Objective:To explore the therapeutic effects of the novel wild edible mushroom Astraeus hygrometricus(Pers.)Morgan(A.hygrometricus)on human acute lymphoblastic leukemia cells.Methods:Extensive screening of the antipro...Objective:To explore the therapeutic effects of the novel wild edible mushroom Astraeus hygrometricus(Pers.)Morgan(A.hygrometricus)on human acute lymphoblastic leukemia cells.Methods:Extensive screening of the antiproliferative and chemopreventive potential of different extracts from 5 wild mushrooms,A.hygrometricus,Phallus sp.,Lentinus sp.,Tricholoma sp.,and Serpula sp.was performed against a panel of 6 cancer cell lines and normal cells using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT)assay.Apoptosis determination,cell cycle profiling,intracellular reactive oxygen species(ROS)and reactive nitrogen species(RNS),and mitochondrial membrane potential were analyzed by flow cytometry.The activity of caspases was measured colorimetrically,and the expression pattern of mitochondrial proteins was analyzed.Results:The methanol extract of A.hygrometricus and MOLT-4 cells were identified as the most potent extract exhibiting antiproliferative activity and most sensitive cell line,respectively.The mushroom extract induced robust selective apoptosis in MOLT-4 cells and arrested cell cycle progression at the G0/G1 stage.The extract disrupted the mitochondrial membrane potential and enhanced ROS production in MOLT-4 cells.The methanol extract induced apoptosis by downregulating the expression of Bcl-2,increasing the expression of Bax,and activating the caspase cascade.Conclusion:The novel wild edible mushroom is a potential repository of biomolecules for the development of antileukemic drugs.展开更多
AIM: 1) To study the participation of Focal Adhesion Kinase (FAK) in regulation of Breast Cancer cell migration in relation with MMP-9 and other signaling proteins. 2) To study the effect of some natural products on F...AIM: 1) To study the participation of Focal Adhesion Kinase (FAK) in regulation of Breast Cancer cell migration in relation with MMP-9 and other signaling proteins. 2) To study the effect of some natural products on FAK. METHODS: Cell culture, Western Blot, Immunoprecipitation, Immunocytochemistry, Zymography, SiRNA transfection, RT-PCR, Real-Time PCR. RESULTS: For our study on FAK, we selected invasive Breast Cancer cell line MDA-MB-231 and treated the cells with Fibronectin (FN). Treatment of FN was found to increase FAK expression, phosphorylation (Tyr 397). FAK was found to be involved in re- gulation of breast cancer cell migration and MMP-9 expression, activity. Fi-bronectin increases association of FAK with integrin α5β1, Paxillin, Actin, ERK, PI3K and localization at Focal Adhesion sites. FAK was found to be involved in modulation of ERK and PI3K phosphorylation. Moreover, FAK signal was found to be transduced through ERK and PI3K, which modulate MMP-9 and thereby cell migration. CONCLUSION: FAK expression, phosphorylation and processing are induced in response to Cell-ECM interactions. Integrin α5β1 is involved in FN induced FAK phosphorylation. FAK is a potent regulator of MMP-9 expression and activity. FAK is involved in regulation of ERK and PI3K phosphorylation. ERK and PI3K are involved in FAK regulated MMP-9 expression & activity. FAK regulates MMP-9 expression and activity and thereby migration of human breast cancer cell. By the regulation of FAK, cell attachment and migration may be regulated by Curcumin, ATRA or EGCG treatment. It may be concluded that invasive potential of breast cancer cells may be modulated by regulation of FAK.展开更多
Increased MMP-1 expression in various tumor cells is significantly correlated with cancer progression. Enhanced secreted and intracellular level of MMP-1 is found in breast cancer cell line MDA-MB-231 in presence of E...Increased MMP-1 expression in various tumor cells is significantly correlated with cancer progression. Enhanced secreted and intracellular level of MMP-1 is found in breast cancer cell line MDA-MB-231 in presence of ECM glycoprotein fibronectin. To extrapolate this study into in vivo system, we observed the expression of MMP-1, fibronectin and α5β1 integrin, which is the receptor for fibronectin, in breast cancer tissue samples. Expression of active form of MMP-1 was increased in tumor samples compared with the non-tumor counterpart. In some samples pro-MMP-1 was decreased but active form was increased in tumor part. The difference was more prominent in advanced stage tumor. ELISA showed appreciable increase in expression of α5 and β1integrins in tumor tissue in comparison to the non tumor counterpart in case of advanced stage tumor. Though there is no appreciable difference in fibronectin concentration, enhanced α5, β1 integrin expression may mediate enhanced cell-ECM interaction to upregulate MMP-1 in tumor samples compared with the matched control.展开更多
