Breast cancer (BC) is the most prevalent malignant disease in females worldwide. Genomic instability in tumor tissue has been associated with tumor progression. These genetic changes may take a variety of forms, including numerical and structural chromosomal abnormalities (CAs), epigenetic changes, and gene expression alterations. Many tumor tissues are made up of genetically different cell populations, and the study of the causes and consequences of this heterogeneity play a central role in cancer research. In this study, CAs in blood and cancer tissues of patients with sporadic BC were examined. Our findings shows that the increase in numerical sex aneuploidy in BC tissues is significantly higher than in blood tissue. These aneuploidy increases in cancer tissues seem to be compatible with the development and increase of cancer, and can play a role in the pathogenesis of cancers. These changes are consistent with early and long-standing exposure to carcinogens, especially estrogens. These findings should clarify our understanding of breast carcinogenesis in breast tissues and promote development of improved methods for risk assessment and BC prevention in women.
{"title":"Cytogenetic differences in blood and cancer tissue samples of the same patient group","authors":"O. Demirhan, D. Korkmaz","doi":"10.31579/2640-1053/070","DOIUrl":"https://doi.org/10.31579/2640-1053/070","url":null,"abstract":"Breast cancer (BC) is the most prevalent malignant disease in females worldwide. Genomic instability in tumor tissue has been associated with tumor progression. These genetic changes may take a variety of forms, including numerical and structural chromosomal abnormalities (CAs), epigenetic changes, and gene expression alterations. Many tumor tissues are made up of genetically different cell populations, and the study of the causes and consequences of this heterogeneity play a central role in cancer research. In this study, CAs in blood and cancer tissues of patients with sporadic BC were examined. Our findings shows that the increase in numerical sex aneuploidy in BC tissues is significantly higher than in blood tissue. These aneuploidy increases in cancer tissues seem to be compatible with the development and increase of cancer, and can play a role in the pathogenesis of cancers. These changes are consistent with early and long-standing exposure to carcinogens, especially estrogens. These findings should clarify our understanding of breast carcinogenesis in breast tissues and promote development of improved methods for risk assessment and BC prevention in women.","PeriodicalId":93018,"journal":{"name":"Journal of cancer research and cellular therapeutics","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43589025","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pembrolizumab has significantly improved outcome of advanced NSCLC. PD-L1 expression has limited utility as a prognostic and predictive biomarker. To improve this several other biomarkers have been evaluated. Useful amongst them are 1. Tumor specific biomarkers include tumor mutation burden, immune cell infiltration (phenotype, genotype, site, type), 2. Changes in cellular, cytokine in peripheral blood. The article provides review of the current status.
{"title":"Response Predictors for Pembrolizumab in Advanced NSCLC beyond PD-L1 Expression","authors":"B. Khamar","doi":"10.31579/2640-1053/056","DOIUrl":"https://doi.org/10.31579/2640-1053/056","url":null,"abstract":"Pembrolizumab has significantly improved outcome of advanced NSCLC. PD-L1 expression has limited utility as a prognostic and predictive biomarker. To improve this several other biomarkers have been evaluated. Useful amongst them are 1. Tumor specific biomarkers include tumor mutation burden, immune cell infiltration (phenotype, genotype, site, type), 2. Changes in cellular, cytokine in peripheral blood. The article provides review of the current status.","PeriodicalId":93018,"journal":{"name":"Journal of cancer research and cellular therapeutics","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41533863","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
In the current study, thermoplasmonic characteristics of Plutonium nanoparticles with spherical, core–shell and rod shapes are investigated. In order to investigate these characteristics, interaction of synchrotron radiation emission as a function of the beam energy and Plutonium nanoparticles were simulated using 3D finite element method. Firstly, absorption and extinction cross sections were calculated. Then, increases in temperature due to synchrotron radiation emission as a function of the beam energy absorption were calculated in Plutonium nanoparticles by solving heat equation. The obtained results show that Plutonium nanorods are more appropriate option for using in optothermal human cancer cells, tissues and tumors treatment method.
