Pub Date : 2019-10-18DOI: 10.31031/nacs.2019.03.000563
C. Gündüz, A. Oğuz
There are two major pathways targeted for the treatment of metastatic renal cell cancer. One is VEGF inhibition that induces tumor shrinkage and increases progression-free survival and the other is Immune checkpoint inhibition that has been shown to increase overall survival. There are two clinically possible ways to block the antiangiogenic (VEGF) pathway. We can use Tyrosine kinase inhibitors (Sunitinib, Pazopanib, Cabozantinib, Axitinib, Sorafenib) that block the intracellular domain of the VEGFR or a monoclonal antibody (Bevacizumab) that binds to circulating VEGF and prevents it from activating VEGFR [1]. Checkpoint inhibition targeting the T lymphocyte-associated antigen 4 (CTLA-4) and/or programmed cell death receptor 1 (PD-1) pathway has led to significant improvements in the treatment of many malignancies, including renal cell carcinoma.
{"title":"Which Way Should be Chosen for Treatment of Metastatic Renal Cell Carcinoma?","authors":"C. Gündüz, A. Oğuz","doi":"10.31031/nacs.2019.03.000563","DOIUrl":"https://doi.org/10.31031/nacs.2019.03.000563","url":null,"abstract":"There are two major pathways targeted for the treatment of metastatic renal cell cancer. One is VEGF inhibition that induces tumor shrinkage and increases progression-free survival and the other is Immune checkpoint inhibition that has been shown to increase overall survival. There are two clinically possible ways to block the antiangiogenic (VEGF) pathway. We can use Tyrosine kinase inhibitors (Sunitinib, Pazopanib, Cabozantinib, Axitinib, Sorafenib) that block the intracellular domain of the VEGFR or a monoclonal antibody (Bevacizumab) that binds to circulating VEGF and prevents it from activating VEGFR [1]. Checkpoint inhibition targeting the T lymphocyte-associated antigen 4 (CTLA-4) and/or programmed cell death receptor 1 (PD-1) pathway has led to significant improvements in the treatment of many malignancies, including renal cell carcinoma.","PeriodicalId":93131,"journal":{"name":"Novel approaches in cancer study","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43952757","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 : 2019-09-30DOI: 10.31031/nacs.2019.03.000562
Shao Yf, Lin Yf, L. Wang, F. Mei, Li Lu
Cancer is one of the main diseases threatening the human life and health. Early recognition is crucial to increase the survival rate of cancer patients. However, current cancer early diagnosis faces many problems. For example, current early clinical diagnostic techniques have low specificity and sensitivity but need high cost. As the progress for the medicine, the new noninvasive and fast cancer early recognition technique has come out, which is of importance to decrease the death rate. Some research results indicate that the cancer patient could emit some special gas [1], and this provides the possibility to utilize the patient’s emission gas for cancer screening, which is noninvasive, simple and sensitive. This diagnostic method has been adopted by using the trained dogs, which have the sensitive sense of smell [2]. And some research results have proven the possibility to use the dogs to realize the early diagnosis for Crimson Publishers Wings to the Research Mini Review
{"title":"Exhaled Breath Analysis for Cancer Diagnosis and Screening","authors":"Shao Yf, Lin Yf, L. Wang, F. Mei, Li Lu","doi":"10.31031/nacs.2019.03.000562","DOIUrl":"https://doi.org/10.31031/nacs.2019.03.000562","url":null,"abstract":"Cancer is one of the main diseases threatening the human life and health. Early recognition is crucial to increase the survival rate of cancer patients. However, current cancer early diagnosis faces many problems. For example, current early clinical diagnostic techniques have low specificity and sensitivity but need high cost. As the progress for the medicine, the new noninvasive and fast cancer early recognition technique has come out, which is of importance to decrease the death rate. Some research results indicate that the cancer patient could emit some special gas [1], and this provides the possibility to utilize the patient’s emission gas for cancer screening, which is noninvasive, simple and sensitive. This diagnostic method has been adopted by using the trained dogs, which have the sensitive sense of smell [2]. And some research results have proven the possibility to use the dogs to realize the early diagnosis for Crimson Publishers Wings to the Research Mini Review","PeriodicalId":93131,"journal":{"name":"Novel approaches in cancer study","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43898907","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 : 2019-09-25DOI: 10.31031/nacs.2019.03.000561
T. Kähkönen, Halleen Jm, J. Bernoulli