Aim: To study Expression and Phosphorylation status of Focal Adhesion Kinase (FAK) in Human Breast Cancer tissue. To study the relation of FAK with standard clinicopathological parameters of Human Breast Cancer. Metho...Aim: To study Expression and Phosphorylation status of Focal Adhesion Kinase (FAK) in Human Breast Cancer tissue. To study the relation of FAK with standard clinicopathological parameters of Human Breast Cancer. Methods: Tissue collection, Protein extraction, RNA isolation, Western Blot, Immunohistochemistry, RT-PCR, ELISA, Statistical analysis. Results: All the four techniques showed upregulated expression, phosphorylation (Tyr-397) and processing of FAK in human breast cancer tissue compared to the adjacent non-tumor tissue of the same patient. Upregulation of FAK was found to be increased parallely with the advancement of cancer. Localisation of FAK was found to be membrano-cytoplasmic. FAK is upregulated both in protein and mRNA level. Expression and phosphorylation of FAK is increased specifically in the tumor regions compared to the surrounding non-tumor region. Upregulation of FAK was frequently found in ER-positive and PR-positive but Her2/neunegative breast cancer cases. Conclusion: FAK has crucial role in development and progression of human breast cancer. FAK may be considered as an indicator of human breast cancer progression. FAK processing may be considered as an indicator of invasive potential of breast cancer. FAK may be considered as a clinical indicator of human breast cancer development and progression.展开更多
AIM: To evaluate the genotype distribution of hepatitis B virus (HBV) in Eastern India and to clarify the phyloge- netic origin and virological characteristics of the recently identifi ed genotype C in this region. ME...AIM: To evaluate the genotype distribution of hepatitis B virus (HBV) in Eastern India and to clarify the phyloge- netic origin and virological characteristics of the recently identifi ed genotype C in this region. METHODS: Genotype determination, T1762/A1764 mutation in the basal core promoter (BCP) and A1896 mutation in the precore region of 230 subjects were de- termined by restriction fragment length polymorphism method (RFLP) and the result was confi rmed by direct sequencing. RESULTS: The predominant genotypes D (HBV/D) and A (HBV/A) were detected in 131/230 (57%) and 57/230 (25%) samples. In addition, genotype C (HBV/C) was detected in 42/230 (18%) isolates. Surface gene region was sequenced from 45 isolates (27 HBV/C, 9 HBV/A and 9 HBV/D). Phylogenetic analysis revealed that all of the HBV/C sequences clustered with South East Asian subgenotype (HBV/Cs). The sequence data showed re- markable similarity with a Thai strain (AF068756) (99.5% ± 0.4% nucleotide identities) in 90% of the genotype C strains analyzed. T1762/A1764 mutation in BCP re- gion, associated with high ALT was signifi cantly higher in HBeAg negative isolates than HBeAg positive isolates. Frequency of A1896 mutation leading to HBeAg negativ- ity was low.CONCLUSION: The present study reports the genotypic distribution and the characteristics of partial genome sequences of HBV/C isolates from Eastern India. Low genetic diversity and confi nement of HBV/C in Eastern India possibly indicate a recent, limited, spread in this region. Genotype C with T1762/A1764 mutation has been reported to increase the risk for hepatocellular car- cinoma; therefore genotype C carriers in Eastern India should be carefully monitored.展开更多
The present study aimed to detect comparative expression of integrin αVβ3 and its involvement in expression and activation of matrix metalloproteinase-2 (MMP-2) in 25 malignant human breast tumor and adjacent normal...The present study aimed to detect comparative expression of integrin αVβ3 and its involvement in expression and activation of matrix metalloproteinase-2 (MMP-2) in 25 malignant human breast tumor and adjacent normal breast tissues from different clinical TNM stages (DCIS to T4) of the disease and possible involvement of known regulating parameters of MMP-2 like TIMP-2, MT1-MMP and EMPRIN. Integrin αVβ3 was highly expressed in tumors than adjacent normal breast tissues. Pro-MMP-2(72-KD) was mainly expressed in adjacent normal tissues compared to tumors. The mature forms of MMP-2 (68 KD and 64 KD) were found only in tumors. Appreciable expression of TIMP-2 and induction of MT1-MMP and EMPRIN in T2-T4 stages suggested their possible role in MMP-2 activation. Over expression Integrin αVβ3 in tumors than adjacent normal breast tissues was an indication of cancer progression with involvement of integrin signaling. We conclude that, the co-precipitation of MMP-2 with αvβ3 by anti-αv antibody is a strong indication that integrin αvβ3 is a surface receptor for MMP-2 and αvβ3-MMP-2 complex on the surface of tumor cells may play a very important role in determining the invasive property and malignant behavior of tumor tissues. The positive expression of endogenous inhibitor of MMP-2, TIMP-2 may have an appreciable role in activation of this protease and risk of malignancy in advanced stage of the disease. The enhanced expression of MT1-MMP and EMPRIN suggested a role for these factors in gelatinase regulation. However the exact mechanism(s) remains to be investigated. Finally, evaluation of integrin αVβ3 associated MMP-2 expression and activity may add valuable information and can possibly be therapeutic target. The clinical exploitation of integrins will provide oncologists with novel therapeutic strategies for the treatment of malignancy in breast cancer.展开更多
