scholarly journals Pathology of Gliomas and the Role Immunotherapy Plays in Combatting Glioma Proliferation

2021 ◽  
Vol 10 (3) ◽  
Author(s):  
Divya Kothakapa ◽  
Anush Swaminathan

Glioma, a type of tumor arising from the brain and/or spinal cord, is a relatively broad term, encompassing three main types of glial cell tumors: astrocytoma, ependymoma, and oligodendroglioma. A prognosis for a glioma can often be extremely poor, with an overall survival rate of 54.84%. With around 20,000 gliomas being diagnosed each year, it is imperative that effective treatments are developed for management of these tumors. A popular treatment pathway for the treatment of gliomas is surgery along with chemo-radiation therapy such as Temozolomide. This current treatment plan, though, has a moderate effect on lengthening glioma patients’ prognoses. The average survival of this plan is 3 to 6 months. New treatments in the field of immunotherapies may have promising effects for glioma patients’ prognoses. Arising developments in immunotherapy glioma treatment and management is an important field to investigate to further improve the effectivity of cancer treatment for glioma patients. Certain immunotherapies in trials have proven to make impactful improvements to glioma prognoses, one trial showing an increase of 2 months in median survival. This literature review will focus on the pathology and characteristics of the proliferation of malignant glioma cells and the role immunotherapy plays in combatting glioma proliferation

2019 ◽  
Vol 28 ◽  
pp. 01016
Author(s):  
Estera Kot ◽  
Krzysztof Siwek

The paper presents an algorithm of segmentation of brain imaging examination results − computed tomography (CT) and positron emission tomography (PET) − to identify, compute, and visualize the brain tumors. Computer software was developed in the MATLAB environment using active contour methods: Edge and Chan-Vese. A review of the current treatment plan for patients with diagnosed glioblastoma multiforme was included to emphasize the significance of the solved problem. The work presents executed steps in the algorithm with a detailed description of thresholding process. Visual results of tumors were performed and presented.


Author(s):  
Diane Moujalled ◽  
Andreas Strasser ◽  
Jeffrey R. Liddell

AbstractTightly orchestrated programmed cell death (PCD) signalling events occur during normal neuronal development in a spatially and temporally restricted manner to establish the neural architecture and shaping the CNS. Abnormalities in PCD signalling cascades, such as apoptosis, necroptosis, pyroptosis, ferroptosis, and cell death associated with autophagy as well as in unprogrammed necrosis can be observed in the pathogenesis of various neurological diseases. These cell deaths can be activated in response to various forms of cellular stress (exerted by intracellular or extracellular stimuli) and inflammatory processes. Aberrant activation of PCD pathways is a common feature in neurodegenerative diseases, such as amyotrophic lateral sclerosis (ALS), Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease, resulting in unwanted loss of neuronal cells and function. Conversely, inactivation of PCD is thought to contribute to the development of brain cancers and to impact their response to therapy. For many neurodegenerative diseases and brain cancers current treatment strategies have only modest effect, engendering the need for investigations into the origins of these diseases. With many diseases of the brain displaying aberrations in PCD pathways, it appears that agents that can either inhibit or induce PCD may be critical components of future therapeutic strategies. The development of such therapies will have to be guided by preclinical studies in animal models that faithfully mimic the human disease. In this review, we briefly describe PCD and unprogrammed cell death processes and the roles they play in contributing to neurodegenerative diseases or tumorigenesis in the brain. We also discuss the interplay between distinct cell death signalling cascades and disease pathogenesis and describe pharmacological agents targeting key players in the cell death signalling pathways that have progressed through to clinical trials.


2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Zhilan Chen ◽  
Chun Zhang ◽  
Jiu Yin ◽  
Xin Xin ◽  
Hemei Li ◽  
...  