Cancer metastases cause high morbidity and mortality in patients. Bone metastases are most common in breast and prostate cancer, but they are also observed in many other cancers such as lung and renal cancer and melanoma [1]. In breast cancer the formation of metastases depends on the tumor subtype, and the major site for metastasis is the skeleton [2]. Patients with bone metastases have a 5-year survival rate of only 21% and a median survival time of 3 years. Prostate cancer is currently described as a bone disease due to high incidence of skeletal metastases. In prostate cancer patients with bone metastases, the 5-year survival rate is about 30% and the median survival time is 3 years [3]. Metastatic cancer patients are treated with conventional cancer therapies that are usually ineffective against bone metastases. Tumor-induced bone loss can also be treated with bone-targeting therapies. Bone marrow is an important immune organ that contains many immune cells, such as myeloid-derived suppressor cells, T cells, B cells and natural killer cells, and it is a cytokine rich microenvironment [4-6]. Immune cells can regulate many aspects of formation and growth of bone metastases [4]. Bone marrow is an immunosuppressive microenvironment, and immune suppressive cells in bone may promote tumor progression [5]. On the contrary, cytotoxic T cells and NK cells can be activated by immunomodulators to mediate anti-tumor effects. In addition, immune cells directly interact with bone cells, promoting tumor-induced effects on bone [6].
{"title":"Potential of Targeting Bone Metastases with Immunotherapies","authors":"T. Kähkönen, Halleen Jm, J. Bernoulli","doi":"10.31031/nacs.2019.03.000561","DOIUrl":"https://doi.org/10.31031/nacs.2019.03.000561","url":null,"abstract":"Cancer metastases cause high morbidity and mortality in patients. Bone metastases are most common in breast and prostate cancer, but they are also observed in many other cancers such as lung and renal cancer and melanoma [1]. In breast cancer the formation of metastases depends on the tumor subtype, and the major site for metastasis is the skeleton [2]. Patients with bone metastases have a 5-year survival rate of only 21% and a median survival time of 3 years. Prostate cancer is currently described as a bone disease due to high incidence of skeletal metastases. In prostate cancer patients with bone metastases, the 5-year survival rate is about 30% and the median survival time is 3 years [3]. Metastatic cancer patients are treated with conventional cancer therapies that are usually ineffective against bone metastases. Tumor-induced bone loss can also be treated with bone-targeting therapies. Bone marrow is an important immune organ that contains many immune cells, such as myeloid-derived suppressor cells, T cells, B cells and natural killer cells, and it is a cytokine rich microenvironment [4-6]. Immune cells can regulate many aspects of formation and growth of bone metastases [4]. Bone marrow is an immunosuppressive microenvironment, and immune suppressive cells in bone may promote tumor progression [5]. On the contrary, cytotoxic T cells and NK cells can be activated by immunomodulators to mediate anti-tumor effects. In addition, immune cells directly interact with bone cells, promoting tumor-induced effects on bone [6].","PeriodicalId":93131,"journal":{"name":"Novel approaches in cancer study","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48316549","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 : 2019-09-23DOI: 10.31031/nacs.2019.03.000560
Riham E Aidrous, A. M. Hussein, Salahaldeen H Dahawi, I. Elkhidir, K. Enan
Breast cancer in women worldwide is considered as the most widespread disease and a most important etiology of mortality [1,2]. Several internal and external factors contribute to the development of this cancer. Internal factors such as age, hormonal effects, lifestyle, obesity, alcohol consumption, smoking, gender, anxiety and stress, genetic predisposition (mutation in BRCA1, 2 and other genes) and family history of breast cancer [3,4]. Exogenous factors include infection with oncogenic viruses such as Mouse Mammary Tumor Virus (MMTV), Human Papilloma Virus (HPV) and Epstein-Barr Virus (EBV). Oncogenic viruses are contributing to 20% of human cancers [5]. Recently, Cytomegalovirus (CMV) has been linked to the development of inflammatory diseases and cancer . EBV It is the causative agent of Infectious Mononucleosis (IM) and has been associated with a growing list of malignancies of both lymphoid and epithelial origin including Burkitt’s lymphoma, B-cell lymphoma in immunocompromised subjects, Hodgkin’s lymphoma, and Nasopharyngeal Carcinoma (NPC). Based on this association, the WHO International Agency for Research on Cancer (IARC) has classified EBV among group I carcinogens which are agents that definitely cause neoplasm in humans [7.