Previous studies have shown that the CC chemokine receptor CCR5 is downregulated on monocyte/macrophage(MO/Mw)surfaces in head and neck squamous cell carcinoma(HNSCC)patients(stage IIIB).Ligands(RANTES,MIP-1a and MIP-...Previous studies have shown that the CC chemokine receptor CCR5 is downregulated on monocyte/macrophage(MO/Mw)surfaces in head and neck squamous cell carcinoma(HNSCC)patients(stage IIIB).Ligands(RANTES,MIP-1a and MIP-1b)of this chemokine receptor were also secreted in lesser quantity from MO/Mw of HNSCC patients in comparison with healthy individuals.In an aim to restore this dysregulated receptor–ligand signaling,we have used neem leaf glycoprotein(NLGP),a novel immunomodulator reported from our laboratory.NLGP upregulated CCR5 expression,as evidenced from studies on MO/Mw of peripheral blood from HNSCC patients as well as healthy individuals.Expression of RANTES,MIP-1a and MIP-1b was also upregulated following NLGP treatment of these cells in vitro.Interestingly,NLGP has little effect on the expression of CCR5 and the ligand RANTES in oral cancer cells.This restored CCR5 receptor–ligand signaling seen in MO/Mw was reflected in improved CCR5-dependent,p38 mitogen-activated protein kinase(MAPK)-mediated migration of MO/Mw after NLGP treatment to a standard chemoattractant.NLGP also induces better antigen presentation and simultaneous costimulation to effector T cells by MO/Mw by upregulating human leucocyte antigen(HLA)-ABC,CD80 and CD86.In addition,NLGP-treated MO/Mw-primed T cells can effectively lyse tumor cells in vitro.The effects of NLGP on monocyte migration and T cell-mediated oral tumor cell killing were further demonstrated in transwell assays with or without CCR5 neutralization.These results suggest a new approach in cancer immunotherapy by modulating dysregulated CCR5 signals from MO/Mw.展开更多
Glioma and cerebral ischemic stroke are two major events that lead to patient death worldwide.Although these conditions have different physiological incidences,~10%of ischemic stroke patients develop cerebral cancer,e...Glioma and cerebral ischemic stroke are two major events that lead to patient death worldwide.Although these conditions have different physiological incidences,~10%of ischemic stroke patients develop cerebral cancer,especially glioma,in the postischemic stages.Additionally,the high proliferation,venous thrombosis and hypercoagulability of the glioma mass increase the significant risk of thromboembolism,including ischemic stroke.Surprisingly,these events share several common pathways,viz.hypoxia,cerebral inflammation,angiogenesis,etc.,but the proper mechanism behind this co-occurrence has yet to be discovered.The hypercoagulability and presence of the D-dimer level in stroke are different in cancer patients than in the noncancerous population.Other factors such as atherosclerosis and coagulopathy involved in the pathogenesis of stroke are partially responsible for cancer,and the reverse is also partially true.Based on clinical and neurosurgical experience,the neuronal structures and functions in the brain and spine are observed to change after a progressive attack of ischemia that leads to hypoxia and atrophy.The major population of cancer cells cannot survive in an adverse ischemic environment that excludes cancer stem cells(CSCs).Cancer cells in stroke patients have already metastasized,but early-stage cancer patients also suffer stroke for multiple reasons.Therefore,stroke is an early manifestation of cancer.Stroke and cancer share many factors that result in an increased risk of stroke in cancer patients,and vice-versa.The intricate mechanisms for stroke with and without cancer are different.This review summarizes the current clinical reports,pathophysiology,probable causes of co-occurrence,prognoses,and treatment possibilities.展开更多
基金indebted toWest Bengal-Department of Science and Technology(1158[Sanc]/ST BT-13015/15/2021-ST SEC)for project funding,University Grants Commission for providing fellowship and contingency to Ribhu Ray,Indian Council of Medical Research for providing fellowship and contingency to Anirban Chouni and UGC-UPE and UGC-CAS program at the Department of Botany,University of Calcutta for financial support.