AbstractChina and the rest of the world are experiencing an outbreak of the 2019 novel coronavirus disease (COVID-19). Patients with cancer are more susceptible to viral infection and are more likely to develop severe complications, as compared to healthy individuals. The growing spread of COVID-19 presents challenges for the clinical care of patients with gynecological malignancies. Ovarian debulking surgery combined with the frequent need for chemotherapy is most likely why ovarian cancer was rated as the gynecologic cancer most affected by COVID-19. Therefore, ovarian cancer presents a particular challenging task. Concerning the ovarian cancer studies with confirmed COVID-19 reported from large-scale general hospitals in Wuhan, we hold that the treatment plan was adjusted appropriately and an individualized remedy was implemented. The recommendations discussed here were developed mainly based on the experience from Wuhan. We advise that the management strategy for ovarian cancer patients should be adjusted in the light of the local epidemic situation and formulated according to the pathological type, tumor stage and the current treatment phase. Online medical service is an effective and convenient communication platform during the pandemic.


2021 ◽  
Vol 19 ◽  
Author(s):  
Julieta Saba ◽  
Federico López Couselo ◽  
Julieta Bruno ◽  
Lila Carniglia ◽  
Daniela Durand ◽  
...  

: Huntington’s disease (HD) is a neurodegenerative genetic disorder caused by a CAG repeat expansion in the huntingtin gene. HD causes motor, cognitive, and behavioral dysfunction. Since no existing treatment affects the course of this disease, new treatments are needed. Inflammation is frequently observed in HD patients before symptom onset. Neuroinflammation, characterized by the presence of reactive microglia and astrocytes and inflammatory factors within the brain, is also detected early. However, in comparison with other neurodegenerative diseases, the role of neuroinflammation in HD is much less known. Work has been dedicated to altered microglial and astrocytic functions in the context of HD, but less attention has been given to glial participation in neuroinflammation. This review describes evidence of inflammation in HD patients and animal models. It also discusses recent knowledge on neuroinflammation in HD, highlighting astrocyte and microglia involvement in the disease and considering anti-inflammatory therapeutic approaches.


Author(s):  
Andreas Luft

Recovery after a stroke is a multidimensional process depending on the individual deficit. Within each functional domain, spontaneous recovery occurs to a variable degree and can be improved by specific neurorehabilitative interventions. The knowledge about the neurophysiology of the processes that lead to recovery and render neurorehabilitative interventions effective is scarce. Such knowledge, however, would be necessary to find new treatments that can fully exploit the brain’s capacity for recovery. Animal models can be an experimental platform to investigate these mechanisms. But it has to be realized that they oversimplify the human condition. The complexity of motor, cognitive, social, emotional, and other factors contributing to recovery in humans cannot be modelled in animals. The opportunities and caveats of animal models are discussed.


2019 ◽  
Vol 3 ◽  
pp. 239821281881068 ◽  
Author(s):  
S. Clare Stanford ◽  
David J. Heal

The late 1960s was a heyday for catecholamine research. Technological developments made it feasible to study the regulation of sympathetic neuronal transmission and to map the distribution of noradrenaline and dopamine in the brain. At last, it was possible to explain the mechanism of action of some important drugs that had been used in the clinic for more than a decade (e.g. the first generation of antidepressants) and to contemplate the rational development of new treatments (e.g. l-dihydroxyphenylalanine therapy, to compensate for the dopaminergic neuropathy in Parkinson’s disease, and β1-adrenoceptor antagonists as antihypertensives). The fact that drug targeting noradrenergic and/or dopaminergic transmission are still the first-line treatments for many psychiatric disorders (e.g. depression, schizophrenia, and attention deficit hyperactivity disorder) is a testament to the importance of these neurotransmitters and the research that has helped us to understand the regulation of their function. This article celebrates some of the highlights of research at that time, pays tribute to some of the subsequent landmark studies, and appraises the options for where it could go next.


Author(s):  
E Spinelli ◽  
G Blevins ◽  
J Mailo ◽  
L Atilano ◽  
H Leonard ◽  
...  

