.doi.org/10.1201/9781351208277-13.

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Hareem, Salwa, Vigneswar Reddy Ashireddygari, Prasad Tammineni, and Rama Krishna Kancha. "Brain Cancer." In Biomedical Aspects of Solid Cancers, 183–200. Singapore: Springer Nature Singapore, 2024. http://dx.doi.org/10.1007/978-981-97-1802-3_16.

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Dolgushin, Mikhail, Valery Kornienko, and Igor Pronin. "Testicular Cancer." In Brain Metastases, 279–81. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-57760-9_21.

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Dolgushin, Mikhail, Valery Kornienko, and Igor Pronin. "Ovarian Cancer." In Brain Metastases, 295–302. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-57760-9_23.

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Dolgushin, Mikhail, Valery Kornienko, and Igor Pronin. "Thyroid Cancer." In Brain Metastases, 303–8. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-57760-9_24.

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Dolgushin, Mikhail, Valery Kornienko, and Igor Pronin. "Lung Cancer (LC)." In Brain Metastases, 99–141. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-57760-9_12.

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Dolgushin, Mikhail, Valery Kornienko, and Igor Pronin. "Breast Cancer (BC)." In Brain Metastases, 143–78. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-57760-9_13.

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Dolgushin, Mikhail, Valery Kornienko, and Igor Pronin. "Colorectal Cancer (CRC)." In Brain Metastases, 233–51. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-57760-9_16.

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Dolgushin, Mikhail, Valery Kornienko, and Igor Pronin. "Stomach Cancer (SC)." In Brain Metastases, 253–62. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-57760-9_17.

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Conference papers on the topic "Brain cancer"

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"Brain Tumor Detection Using Deep Convolutional Neural Network." In The International Conference on scientific innovations in Science, Technology, and Management. International Journal of Advanced Trends in Engineering and Management, 2023. http://dx.doi.org/10.59544/poda4062/ngcesi23p130.

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Brain tumor is the third-most common cause of cancer related deaths in the world. Fortunately, it can be detected using MRI. Computer-aided diagnosis (CADx) systems can help clinicians identify cancer from brain diseases more accurately. In this project, propose a CAD system that distinguishes and classifies brain tumor from pre-cancerous conditions. The system uses a deplearning model. Deep CNN which involves depth wise separable convolutions, to classify cancer and non-cancers. The proposed method consist of two steps: Google’s Auto Augment for augmentation and the CV2 based feature selection for image segmentation during pre- processing. These approaches produce a feasible methods of distinguishing and classifying cancers from other brain diseases. Our methods are fully automated without the manual specification of region-of-interests for the test and with a random selection of images for model training. This methodology may play a crucial role in selecting effective treatment options without the need for a surgical biopsy.
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"Progesterone and Brain Cancer." In 4th International Conference on Advances in Agricultural, Biological & Ecological Sciences. International Institute of Chemical, Biological & Environmental Engineering (IICBEE), 2016. http://dx.doi.org/10.15242/iicbe.c1216058.

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Stepp, Herbert, Ronald Sroka, and Walter Stummer. "Intra-operative Brain Tumor Imaging." In Cancer Imaging and Therapy. Washington, D.C.: OSA, 2016. http://dx.doi.org/10.1364/cancer.2016.jm2a.1.

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Wang, C., S. Pacheco, B. K. Baggett, M. K. Chawla, D. T. Gray, U. Utzinger, C. A. Barnes, and R. Liang. "Whole brain imaging with a scalable microscope." In Cancer Imaging and Therapy. Washington, D.C.: OSA, 2016. http://dx.doi.org/10.1364/cancer.2016.jw3a.30.

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Leblond, Frederic. "Intraoperative Optical Spectroscopy of Brain Tumors for Guiding Resection." In Cancer Imaging and Therapy. Washington, D.C.: OSA, 2016. http://dx.doi.org/10.1364/cancer.2016.jm2a.4.

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Wang, Tianxiong, Naidi Sun, Rui Cao, Bo Ning, and Song Hu. "High-speed Functional Photoacoustic Microscopy of the Mouse Brain." In Cancer Imaging and Therapy. Washington, D.C.: OSA, 2016. http://dx.doi.org/10.1364/cancer.2016.jw3a.20.

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Leung, Y. Y., C. Q. Chang, Y. S. Hung, and P. C. W. Fung. "Gene selection for Brain Cancer Classification." In Conference Proceedings. Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2006. http://dx.doi.org/10.1109/iembs.2006.260197.

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Leung, Y. Y., C. Q. Chang, Y. S. Hung, and P. C. W. Fung. "Gene selection for Brain Cancer Classification." In Conference Proceedings. Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2006. http://dx.doi.org/10.1109/iembs.2006.4398787.

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Tang, Jianbo, Xianjin Dai, and Huabei Jiang. "Miniaturized Scanning Photoacoustic Imaging for Brain Study in Behaving Rats." In Cancer Imaging and Therapy. Washington, D.C.: OSA, 2016. http://dx.doi.org/10.1364/cancer.2016.jtu3a.28.

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Milej, Daniel, Androu Abdalmalak, Hassan Ahmed, Mamadou Diop, Ting-Yim Lee, and Keith St. Lawrence. "Quantification of blood–brain barrier permeability by time-resolved NIRS." In Cancer Imaging and Therapy. Washington, D.C.: OSA, 2016. http://dx.doi.org/10.1364/cancer.2016.ptu3a.2.