{"title":"Simulation of Interaction of Synchrotron Radiation Emission as A Function of the Beam Energy and Plutonium Nanoparticles Using 3d Finite Element Method (Fem) as an Optothermal Human Cancer Cells, Tiss","authors":"A. Heidari, K. Schmitt, M. Henderson, E. Besana","doi":"10.31579/2640-1053/060","DOIUrl":"https://doi.org/10.31579/2640-1053/060","url":null,"abstract":"In the current study, thermoplasmonic characteristics of Plutonium nanoparticles with spherical, core–shell and rod shapes are investigated. In order to investigate these characteristics, interaction of synchrotron radiation emission as a function of the beam energy and Plutonium nanoparticles were simulated using 3D finite element method. Firstly, absorption and extinction cross sections were calculated. Then, increases in temperature due to synchrotron radiation emission as a function of the beam energy absorption were calculated in Plutonium nanoparticles by solving heat equation. The obtained results show that Plutonium nanorods are more appropriate option for using in optothermal human cancer cells, tissues and tumors treatment method.","PeriodicalId":93018,"journal":{"name":"Journal of cancer research and cellular therapeutics","volume":"21 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70017987","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-11-19DOI: 10.14302/issn.2641-7669.ject-19-3040
Abdul Kader Mohiuddin
Many lay people along with some so called “key opinion leaders” have a common slogan “There's no answer for cancer”. Again, mistake delays proper treatment and make situation worse, more often. Compliance is crucial to obtain optimal health outcomes, such as cure or improvement in QoL. Patients may delay treatment or fail to seek care because of high out-of- pocket expenditures. Despite phenomenal development, conventional therapy falls short in cancer management. There are two major hurdles in anticancer drug development: dose-limiting toxic side effects that reduce either drug effectiveness or the QoL of patients and complicated drug development processes that are costly and time consuming. Cancer patients are increasingly seeking out alternative medicine and might be reluctant to disclose its use to their oncology treatment physicians. But there is limited available information on patterns of utilization and efficacy of alternative medicine for patients with cancer. As adjuvant therapy, many traditional medicines shown efficacy against brain, head and neck, skin, breast, liver, pancreas, kidney, bladder, prostate, colon and blood cancers. The literature reviews non-pharmacological interventions used against cancer, published trials, systematic reviews and meta-analyses.
{"title":"Complementary and Alternative Treatments for Cancer Prevention and Cure [Part 1]","authors":"Abdul Kader Mohiuddin","doi":"10.14302/issn.2641-7669.ject-19-3040","DOIUrl":"https://doi.org/10.14302/issn.2641-7669.ject-19-3040","url":null,"abstract":"Many lay people along with some so called “key opinion leaders” have a common slogan “There's no answer for cancer”. Again, mistake delays proper treatment and make situation worse, more often. Compliance is crucial to obtain optimal health outcomes, such as cure or improvement in QoL. Patients may delay treatment or fail to seek care because of high out-of- pocket expenditures. Despite phenomenal development, conventional therapy falls short in cancer management. There are two major hurdles in anticancer drug development: dose-limiting toxic side effects that reduce either drug effectiveness or the QoL of patients and complicated drug development processes that are costly and time consuming. Cancer patients are increasingly seeking out alternative medicine and might be reluctant to disclose its use to their oncology treatment physicians. But there is limited available information on patterns of utilization and efficacy of alternative medicine for patients with cancer. As adjuvant therapy, many traditional medicines shown efficacy against brain, head and neck, skin, breast, liver, pancreas, kidney, bladder, prostate, colon and blood cancers. The literature reviews non-pharmacological interventions used against cancer, published trials, systematic reviews and meta-analyses.","PeriodicalId":93018,"journal":{"name":"Journal of cancer research and cellular therapeutics","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45325642","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lymphomatoid papulosis (LyP) Type E is a recently introduced subtype of LyP presenting with escar-like lesions and characterized with angiocentric invasion of dermal blood vessels by CD30 positive atypical lymphocytes resulting necrosis of their walls. Owing to its considerable histologic characteristics such as dense dermal infiltration of CD30 positive large atypical lymphocytes showing high mitotic activity, and angiodestructive invasion, it is challengible to discriminate LyP Type E to aggressive cutanoues lymphomas.