{"title":"Molecular Detection of Epstein-Barr Virus and Human Cytomegalovirus Antigen Expression in Breast Cancer in Khartoum State, Sudan 2018","authors":"Riham E Aidrous, A. M. Hussein, Salahaldeen H Dahawi, I. Elkhidir, K. Enan","doi":"10.31031/nacs.2019.03.000560","DOIUrl":"https://doi.org/10.31031/nacs.2019.03.000560","url":null,"abstract":"Breast cancer in women worldwide is considered as the most widespread disease and a most important etiology of mortality [1,2]. Several internal and external factors contribute to the development of this cancer. Internal factors such as age, hormonal effects, lifestyle, obesity, alcohol consumption, smoking, gender, anxiety and stress, genetic predisposition (mutation in BRCA1, 2 and other genes) and family history of breast cancer [3,4]. Exogenous factors include infection with oncogenic viruses such as Mouse Mammary Tumor Virus (MMTV), Human Papilloma Virus (HPV) and Epstein-Barr Virus (EBV). Oncogenic viruses are contributing to 20% of human cancers [5]. Recently, Cytomegalovirus (CMV) has been linked to the development of inflammatory diseases and cancer . EBV It is the causative agent of Infectious Mononucleosis (IM) and has been associated with a growing list of malignancies of both lymphoid and epithelial origin including Burkitt’s lymphoma, B-cell lymphoma in immunocompromised subjects, Hodgkin’s lymphoma, and Nasopharyngeal Carcinoma (NPC). Based on this association, the WHO International Agency for Research on Cancer (IARC) has classified EBV among group I carcinogens which are agents that definitely cause neoplasm in humans [7.","PeriodicalId":93131,"journal":{"name":"Novel approaches in cancer study","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43258035","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 : 2019-09-16DOI: 10.31031/nacs.2019.03.000559
M. Szaryńska, Agata Olejniczak Kęder
The Fas signaling is known to exert very variable effects in wide spectrum of cells. The FasR/ FasL (CD95/ CD95L) proteins can be associated with both positive (physiological) and negative (pathological) effects. Nowadays, there is a growing interest in the elucidation of the Fas signaling role in the pathogenesis and progression of various cancers. Additionally, it was proven that the expression of FasR/ FasL in colorectal cancer is associated with worse prognosis, metastasis and recurrence [1-6] the aspects of cancer biology which cancer stem cells are responsible for [7]. On the one hand, Fas signaling pathway is considered as a potential target for anticancer therapy and, on the other hand, is hoped to be exploit as therapeutic tool. The approach to this issue is dynamically update since the state of knowledge concerning Fas signaling functions is rapidly developing. The most established pro-apoptotic activity of FasR/L signaling is the elimination of non-CSC cancerous, virus-infected or useless/ autoreactive T cells by cytotoxic T lymphocytes [8]. Drug therapy combining the multi-kinase inhibitor Sorafenib and the histone deacetylase inhibitor Vorinostat was shown to activate Fas-mediated apoptosis by promoting receptor tyrosine phosphorylation or contribution to FasR activation via initial facilitation of ROS generation and subsequent FasL expression [9]. Additionally, Fas signaling was proven to be associated with HSPs. Although it was originally demonstrated in rat global brain ischemia model, we assume that similar relationships exist in cancer cells as well. Inhibition of HSP90 proteins reduced FasL expression and induced neuroprotective effect [10]. Moreover, the heat shock proteins accumulation was demonstrated as a specific mechanism increasing protein stability and reducing a turnover during Fas-mediated apoptosis in Jurkat cells [11].
