R. Das, S. Karmakar, Ishita Saha, R. Sahoo, S. K. Medda, R. Kottapalli
The glucose level linkages with breast cancer (BC) biomarkers are focused in the article adopting probabilistic modeling with a real data set surveyed from 64 BC women and 52 normal women along with 10 interested study factors. It is derived that mean glucose levels are over for BC women (P=0.02224) than normal. Mean glucose levels are inversely linked with insulin (P< 0.00001), interaction effects of leptin and adiponectin (leptin*adiponectin) (P=0.08834), homeostasis model assessment score insulin resistance (HOMA-IR) and leptin (HOMA-IR*leptin) (P<0.00001), while they are directly linked with HOMA-IR (P<0.00001) and leptin (P<0.00001). The variance of glucose levels is inversely linked with leptin (P=0.00022), insulin (P=0.01365), monocyte chemoattractant protein-1 (MCP-1) (P=0.01153), insulin*HOMA-IR (P=0.00022), age*resistin (P=0.03974), age*HOMA-IR(P=0.03102), while it is directly linked with HOMA-IR (P<0.00001), resistin (P=0.02182) and age (P=0.00133). Glucose levels are higher for BC women, and they increase along with the increased levels of HOMA-IR, leptin, and the decreased levels of insulin, HOMA-IR*leptin, leptin*adiponectin.
{"title":"The glucose level linkages with breast cancer markers","authors":"R. Das, S. Karmakar, Ishita Saha, R. Sahoo, S. K. Medda, R. Kottapalli","doi":"10.31579/2640-1053/083","DOIUrl":"https://doi.org/10.31579/2640-1053/083","url":null,"abstract":"The glucose level linkages with breast cancer (BC) biomarkers are focused in the article adopting probabilistic modeling with a real data set surveyed from 64 BC women and 52 normal women along with 10 interested study factors. It is derived that mean glucose levels are over for BC women (P=0.02224) than normal. Mean glucose levels are inversely linked with insulin (P< 0.00001), interaction effects of leptin and adiponectin (leptin*adiponectin) (P=0.08834), homeostasis model assessment score insulin resistance (HOMA-IR) and leptin (HOMA-IR*leptin) (P<0.00001), while they are directly linked with HOMA-IR (P<0.00001) and leptin (P<0.00001). The variance of glucose levels is inversely linked with leptin (P=0.00022), insulin (P=0.01365), monocyte chemoattractant protein-1 (MCP-1) (P=0.01153), insulin*HOMA-IR (P=0.00022), age*resistin (P=0.03974), age*HOMA-IR(P=0.03102), while it is directly linked with HOMA-IR (P<0.00001), resistin (P=0.02182) and age (P=0.00133). Glucose levels are higher for BC women, and they increase along with the increased levels of HOMA-IR, leptin, and the decreased levels of insulin, HOMA-IR*leptin, leptin*adiponectin.","PeriodicalId":93018,"journal":{"name":"Journal of cancer research and cellular therapeutics","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43361648","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}
Hematopoietic microenvironment or niche keeps stem cells in multi-potent/ uni-potent state which prevents precocious differentiation. The niche employs a variety of factors includes growth factors, cytokines and cell adhesion molecules too. In this section, we try to have a better understanding about the role of hematopoietic stem cells, niche and hematopoiesis as well as we demonstrate that leukemia induced reprogramming initially and then remodeling of the bone marrow (BM) microenvironment which can be a major part of leukemogenesis and is a potential prognostic parameter in malignant hematopoietic disease as well.