文摘Objective:To explore the therapeutic effects of the novel wild edible mushroom Astraeus hygrometricus(Pers.)Morgan(A.hygrometricus)on human acute lymphoblastic leukemia cells.Methods:Extensive screening of the antiproliferative and chemopreventive potential of different extracts from 5 wild mushrooms,A.hygrometricus,Phallus sp.,Lentinus sp.,Tricholoma sp.,and Serpula sp.was performed against a panel of 6 cancer cell lines and normal cells using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT)assay.Apoptosis determination,cell cycle profiling,intracellular reactive oxygen species(ROS)and reactive nitrogen species(RNS),and mitochondrial membrane potential were analyzed by flow cytometry.The activity of caspases was measured colorimetrically,and the expression pattern of mitochondrial proteins was analyzed.Results:The methanol extract of A.hygrometricus and MOLT-4 cells were identified as the most potent extract exhibiting antiproliferative activity and most sensitive cell line,respectively.The mushroom extract induced robust selective apoptosis in MOLT-4 cells and arrested cell cycle progression at the G0/G1 stage.The extract disrupted the mitochondrial membrane potential and enhanced ROS production in MOLT-4 cells.The methanol extract induced apoptosis by downregulating the expression of Bcl-2,increasing the expression of Bax,and activating the caspase cascade.Conclusion:The novel wild edible mushroom is a potential repository of biomolecules for the development of antileukemic drugs.
文摘AIM: 1) To study the participation of Focal Adhesion Kinase (FAK) in regulation of Breast Cancer cell migration in relation with MMP-9 and other signaling proteins. 2) To study the effect of some natural products on FAK. METHODS: Cell culture, Western Blot, Immunoprecipitation, Immunocytochemistry, Zymography, SiRNA transfection, RT-PCR, Real-Time PCR. RESULTS: For our study on FAK, we selected invasive Breast Cancer cell line MDA-MB-231 and treated the cells with Fibronectin (FN). Treatment of FN was found to increase FAK expression, phosphorylation (Tyr 397). FAK was found to be involved in re- gulation of breast cancer cell migration and MMP-9 expression, activity. Fi-bronectin increases association of FAK with integrin α5β1, Paxillin, Actin, ERK, PI3K and localization at Focal Adhesion sites. FAK was found to be involved in modulation of ERK and PI3K phosphorylation. Moreover, FAK signal was found to be transduced through ERK and PI3K, which modulate MMP-9 and thereby cell migration. CONCLUSION: FAK expression, phosphorylation and processing are induced in response to Cell-ECM interactions. Integrin α5β1 is involved in FN induced FAK phosphorylation. FAK is a potent regulator of MMP-9 expression and activity. FAK is involved in regulation of ERK and PI3K phosphorylation. ERK and PI3K are involved in FAK regulated MMP-9 expression & activity. FAK regulates MMP-9 expression and activity and thereby migration of human breast cancer cell. By the regulation of FAK, cell attachment and migration may be regulated by Curcumin, ATRA or EGCG treatment. It may be concluded that invasive potential of breast cancer cells may be modulated by regulation of FAK.
文摘Increased MMP-1 expression in various tumor cells is significantly correlated with cancer progression. Enhanced secreted and intracellular level of MMP-1 is found in breast cancer cell line MDA-MB-231 in presence of ECM glycoprotein fibronectin. To extrapolate this study into in vivo system, we observed the expression of MMP-1, fibronectin and α5β1 integrin, which is the receptor for fibronectin, in breast cancer tissue samples. Expression of active form of MMP-1 was increased in tumor samples compared with the non-tumor counterpart. In some samples pro-MMP-1 was decreased but active form was increased in tumor part. The difference was more prominent in advanced stage tumor. ELISA showed appreciable increase in expression of α5 and β1integrins in tumor tissue in comparison to the non tumor counterpart in case of advanced stage tumor. Though there is no appreciable difference in fibronectin concentration, enhanced α5, β1 integrin expression may mediate enhanced cell-ECM interaction to upregulate MMP-1 in tumor samples compared with the matched control.