{"title":"Different Faces of Fas Signaling in Cancer Cells","authors":"M. Szaryńska, Agata Olejniczak Kęder","doi":"10.31031/nacs.2019.03.000559","DOIUrl":"https://doi.org/10.31031/nacs.2019.03.000559","url":null,"abstract":"The Fas signaling is known to exert very variable effects in wide spectrum of cells. The FasR/ FasL (CD95/ CD95L) proteins can be associated with both positive (physiological) and negative (pathological) effects. Nowadays, there is a growing interest in the elucidation of the Fas signaling role in the pathogenesis and progression of various cancers. Additionally, it was proven that the expression of FasR/ FasL in colorectal cancer is associated with worse prognosis, metastasis and recurrence [1-6] the aspects of cancer biology which cancer stem cells are responsible for [7]. On the one hand, Fas signaling pathway is considered as a potential target for anticancer therapy and, on the other hand, is hoped to be exploit as therapeutic tool. The approach to this issue is dynamically update since the state of knowledge concerning Fas signaling functions is rapidly developing. The most established pro-apoptotic activity of FasR/L signaling is the elimination of non-CSC cancerous, virus-infected or useless/ autoreactive T cells by cytotoxic T lymphocytes [8]. Drug therapy combining the multi-kinase inhibitor Sorafenib and the histone deacetylase inhibitor Vorinostat was shown to activate Fas-mediated apoptosis by promoting receptor tyrosine phosphorylation or contribution to FasR activation via initial facilitation of ROS generation and subsequent FasL expression [9]. Additionally, Fas signaling was proven to be associated with HSPs. Although it was originally demonstrated in rat global brain ischemia model, we assume that similar relationships exist in cancer cells as well. Inhibition of HSP90 proteins reduced FasL expression and induced neuroprotective effect [10]. Moreover, the heat shock proteins accumulation was demonstrated as a specific mechanism increasing protein stability and reducing a turnover during Fas-mediated apoptosis in Jurkat cells [11].","PeriodicalId":93131,"journal":{"name":"Novel approaches in cancer study","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48498494","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 : 2019-09-11DOI: 10.31031/nacs.2019.03.000558
Prashanthi Dharanipragada, N. Parekh
Diffuse Large B-cell Lymphoma (DLBCL) is the most common lymphoid malignancy in adults, accounting for ~35% of Non-Hodgkin’s lymphoma cases worldwide. Several classification systems have been proposed based on shared morphology, immunophenotype, genetic alterations, clinical outcomes, etc., to decipher the mechanisms of pathogenesis and design suitable therapy. Classification of DLBCL into cell-of-origin (COO) subtypes, Germinal Centre B-cell (GCB) and Activated B-cell (ABC), has been traditionally defined as lowand highrisk patient groups respectively when treated with chemotherapy [1]. Several previous studies have shown a diverse set of genetic and epigenetic factors affecting few key pathways in each subtype. For example, the GCB subtype is mostly characterized with alterations in chromatinmodifying enzymes, activated PI3K pathway, disruption of Gα migration pathway components and frequent structural variants of BCL2 gene, while ABC subtype is often associated with increased NF-κB activity, altered BCR signalling, perturbed terminal B cell differentiation, etc. The differences in the genetic profiles of the two subtypes have been associated with differential response to treatment, with ABC subtype exhibiting poorer outcomes compared to GCB subtype when treated with standard rituximab, cyclophosphamide, doxorubicin (Adriamycin), vincristine (Oncovin) and prednisone (R-CHOP) immuno-chemotherapy. Moreover, relapsed/refractory DLBCL is observed in ~30-40% of the treated cases.