{"title":"Why Is Importance the Reprogramming and Remodeling In Malignant Hematopoietic Microenvironment and Its Hematopoietic Stem Cells Too","authors":"A. Rahnemoon","doi":"10.31579/2640-1053/086","DOIUrl":"https://doi.org/10.31579/2640-1053/086","url":null,"abstract":"Hematopoietic microenvironment or niche keeps stem cells in multi-potent/ uni-potent state which prevents precocious differentiation. The niche employs a variety of factors includes growth factors, cytokines and cell adhesion molecules too. In this section, we try to have a better understanding about the role of hematopoietic stem cells, niche and hematopoiesis as well as we demonstrate that leukemia induced reprogramming initially and then remodeling of the bone marrow (BM) microenvironment which can be a major part of leukemogenesis and is a potential prognostic parameter in malignant hematopoietic disease as well.","PeriodicalId":93018,"journal":{"name":"Journal of cancer research and cellular therapeutics","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44122800","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}
A. Cardoso, Maria Luiza Mukai Franciosi, A. Wagner
Since our publication “Purinergic Signaling and Tumor Microenvironment in Cervical Cancer” [1], in early 2020, there has been a significant change in purinergic signaling research. The Coronavirus disease 2019 (COVID-19) significantly impacted the prevention, diagnosis, and treatment of cervical cancer [2]. In that previous review, we had addressed the possibilities of purinergic signaling in the tumor microenvironment of this type of cancer [1]. The conclusions were: the extracellular medium of cervical cancer is rich in adenosine triphosphate (ATP) and adenosine [3, 4, 5]; ATP is a pro-inflammatory molecule that has an affinity for P2X2, P2X4, and P2X7 receptors [6]; this activation leads to apoptosis of the cells of the cervix [7]; P2X7 is still involved in stimulating factors that lead to mitogenic and angiogenic pathways [8]; there is a variant of P2X7 in cervical cancer cells, P2X7j, which decreases permeability and cell death [9, 10, 11]. The P2Y1, P2Y2, and P2Y6 receptors, in turn, have the effect of tumor progression [12]. The review also contributed to the understanding of adenosine, which would activate A2A receptors on T lymphocytes, which would promote a decrease in the proliferation and effector function of such cells
{"title":"What is new in Purinergic Signaling and Cervical Cancer?","authors":"A. Cardoso, Maria Luiza Mukai Franciosi, A. Wagner","doi":"10.31579/2640-1053/084","DOIUrl":"https://doi.org/10.31579/2640-1053/084","url":null,"abstract":"Since our publication “Purinergic Signaling and Tumor Microenvironment in Cervical Cancer” [1], in early 2020, there has been a significant change in purinergic signaling research. The Coronavirus disease 2019 (COVID-19) significantly impacted the prevention, diagnosis, and treatment of cervical cancer [2]. In that previous review, we had addressed the possibilities of purinergic signaling in the tumor microenvironment of this type of cancer [1]. The conclusions were: the extracellular medium of cervical cancer is rich in adenosine triphosphate (ATP) and adenosine [3, 4, 5]; ATP is a pro-inflammatory molecule that has an affinity for P2X2, P2X4, and P2X7 receptors [6]; this activation leads to apoptosis of the cells of the cervix [7]; P2X7 is still involved in stimulating factors that lead to mitogenic and angiogenic pathways [8]; there is a variant of P2X7 in cervical cancer cells, P2X7j, which decreases permeability and cell death [9, 10, 11]. The P2Y1, P2Y2, and P2Y6 receptors, in turn, have the effect of tumor progression [12]. The review also contributed to the understanding of adenosine, which would activate A2A receptors on T lymphocytes, which would promote a decrease in the proliferation and effector function of such cells","PeriodicalId":93018,"journal":{"name":"Journal of cancer research and cellular therapeutics","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46541610","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}
Signet-ring cell carcinoma of the urinary bladder is an uncommon histopathology variant of carcinoma of urinary bladder which has been stated to account for 0.5% and 2% of primary malignant tumours of the urinary bladder. Signet-ring cell carcinoma of the urinary bladder is stated to either arise from the wall of the urinary bladder or from remnants of the urachus, or signet-ring cell carcinoma of the urinary bladder could also develop as a metastatic tumour that has ensued a primary signet-ring cell carcinoma that had arisen from a number sites of the body some of which include: the stomach, colon, or breast, the appendix and other organs. It has been iterated that the least common type of signet-ring cell carcinoma is primary signet-ring cell carcinoma and that up to 2013 less than 100 cases had been reported. Signet-ring cell carcinoma of the urinary bladder can affect males as well as females, young individuals or adults. Signet-ring cell carcinoma of the urinary bladder could be diagnosed incidentally or it may present with non-specific symptoms that simulate the symptoms of other urinary bladder tumours including: lower urinary tract symptoms, haematuria, abdominal pain / discomfort or loin pain, retention of urine, feeling unwell, or weight loss. Microscopy examination of the tumour whether it was obtained by means of trans-urethral resection or by cystectomy would tend to demonstrate a tumour that is comprised of signet-ring cells that contain peripherally pushed hyperchromatic nuclei, intra-cytoplasmic mucin, as well as lakes of extracellular mucin. The tumour cells could be arranged in lobules, and separated by fibrovascular septae. There tends to be visualization