{"title":"To be a “Lymphomatoid Papulosis Type E” or not to be? That Is a Question","authors":"Yong-Moon Lee","doi":"10.31579/2640-1053/055","DOIUrl":"https://doi.org/10.31579/2640-1053/055","url":null,"abstract":"Lymphomatoid papulosis (LyP) Type E is a recently introduced subtype of LyP presenting with escar-like lesions and characterized with angiocentric invasion of dermal blood vessels by CD30 positive atypical lymphocytes resulting necrosis of their walls. Owing to its considerable histologic characteristics such as dense dermal infiltration of CD30 positive large atypical lymphocytes showing high mitotic activity, and angiodestructive invasion, it is challengible to discriminate LyP Type E to aggressive cutanoues lymphomas.","PeriodicalId":93018,"journal":{"name":"Journal of cancer research and cellular therapeutics","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42426119","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Primary tumor of inferior vena cava with infrarenal, suprarenal and suprahepatic extension.","authors":"A. Reina","doi":"10.31579/2640-1053/034","DOIUrl":"https://doi.org/10.31579/2640-1053/034","url":null,"abstract":"","PeriodicalId":93018,"journal":{"name":"Journal of cancer research and cellular therapeutics","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43491688","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The chromatin remodeling factor chromodomain helicase DNA-binding protein 4 (CHD4) is a core component of the nucleosome remodeling and deacetylase (NuRD) complex. Due to its important role in DNA damage repair, CHD4 has been identified as a key determinant in cancer progression, stem cell differentiation, and T cell and B cell development. Accumulating evidence has revealed that CHD4 can function in NuRD dependent and independent manner in response to DNA damage. Mutations of CHD4 have been shown to diminish its functions, which indicates that interpretation of its mutations may provide tangible benefit for patients. The expression of CHD4 play a dual role in sensitizing cancer cells to chemotherapeutic agents, which provides new insights into the contribution of CHD4 to tumor biology and new therapeutic avenues.
{"title":"The Tale of CHD4 in DNA Damage Response and Chemotherapeutic Response","authors":"Jing Zhang, D. Shih, Shiaw-Yih Lin","doi":"10.31579/2640-1053/052","DOIUrl":"https://doi.org/10.31579/2640-1053/052","url":null,"abstract":"The chromatin remodeling factor chromodomain helicase DNA-binding protein 4 (CHD4) is a core component of the nucleosome remodeling and deacetylase (NuRD) complex. Due to its important role in DNA damage repair, CHD4 has been identified as a key determinant in cancer progression, stem cell differentiation, and T cell and B cell development. Accumulating evidence has revealed that CHD4 can function in NuRD dependent and independent manner in response to DNA damage. Mutations of CHD4 have been shown to diminish its functions, which indicates that interpretation of its mutations may provide tangible benefit for patients. The expression of CHD4 play a dual role in sensitizing cancer cells to chemotherapeutic agents, which provides new insights into the contribution of CHD4 to tumor biology and new therapeutic avenues.","PeriodicalId":93018,"journal":{"name":"Journal of cancer research and cellular therapeutics","volume":"167 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79081014","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
J.A. Enríquez-Castroa, G. Estévez-Díazb, J.G. Segoviano-Parrac
Giant cell tumours (GCT) are usually benign, locally aggressive tumours. They tend to occur in long bones and rarely in small bones, with an incidence rate of 1.2 to 2.4% in the bones of the foot. The objective is to present a unique case in the literature of a GCT that only affected the first cuneiform. We present the case of a 35-year-old male patient seen at Hospital General de México (HGM) with seven months history of pain and increased volume in the medial region of the right foot, with X-ray and MRI images consistent with GCT in first cuneiform of the right foot. The excisional biopsy confirmed GCT. The definitive treatment consisted of curettage, cryotherapy with nitrogen and heterologous bone graft placement. Evolution was satisfactory, with no pain, no volume increase, normal gait and radiographic bone graft integration. Follow-up was at six years.