{"title":"Identifying Biomarkers for Diffuse Large B-Cell Lymphoma Subtypes","authors":"Prashanthi Dharanipragada, N. Parekh","doi":"10.31031/nacs.2019.03.000558","DOIUrl":"https://doi.org/10.31031/nacs.2019.03.000558","url":null,"abstract":"Diffuse Large B-cell Lymphoma (DLBCL) is the most common lymphoid malignancy in adults, accounting for ~35% of Non-Hodgkin’s lymphoma cases worldwide. Several classification systems have been proposed based on shared morphology, immunophenotype, genetic alterations, clinical outcomes, etc., to decipher the mechanisms of pathogenesis and design suitable therapy. Classification of DLBCL into cell-of-origin (COO) subtypes, Germinal Centre B-cell (GCB) and Activated B-cell (ABC), has been traditionally defined as lowand highrisk patient groups respectively when treated with chemotherapy [1]. Several previous studies have shown a diverse set of genetic and epigenetic factors affecting few key pathways in each subtype. For example, the GCB subtype is mostly characterized with alterations in chromatinmodifying enzymes, activated PI3K pathway, disruption of Gα migration pathway components and frequent structural variants of BCL2 gene, while ABC subtype is often associated with increased NF-κB activity, altered BCR signalling, perturbed terminal B cell differentiation, etc. The differences in the genetic profiles of the two subtypes have been associated with differential response to treatment, with ABC subtype exhibiting poorer outcomes compared to GCB subtype when treated with standard rituximab, cyclophosphamide, doxorubicin (Adriamycin), vincristine (Oncovin) and prednisone (R-CHOP) immuno-chemotherapy. Moreover, relapsed/refractory DLBCL is observed in ~30-40% of the treated cases.","PeriodicalId":93131,"journal":{"name":"Novel approaches in cancer study","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42533256","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 : 2019-08-26DOI: 10.31031/nacs.2019.03.000556
J. Trosko
Is searching for a “Rose in a Dung Heap” the correct strategy for future cancer research? Starting from the view point that there are two philosophical approaches to solve the extremely complex problem of preventing and treating cancers, namely (a) the empirical, unbiased approach of collecting large amount of observations in hopes of finding a pattern (i.e., current use of data mining or computational biology and “Artificial Intelligence ”) or (b) a specific hypothesis-mechanistically based, deductive approach), it seems, while both approaches are being used, we still have made no “conceptual” breakthrough. In spite everyone today recognizing that this cancer problem requires a true multi-disciplinary approach, it still must be based on some biological facts. With all the known facts about many physical (radiations), chemical (natural toxins/synthetic toxicants) and biologics (viruses, bacteria, fungi) having some influence on human carcinogenesis, the link to these factors is only somewhat known to be involved in the multi-stage/multi-mechanism of human carcinogenesis [2,3]. Yet, the integration of the psychological, social, anthropological, cultural, economic, political and ecological sciences has only been weakly linked to the evolutionary and biological sciences [4-7]. As this article is grounded in my limited 50 years of experience in but a few disciplines, as an “opinion” writer, I feel, while the multidisciplinary field of carcinogenesis is still very incomplete, there is sufficient solid scientific information that could supply a new direction. First, we know that there are genetic, racial, developmental, gender, environmental, dietary, nutritional, immunological, behavioral, ecological, cultural, and economic/political factors that influence the cancer process. In addition, we know that cancers have their origin in a single cell [ 8,9]. Today, there is a substantial evidence that the organ-specific adult stem cell and its early progenitor daughter are the target cells to become, in time, a “cancer stem cell” [10-12]. It is now thought that these “cancer stem cells” ought to be the target for both prevention and therapy [13,14]. Moreover, there is ample evidence of the power of nutrition and diets to influence, either positively or negatively, the frequency of many cancers, especially with the observations of caloric restricted, excess calories, and changes in diets due to diaspora of both peoples and foods, especially in large populations during the Second War in Europe and Japan [15,16]. This is now leading some investigators to view that pregnant women, exposed Crimson Publishers Wings to the Research Opinion