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Reports on the topic "Brain cancer"

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Marchetti, Dario. Heparanase Mechanisms in Brain-metastatic Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2013. http://dx.doi.org/10.21236/ada585985.

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Marchetti, Dario. Heparanase Mechanisms in Brain-Metastatic Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, November 2013. http://dx.doi.org/10.21236/ada596541.

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Marchetti, Dario. Heparanase Mechanisms in Brain - Metastatic Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2012. http://dx.doi.org/10.21236/ada560853.

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Price, Janet E. The Biology of Breast Cancer in Brain Metastasis. Fort Belvoir, VA: Defense Technical Information Center, April 2001. http://dx.doi.org/10.21236/ada395698.

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Alex Rossi, Alex Rossi. How Do Fats Help Us Treat Brain Cancer? Experiment, May 2014. http://dx.doi.org/10.18258/2648.

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Song, Yaowen, Shuiyu Lin, Jun Chen, Silu Ding, and Jun Dang. First-line treatment with TKI plus brain radiotherapy vs TKI alone in EGFR-mutated non-small-cell lung cancer with brain metastases: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2023. http://dx.doi.org/10.37766/inplasy2023.1.0013.

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Review question / Objective: It remains uncertain whether first-line treatment with upfront brain radiotherapy (RT) in combination with epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) is superior to EGFR-TKIs alone in EGFR-mutated non-small-cell lung cancer with newly diagnosed brain metastases (BMs). We performed a meta-analysis to address this issue. Condition being studied: Brain radiotherapy (RT) has been shown to damage the blood-brain barrier (BBB) and improve the concentration of EGFR-TKIs in the CSF. Additionally, RT can result in a reduction of EGFR-TKIs resistance. Therefore, EGFR-TKIs in combination with brain RT should be more effective than EGFR-TKIs alone theoretically. However, results from retrospective studies are inconsistent. There is the possibility that patients characteristics or brain RT technique affect the efficacy of treatments. To date, there is still no randomized controlled trials (RCTs) comparing the two treatment strategies.
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Garsa, Adam, Julie K. Jang, Sangita Baxi, Christine Chen, Olamigoke Akinniranye, Owen Hall, Jody Larkin, Aneesa Motala, Sydne Newberry, and Susanne Hempel. Radiation Therapy for Brain Metasases. Agency for Healthcare Research and Quality (AHRQ), June 2021. http://dx.doi.org/10.23970/ahrqepccer242.

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Objective. This evidence report synthesizes the available evidence on radiation therapy for brain metastases. Data sources. We searched PubMed®, Embase®, Web of Science, Scopus, CINAHL®, clinicaltrials.gov, and published guidelines in July 2020; assessed independently submitted data; consulted with experts; and contacted authors. Review methods. The protocol was informed by Key Informants. The systematic review was supported by a Technical Expert Panel and is registered in PROSPERO (CRD42020168260). Two reviewers independently screened citations; data were abstracted by one reviewer and checked by an experienced reviewer. We included randomized controlled trials (RCTs) and large observational studies (for safety assessments), evaluating whole brain radiation therapy (WBRT) and stereotactic radiosurgery (SRS) alone or in combination, as initial or postoperative treatment, with or without systemic therapy for adults with brain metastases due to non-small cell lung cancer, breast cancer, or melanoma. Results. In total, 97 studies, reported in 190 publications, were identified, but the number of analyses was limited due to different intervention and comparator combinations as well as insufficient reporting of outcome data. Risk of bias varied; 25 trials were terminated early, predominantly due to poor accrual. Most studies evaluated WBRT, alone or in combination with SRS, as initial treatment; 10 RCTs reported on post-surgical interventions. The combination treatment SRS plus WBRT compared to SRS alone or WBRT alone showed no statistically significant difference in overall survival (hazard ratio [HR], 1.09; confidence interval [CI], 0.69 to 1.73; 4 RCTs; low strength of evidence [SoE]) or death due to brain metastases (relative risk [RR], 0.93; CI, 0.48 to 1.81; 3 RCTs; low SoE). Radiation therapy after surgery did not improve overall survival compared with surgery alone (HR, 0.98; CI, 0.76 to 1.26; 5 RCTs; moderate SoE). Data for quality of life, functional status, and cognitive effects were insufficient to determine effects of WBRT, SRS, or post-surgical interventions. We did not find systematic differences across interventions in serious adverse events radiation necrosis, fatigue, or seizures (all low or moderate SoE). WBRT plus systemic therapy (RR, 1.44; CI, 1.03 to 2.00; 14 studies; moderate SoE) was associated with increased risks for vomiting compared to WBRT alone. Conclusion. Despite the substantial research literature on radiation therapy, comparative effectiveness information is limited. There is a need for more data on patient-relevant outcomes such as quality of life, functional status, and cognitive effects.
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Watson, Mark A. Genomic Characterization of Brain Metastasis in Non-Small Cell Lung Cancer Patients. Fort Belvoir, VA: Defense Technical Information Center, January 2014. http://dx.doi.org/10.21236/ada606182.

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Fei, Fan, Yu Fei, Ruxiang Xu, Xiaoling Liao, Yongsheng He, Lina Hao, Zongze He, and Wentao Dong. Lapatinib with whole brain radiotherapy in breast cancer patients with brain metastases: study protocol of a systematic review and pooled analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2020. http://dx.doi.org/10.37766/inplasy2020.12.0089.

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Lin, Lilie. F18 EF5 PET/CT Imaging in Patients with Brain Metastases from Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2014. http://dx.doi.org/10.21236/ada613489.

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