文摘Aim: To study Expression and Phosphorylation status of Focal Adhesion Kinase (FAK) in Human Breast Cancer tissue. To study the relation of FAK with standard clinicopathological parameters of Human Breast Cancer. Methods: Tissue collection, Protein extraction, RNA isolation, Western Blot, Immunohistochemistry, RT-PCR, ELISA, Statistical analysis. Results: All the four techniques showed upregulated expression, phosphorylation (Tyr-397) and processing of FAK in human breast cancer tissue compared to the adjacent non-tumor tissue of the same patient. Upregulation of FAK was found to be increased parallely with the advancement of cancer. Localisation of FAK was found to be membrano-cytoplasmic. FAK is upregulated both in protein and mRNA level. Expression and phosphorylation of FAK is increased specifically in the tumor regions compared to the surrounding non-tumor region. Upregulation of FAK was frequently found in ER-positive and PR-positive but Her2/neunegative breast cancer cases. Conclusion: FAK has crucial role in development and progression of human breast cancer. FAK may be considered as an indicator of human breast cancer progression. FAK processing may be considered as an indicator of invasive potential of breast cancer. FAK may be considered as a clinical indicator of human breast cancer development and progression.
基金Supported by Indian Council of Medical Research, Government of India. Arup Banerjee and Sibnarayan Datta are recipient of senior research fellowship of the Indian Council of Medical Research and University Grants Commission, Government of India, respectively
文摘AIM: To evaluate the genotype distribution of hepatitis B virus (HBV) in Eastern India and to clarify the phyloge- netic origin and virological characteristics of the recently identifi ed genotype C in this region. METHODS: Genotype determination, T1762/A1764 mutation in the basal core promoter (BCP) and A1896 mutation in the precore region of 230 subjects were de- termined by restriction fragment length polymorphism method (RFLP) and the result was confi rmed by direct sequencing. RESULTS: The predominant genotypes D (HBV/D) and A (HBV/A) were detected in 131/230 (57%) and 57/230 (25%) samples. In addition, genotype C (HBV/C) was detected in 42/230 (18%) isolates. Surface gene region was sequenced from 45 isolates (27 HBV/C, 9 HBV/A and 9 HBV/D). Phylogenetic analysis revealed that all of the HBV/C sequences clustered with South East Asian subgenotype (HBV/Cs). The sequence data showed re- markable similarity with a Thai strain (AF068756) (99.5% ± 0.4% nucleotide identities) in 90% of the genotype C strains analyzed. T1762/A1764 mutation in BCP re- gion, associated with high ALT was signifi cantly higher in HBeAg negative isolates than HBeAg positive isolates. Frequency of A1896 mutation leading to HBeAg negativ- ity was low.CONCLUSION: The present study reports the genotypic distribution and the characteristics of partial genome sequences of HBV/C isolates from Eastern India. Low genetic diversity and confi nement of HBV/C in Eastern India possibly indicate a recent, limited, spread in this region. Genotype C with T1762/A1764 mutation has been reported to increase the risk for hepatocellular car- cinoma; therefore genotype C carriers in Eastern India should be carefully monitored.
文摘The present study aimed to detect comparative expression of integrin αVβ3 and its involvement in expression and activation of matrix metalloproteinase-2 (MMP-2) in 25 malignant human breast tumor and adjacent normal breast tissues from different clinical TNM stages (DCIS to T4) of the disease and possible involvement of known regulating parameters of MMP-2 like TIMP-2, MT1-MMP and EMPRIN. Integrin αVβ3 was highly expressed in tumors than adjacent normal breast tissues. Pro-MMP-2(72-KD) was mainly expressed in adjacent normal tissues compared to tumors. The mature forms of MMP-2 (68 KD and 64 KD) were found only in tumors. Appreciable expression of TIMP-2 and induction of MT1-MMP and EMPRIN in T2-T4 stages suggested their possible role in MMP-2 activation. Over expression Integrin αVβ3 in tumors than adjacent normal breast tissues was an indication of cancer progression with involvement of integrin signaling. We conclude that, the co-precipitation of MMP-2 with αvβ3 by anti-αv antibody is a strong indication that integrin αvβ3 is a surface receptor for MMP-2 and αvβ3-MMP-2 complex on the surface of tumor cells may play a very important role in determining the invasive property and malignant behavior of tumor tissues. The positive expression of endogenous inhibitor of MMP-2, TIMP-2 may have an appreciable role in activation of this protease and risk of malignancy in advanced stage of the disease. The enhanced expression of MT1-MMP and EMPRIN suggested a role for these factors in gelatinase regulation. However the exact mechanism(s) remains to be investigated. Finally, evaluation of integrin αVβ3 associated MMP-2 expression and activity may add valuable information and can possibly be therapeutic target. The clinical exploitation of integrins will provide oncologists with novel therapeutic strategies for the treatment of malignancy in breast cancer.