{"title":"Are We Still Missing the Target in Trying to Prevent and Treat Human Cancers?","authors":"J. Trosko","doi":"10.31031/nacs.2019.03.000556","DOIUrl":"https://doi.org/10.31031/nacs.2019.03.000556","url":null,"abstract":"Is searching for a “Rose in a Dung Heap” the correct strategy for future cancer research? Starting from the view point that there are two philosophical approaches to solve the extremely complex problem of preventing and treating cancers, namely (a) the empirical, unbiased approach of collecting large amount of observations in hopes of finding a pattern (i.e., current use of data mining or computational biology and “Artificial Intelligence ”) or (b) a specific hypothesis-mechanistically based, deductive approach), it seems, while both approaches are being used, we still have made no “conceptual” breakthrough. In spite everyone today recognizing that this cancer problem requires a true multi-disciplinary approach, it still must be based on some biological facts. With all the known facts about many physical (radiations), chemical (natural toxins/synthetic toxicants) and biologics (viruses, bacteria, fungi) having some influence on human carcinogenesis, the link to these factors is only somewhat known to be involved in the multi-stage/multi-mechanism of human carcinogenesis [2,3]. Yet, the integration of the psychological, social, anthropological, cultural, economic, political and ecological sciences has only been weakly linked to the evolutionary and biological sciences [4-7]. As this article is grounded in my limited 50 years of experience in but a few disciplines, as an “opinion” writer, I feel, while the multidisciplinary field of carcinogenesis is still very incomplete, there is sufficient solid scientific information that could supply a new direction. First, we know that there are genetic, racial, developmental, gender, environmental, dietary, nutritional, immunological, behavioral, ecological, cultural, and economic/political factors that influence the cancer process. In addition, we know that cancers have their origin in a single cell [ 8,9]. Today, there is a substantial evidence that the organ-specific adult stem cell and its early progenitor daughter are the target cells to become, in time, a “cancer stem cell” [10-12]. It is now thought that these “cancer stem cells” ought to be the target for both prevention and therapy [13,14]. Moreover, there is ample evidence of the power of nutrition and diets to influence, either positively or negatively, the frequency of many cancers, especially with the observations of caloric restricted, excess calories, and changes in diets due to diaspora of both peoples and foods, especially in large populations during the Second War in Europe and Japan [15,16]. This is now leading some investigators to view that pregnant women, exposed Crimson Publishers Wings to the Research Opinion","PeriodicalId":93131,"journal":{"name":"Novel approaches in cancer study","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42595407","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 : 2019-08-02DOI: 10.31031/NACS.2019.03.000555
T. Haye
Epidemiology of stomach cancer varies depending on several parameters including demographic, histological and geographic features. On the other hand, the measures of the associations of gastric cancer with putative risk factors are relatively robust with regard to these variations [1]. Each year approximately 990,000 people are diagnosed with gastric cancer worldwide, of whom about 738,000 die from this disease, making gastric cancer the 4th most common incident cancer and the 2nd most common cause of cancer death [2]. However, its incidence rates in different geographical regions are distinctly varied. Etiologically, gastric cancer is associated with Helicobacter pylori infection, nutritional and lifestyle factors, and genetics [3,4]. This review provides an update of the current trends of gastric cancer. Overall, in most developed countries, its incidence has decreased substantially in the past five decades, with the disorder now the 14th most common neoplasm in the USA. However, in many developing countries, the incidence of gastric cancer has increased during the same period. In the Middle East, the incidence varies from high in Iran (age-standardized incidence rate 26·1 per 100 000 individuals per year) to low in Israel (12·5 per 100 000 per year) and Egypt (3·4 per 100 000 per year).Gastric cancer is the most common malignant disease in Iran and Oman [5-7].