of mitosis as well as evidence of necrosis. The tumour tends to be seen within the underlying stroma and quite often within the detrusor muscle and up to the extra-vesical fat quite often. Immunohistochemistry staining studies of signet-ring cell carcinoma of the urinary bladder would tend to show tumour cells that exhibit positive staining for: Cytokeratin including cytokeratin 7, CAM 5.2, AE1/3, and 34ßE12; Vimentin; Peanut lectin agglutinin; Ulex europaeus agglutinin. In signet ring cell carcinoma of urinary bladder immunohistochemistry staining of the tumour may also show tumour cells that exhibit positive staining for the following tumour markers: CK, CK7, CK20; CDX2; Villin - There could be a small amount of positive staining for Villin. In signet-ring cell carcinoma of the urinary bladder, immunohistochemistry studies of the tumour may demonstrate tumour cells that do exhibit negative staining for the ensuing tumour markers: Vimentin, (this does show therefore that some tumours would stain positive and others would stain negative); GATA3, and P53. To confirm whether a signet-ring cell carcinoma of the urinary bladder is a pure primary tumour or metastatic tumour does require detailed history taking with evidence of previously treated signet-ring cell carcinoma elsewhere
{"title":"Signet-Ring Cell Carcinoma of the Urinary Bladder: A Review and Update","authors":"A. Kodzo-Grey Venyo","doi":"10.31579/2640-1053/081","DOIUrl":"https://doi.org/10.31579/2640-1053/081","url":null,"abstract":"Signet-ring cell carcinoma of the urinary bladder is an uncommon histopathology variant of carcinoma of urinary bladder which has been stated to account for 0.5% and 2% of primary malignant tumours of the urinary bladder. Signet-ring cell carcinoma of the urinary bladder is stated to either arise from the wall of the urinary bladder or from remnants of the urachus, or signet-ring cell carcinoma of the urinary bladder could also develop as a metastatic tumour that has ensued a primary signet-ring cell carcinoma that had arisen from a number sites of the body some of which include: the stomach, colon, or breast, the appendix and other organs. It has been iterated that the least common type of signet-ring cell carcinoma is primary signet-ring cell carcinoma and that up to 2013 less than 100 cases had been reported. Signet-ring cell carcinoma of the urinary bladder can affect males as well as females, young individuals or adults. Signet-ring cell carcinoma of the urinary bladder could be diagnosed incidentally or it may present with non-specific symptoms that simulate the symptoms of other urinary bladder tumours including: lower urinary tract symptoms, haematuria, abdominal pain / discomfort or loin pain, retention of urine, feeling unwell, or weight loss. Microscopy examination of the tumour whether it was obtained by means of trans-urethral resection or by cystectomy would tend to demonstrate a tumour that is comprised of signet-ring cells that contain peripherally pushed hyperchromatic nuclei, intra-cytoplasmic mucin, as well as lakes of extracellular mucin. The tumour cells could be arranged in lobules, and separated by fibrovascular septae. There tends to be visualization of mitosis as well as evidence of necrosis. The tumour tends to be seen within the underlying stroma and quite often within the detrusor muscle and up to the extra-vesical fat quite often. Immunohistochemistry staining studies of signet-ring cell carcinoma of the urinary bladder would tend to show tumour cells that exhibit positive staining for: Cytokeratin including cytokeratin 7, CAM 5.2, AE1/3, and 34ßE12; Vimentin; Peanut lectin agglutinin; Ulex europaeus agglutinin. In signet ring cell carcinoma of urinary bladder immunohistochemistry staining of the tumour may also show tumour cells that exhibit positive staining for the following tumour markers: CK, CK7, CK20; CDX2; Villin - There could be a small amount of positive staining for Villin. In signet-ring cell carcinoma of the urinary bladder, immunohistochemistry studies of the tumour may demonstrate tumour cells that do exhibit negative staining for the ensuing tumour markers: Vimentin, (this does show therefore that some tumours would stain positive and others would stain negative); GATA3, and P53. To confirm whether a signet-ring cell carcinoma of the urinary bladder is a pure primary tumour or metastatic tumour does require detailed history taking with evidence of previously treated signet-ring cell carcinoma elsewhere","PeriodicalId":93018,"journal":{"name":"Journal of cancer research and cellular therapeutics","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45422402","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}
Obesity and its related complications have been the pressing disease pandemic affecting the developed world. It is well-established that the direct consequence of obesity in the cardiovascular system resulting in many diseases. However, its implications in carcinogenesis, cancer treatment and one’s anti-tumour immunity are gradually unfolding. To understand how fat cells can affect these, one needs to explore how the fat cell affects epithelial and immune cells. To this end, we explore the way how the adipocytes, via its production of adipokines, influence these cells, resulting in early epithelial cell transformation into cancer cells and influencing anti-tumour immunity once the cancer is established. In order to simplify our discussion, we focus this review on breast cancer. We propose that to have an effective therapy for cancer treatment, we need to intervene at the adipokine interaction with epithelial cells, cancer cells, and immune cells. In this review we also decipher the potential therapeutic targets in controlling carcinogenesis and disease progression.