基金supports from the Indian Council of Medical Research,New Delhi(Grant Nos.3/2/2/131/2007/NCD-III and Immuno/18/11/08/2006-ECD-I)University Grant Commission,New Delhi(Grant No.F.2-3/2000(SA-1)to AB and TC)are acknowledged.
文摘Previous studies have shown that the CC chemokine receptor CCR5 is downregulated on monocyte/macrophage(MO/Mw)surfaces in head and neck squamous cell carcinoma(HNSCC)patients(stage IIIB).Ligands(RANTES,MIP-1a and MIP-1b)of this chemokine receptor were also secreted in lesser quantity from MO/Mw of HNSCC patients in comparison with healthy individuals.In an aim to restore this dysregulated receptor–ligand signaling,we have used neem leaf glycoprotein(NLGP),a novel immunomodulator reported from our laboratory.NLGP upregulated CCR5 expression,as evidenced from studies on MO/Mw of peripheral blood from HNSCC patients as well as healthy individuals.Expression of RANTES,MIP-1a and MIP-1b was also upregulated following NLGP treatment of these cells in vitro.Interestingly,NLGP has little effect on the expression of CCR5 and the ligand RANTES in oral cancer cells.This restored CCR5 receptor–ligand signaling seen in MO/Mw was reflected in improved CCR5-dependent,p38 mitogen-activated protein kinase(MAPK)-mediated migration of MO/Mw after NLGP treatment to a standard chemoattractant.NLGP also induces better antigen presentation and simultaneous costimulation to effector T cells by MO/Mw by upregulating human leucocyte antigen(HLA)-ABC,CD80 and CD86.In addition,NLGP-treated MO/Mw-primed T cells can effectively lyse tumor cells in vitro.The effects of NLGP on monocyte migration and T cell-mediated oral tumor cell killing were further demonstrated in transwell assays with or without CCR5 neutralization.These results suggest a new approach in cancer immunotherapy by modulating dysregulated CCR5 signals from MO/Mw.
基金This work was supported by grants received from DST(NanoMission:DST/NM/NT/2018/105(G)&SR/NM/NS-1058/2015,and SERB:EMR/2017/000992/HS)Govt.of India.
文摘Glioma and cerebral ischemic stroke are two major events that lead to patient death worldwide.Although these conditions have different physiological incidences,~10%of ischemic stroke patients develop cerebral cancer,especially glioma,in the postischemic stages.Additionally,the high proliferation,venous thrombosis and hypercoagulability of the glioma mass increase the significant risk of thromboembolism,including ischemic stroke.Surprisingly,these events share several common pathways,viz.hypoxia,cerebral inflammation,angiogenesis,etc.,but the proper mechanism behind this co-occurrence has yet to be discovered.The hypercoagulability and presence of the D-dimer level in stroke are different in cancer patients than in the noncancerous population.Other factors such as atherosclerosis and coagulopathy involved in the pathogenesis of stroke are partially responsible for cancer,and the reverse is also partially true.Based on clinical and neurosurgical experience,the neuronal structures and functions in the brain and spine are observed to change after a progressive attack of ischemia that leads to hypoxia and atrophy.The major population of cancer cells cannot survive in an adverse ischemic environment that excludes cancer stem cells(CSCs).Cancer cells in stroke patients have already metastasized,but early-stage cancer patients also suffer stroke for multiple reasons.Therefore,stroke is an early manifestation of cancer.Stroke and cancer share many factors that result in an increased risk of stroke in cancer patients,and vice-versa.The intricate mechanisms for stroke with and without cancer are different.This review summarizes the current clinical reports,pathophysiology,probable causes of co-occurrence,prognoses,and treatment possibilities.