Background: Sarcoidosis is a multiorgan autoimmune disease characterized by the presence of non-caseating granulomas. The diagnosis can be difficult, particularly with central nervous system (CNS) involvement, and pathology outside of the CNS has to be carefully evaluated. Early and correct diagnosis is crucial for appropriate management particularly in children where sarcoidosis and neurosarcoidosis are rare. Methods: We describe a 16 year old previously healthy boy who presented with progressive pyramidal neurological signs and symptoms localizable primarily to the brain stem. Results: Initial imaging revealed striking brainstem, as well as cerebral, cerebellar and spinal cord perivascular enhancement. Lung involvement was subclinical with a miliary pattern on chest imaging and needle biopsy revealed an interstitial lymphocytic infiltration. Extensive serum and CSF rheumatological, autoimmune and infectious investigations were noncontributory. Serum ACE levels were at first within normal limits. Steroid treatment stabilized symptoms and perhaps coincidentally, separate rituximab treatments were followed within days by vertigo (with a new pontine lesion) or a respiratory decompensation. A wedge lung biopsy revealed granulomatosis. Current treatment consists of mycophenolate, methotrexate with a prednisone wean. Conclusions: This case report reinforces the varied manifestations and mimics of sarcoidosis (including CLIPPERS) and highlights the need for a high index of suspicion despite apparently negative investigations.


1999 ◽  
Vol 15 (1) ◽  
pp. 207-219 ◽  
Author(s):  
Gisela Kobelt ◽  
Linus Jönsson

Several new topical agents have been introduced recently and it can be expected that the treatment of glaucoma will change, depending on how effectively these agents control intraocular pressure (IOP). IOP is considered the major risk factor in the development of glaucomatous damage. In order to estimate the impact of these new agents on the cost of treating glaucoma, a simulation model was created to estimate the cost of treating patients with a recent diagnosis of primary open-angle glaucoma or ocular hypertension in different countries. The Markov model is based on retrospective chart reviews in different countries and calculates only cost, not outcome. Results are presented for France and the United Kingdom, where current treatment appeared to be comparable. Average one-year costs per patient with current treatment were FF2,389 (US $389) and £380 (US $627), respectively. Costs with the new treatments were lower than with current therapy.


2018 ◽  
Vol 46 (3) ◽  
pp. 1241-1251 ◽  
Author(s):  
Tinghong Ye ◽  
Tingting Wang ◽  
Xiaoxue Yang ◽  
Xiaoli Fan ◽  
Maoyao Wen ◽  
...  

Background/Aims: Autoimmune hepatitis (AIH) is a chronic necroinflammatory disease of the liver whose pathogenic mechanisms have not yet been elucidated. Moreover, the current treatment used for the vast majority of AIH patients is largely dependent on immunosuppressant administration and liver transplantation. However, research on the pathogenesis of AIH and effective new treatments for AIH have been hampered by a lack of animal models that accurately reproduce the human condition. Methods: AIH models created by concanavalin A (ConA) injections at different times and doses. The levels of ALT, AST, LDH and inflammatory cytokines were examined at various times after 20 mg/kg ConA was administered by ELISA using commercially available kits. Moreover, liver pathological changes were observed by flow cytometry (FCM) and H&E staining. Results: Our experiments demonstrated that the levels of ALT, AST, LDH and several inflammatory cytokines, including TNF-α, IFN-γ, and IL-6, were higher in the 20 mg/kg 12 h ConA group than in the other groups. Importantly, the numbers of activated CD4+ and CD8+ T lymphocytes in the blood, spleen and liver were calculated. These results showed that ConA (20 mg/kg for 12 h)-induced hepatitis was similar to that in clinical AIH patients. Furthermore, we found that the number of MDSCs in the blood was significantly increased in the ConA (20 mg/kg for 12 h) group compared with controls. Our findings indicated that ConA (20 mg/kg for 12 h)-induced hepatitis could be used as an experimental murine model that mirrors most of the pathogenic properties of human type I AIH. Conclusion: This model [ConA (20 mg/kg for 12 h)] provides a valuable tool for studying AIH immunopathogenesis and rapidly assessing novel therapeutic approaches.


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