{"title":"Giant Cell Tumour of the First Cuneiform: Case Study","authors":"J.A. Enríquez-Castroa, G. Estévez-Díazb, J.G. Segoviano-Parrac","doi":"10.31579/2640-1053/053","DOIUrl":"https://doi.org/10.31579/2640-1053/053","url":null,"abstract":"Giant cell tumours (GCT) are usually benign, locally aggressive tumours. They tend to occur in long bones and rarely in small bones, with an incidence rate of 1.2 to 2.4% in the bones of the foot. The objective is to present a unique case in the literature of a GCT that only affected the first cuneiform. We present the case of a 35-year-old male patient seen at Hospital General de México (HGM) with seven months history of pain and increased volume in the medial region of the right foot, with X-ray and MRI images consistent with GCT in first cuneiform of the right foot. The excisional biopsy confirmed GCT. The definitive treatment consisted of curettage, cryotherapy with nitrogen and heterologous bone graft placement. Evolution was satisfactory, with no pain, no volume increase, normal gait and radiographic bone graft integration. Follow-up was at six years.","PeriodicalId":93018,"journal":{"name":"Journal of cancer research and cellular therapeutics","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41325643","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Edward J. Kim, Jasmine C. Huynh, Justin A. Chen, Mili Arora, M. Cho
Inhibition of mitosis is an established therapeutic approach in the treatment of cancer. However, existing drugs that use this mechanism including taxanes cause off-target effects leading to dose-limiting toxicity such as sensory neuropathy. Development of inhibitors of mitosis-specific targets has created the next generation of mitosis inhibitors with the goal of achieving similar anti-tumor efficacy but with less toxicity. Aurora Kinase A is one example of a mitosis-specific target for which multiple drugs have been developed as anti-cancer therapy. Although early preclinical studies have showed on-target effects, clinical development has been slowed by minimal efficacy as monotherapy. However, strategic combinations of Aurora Kinase A inhibition with various targeted drugs has shown promise and led to renewed interest in the potential of inhibiting this mitosis-specific target.
{"title":"Strategic Combinations of Aurora Kinase an Inhibiton with Targeted Drugs for Synergistic Anti-Tumor Effect","authors":"Edward J. Kim, Jasmine C. Huynh, Justin A. Chen, Mili Arora, M. Cho","doi":"10.31579/2640-1053/051","DOIUrl":"https://doi.org/10.31579/2640-1053/051","url":null,"abstract":"Inhibition of mitosis is an established therapeutic approach in the treatment of cancer. However, existing drugs that use this mechanism including taxanes cause off-target effects leading to dose-limiting toxicity such as sensory neuropathy. Development of inhibitors of mitosis-specific targets has created the next generation of mitosis inhibitors with the goal of achieving similar anti-tumor efficacy but with less toxicity. Aurora Kinase A is one example of a mitosis-specific target for which multiple drugs have been developed as anti-cancer therapy. Although early preclinical studies have showed on-target effects, clinical development has been slowed by minimal efficacy as monotherapy. However, strategic combinations of Aurora Kinase A inhibition with various targeted drugs has shown promise and led to renewed interest in the potential of inhibiting this mitosis-specific target.","PeriodicalId":93018,"journal":{"name":"Journal of cancer research and cellular therapeutics","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43249997","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
In the case of cancer, the basic problem is stopping the multiplication of cancer cells. Responsible for this process is part of the defective DNA that determines the rate of cell multiplication in a given tissue. Because this piece of DNA has its length and complex internal structure, a defect may appear in various spots. A particularly sensitive moment is the division of the cell, when the DNA in the chromosomes is divided into two parts. If "carcinogenic substances" occur in the DNA division environment then, a structural defect of DNA is created that determines the continuous multiplication of the cell.
{"title":"Can we win the fight against cancer?","authors":"M. Pawlikowski","doi":"10.31579/2640-1053/010/","DOIUrl":"https://doi.org/10.31579/2640-1053/010/","url":null,"abstract":"In the case of cancer, the basic problem is stopping the multiplication of cancer cells. Responsible for this process is part of the defective DNA that determines the rate of cell multiplication in a given tissue. Because this piece of DNA has its length and complex internal structure, a defect may appear in various spots. A particularly sensitive moment is the division of the cell, when the DNA in the chromosomes is divided into two parts. If \"carcinogenic substances\" occur in the DNA division environment then, a structural defect of DNA is created that determines the continuous multiplication of the cell.","PeriodicalId":93018,"journal":{"name":"Journal of cancer research and cellular therapeutics","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45886870","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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