{"title":"Review on Gastric Cancer","authors":"T. Haye","doi":"10.31031/NACS.2019.03.000555","DOIUrl":"https://doi.org/10.31031/NACS.2019.03.000555","url":null,"abstract":"Epidemiology of stomach cancer varies depending on several parameters including demographic, histological and geographic features. On the other hand, the measures of the associations of gastric cancer with putative risk factors are relatively robust with regard to these variations [1]. Each year approximately 990,000 people are diagnosed with gastric cancer worldwide, of whom about 738,000 die from this disease, making gastric cancer the 4th most common incident cancer and the 2nd most common cause of cancer death [2]. However, its incidence rates in different geographical regions are distinctly varied. Etiologically, gastric cancer is associated with Helicobacter pylori infection, nutritional and lifestyle factors, and genetics [3,4]. This review provides an update of the current trends of gastric cancer. Overall, in most developed countries, its incidence has decreased substantially in the past five decades, with the disorder now the 14th most common neoplasm in the USA. However, in many developing countries, the incidence of gastric cancer has increased during the same period. In the Middle East, the incidence varies from high in Iran (age-standardized incidence rate 26·1 per 100 000 individuals per year) to low in Israel (12·5 per 100 000 per year) and Egypt (3·4 per 100 000 per year).Gastric cancer is the most common malignant disease in Iran and Oman [5-7].","PeriodicalId":93131,"journal":{"name":"Novel approaches in cancer study","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46521679","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 : 2019-07-30DOI: 10.31031/nacs.2019.03.000554
Yufeng Cheng
Background: Expression of P 16 gene that is the key regulatory protein of the cell cycle has been linked with the prognosis of Esophageal squamous cell carcinoma patients. Materials and method: By immunohistochemistry, we examined the expression status of P 16 of 110 esophageal squamous cell carcinoma patients on the tissue microarrays (TMAs). The nuclear staining intensity was calculated by immunoreactivity score ranging from (0-12) and split them into two groups: No-expression & Overexpression group. Result: Postoperatively median follow-up period of our study was 70 months. Down-regulation of P 16 expression pointedly predicted decreased 5-year overall survival (P=0.001) and progression-free survival, which is statistically significant & demonstrated by Kaplan-Meier estimates using the log-rank test. Hence, P 16 protein acts as an independent prognostic factor for overall survival and progression-free survival that demonstrated by multivariate Cox-regression analysis (HR=0.046 with 95% CI 0.006-0.333, P=0.002 and HR=0.064 with 95% CI 0.009-0.466, P=0.005 respectively OS & PFS). Conclusion: P 16 is a promising biomarker that is down regulated in ESCC patients and prognostic indicator for poor survival postoperatively.
{"title":"Decreased Expression of P16 Indicates the Postoperative Poor Prognosis of Esophageal Squamous Cell Carcinoma Patients","authors":"Yufeng Cheng","doi":"10.31031/nacs.2019.03.000554","DOIUrl":"https://doi.org/10.31031/nacs.2019.03.000554","url":null,"abstract":"Background: Expression of P 16 gene that is the key regulatory protein of the cell cycle has been linked with the prognosis of Esophageal squamous cell carcinoma patients. Materials and method: By immunohistochemistry, we examined the expression status of P 16 of 110 esophageal squamous cell carcinoma patients on the tissue microarrays (TMAs). The nuclear staining intensity was calculated by immunoreactivity score ranging from (0-12) and split them into two groups: No-expression & Overexpression group. Result: Postoperatively median follow-up period of our study was 70 months. Down-regulation of P 16 expression pointedly predicted decreased 5-year overall survival (P=0.001) and progression-free survival, which is statistically significant & demonstrated by Kaplan-Meier estimates using the log-rank test. Hence, P 16 protein acts as an independent prognostic factor for overall survival and progression-free survival that demonstrated by multivariate Cox-regression analysis (HR=0.046 with 95% CI 0.006-0.333, P=0.002 and HR=0.064 with 95% CI 0.009-0.466, P=0.005 respectively OS & PFS). Conclusion: P 16 is a promising biomarker that is down regulated in ESCC patients and prognostic indicator for poor survival postoperatively.","PeriodicalId":93131,"journal":{"name":"Novel approaches in cancer study","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43961766","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 : 2019-07-16DOI: 10.31031/nacs.2019.03.000553
Ti’ara L. Griffen
Chronic Lymphocytic Leukemia (CLL) is an adult heme malignancy characterized by the presence of ma-ture-appearing CD5+ B cells in the blood, bone marrow, and secondary lymphoid organs. CLL is heterogeneous in its progression and clinical outcomes. Factors that contribute to the heterogeneity include the immunoglobulin heavy chain (IGHV) status and chromosomal aberrations. CLL’s heterogeneous behavior has made it difficult to understand its biology and find a cure. Systems biology approaches are commonly used to establish biomarkers for cancer. Because proteins are targets of FDA approved therapies, proteomics approaches have been used to decipher the c mplex behavior of CLL pathogenesis and identify actionable targets. In this minireview, we highlight factors that contribute to CLL, new insights discovered from proteomics studies, and future directions.
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