{"title":"Complex interaction of adipokines in breast cancer and anti-tumour immunity; a new paradigm for cancer treatment","authors":"Peng H Tan, Ming-rui Xie, E. Sfakianakis","doi":"10.31579/2640-1053/077","DOIUrl":"https://doi.org/10.31579/2640-1053/077","url":null,"abstract":"Obesity and its related complications have been the pressing disease pandemic affecting the developed world. It is well-established that the direct consequence of obesity in the cardiovascular system resulting in many diseases. However, its implications in carcinogenesis, cancer treatment and one’s anti-tumour immunity are gradually unfolding. To understand how fat cells can affect these, one needs to explore how the fat cell affects epithelial and immune cells. To this end, we explore the way how the adipocytes, via its production of adipokines, influence these cells, resulting in early epithelial cell transformation into cancer cells and influencing anti-tumour immunity once the cancer is established. In order to simplify our discussion, we focus this review on breast cancer. We propose that to have an effective therapy for cancer treatment, we need to intervene at the adipokine interaction with epithelial cells, cancer cells, and immune cells. In this review we also decipher the potential therapeutic targets in controlling carcinogenesis and disease progression.","PeriodicalId":93018,"journal":{"name":"Journal of cancer research and cellular therapeutics","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43127871","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}
Prostate cancer is the most common cancer and among the leading causes of cancer death in men and its clinical symptoms vary a lot. The most common metastatic site is the bones, but rarely prostate cancer can metastasize to brain in very advanced stages of the disease. However, brain metastases giving neurological symptoms as first manifestation of prostate cancers have been reported. Research of international literature revealed only seventeen patients (including our own) that were diagnosed with prostate cancer presented with neurological symptoms.
{"title":"Prostate cancer presented with de novo brain metastases as initial manifestation: A case report with review of the literature","authors":"K. Tsapakidis","doi":"10.31579/2640-1053/073","DOIUrl":"https://doi.org/10.31579/2640-1053/073","url":null,"abstract":"Prostate cancer is the most common cancer and among the leading causes of cancer death in men and its clinical symptoms vary a lot. The most common metastatic site is the bones, but rarely prostate cancer can metastasize to brain in very advanced stages of the disease. However, brain metastases giving neurological symptoms as first manifestation of prostate cancers have been reported. Research of international literature revealed only seventeen patients (including our own) that were diagnosed with prostate cancer presented with neurological symptoms.","PeriodicalId":93018,"journal":{"name":"Journal of cancer research and cellular therapeutics","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43117566","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}
Background: A mouse model for thymoma was previously created serendipitously by the random introduction of a transgene consisting of a mouse α-cardiac promoter, a constitutively active human transforming growth factor-β, and a simian virus 40 integration sequence into C3HeB/FeJ mice. Previous data demonstrated that the likely cause of thymomas in the thymoma mouse model was due to insertional mutagenesis by the transgene. At the time, fluorescence in situ hybridization was used to localize the transgene to the short arm of chromosome 2 (Chr2qF2-G region). In this exploratory study, we aimed to identify the exact insertion site of the transgene as this could provide clues to the genetic causation of thymomas in humans. Materials and Methods: To identify the insertion site of the transgene, germline DNA from the thymoma mouse model was sequenced using low-pass, fragment-library, whole genome sequencing. Long-insert mate pair whole genome sequencing was employed to traverse the repetitive regions of the mouse’s genome and identify the integration site. Results: The transgene was found to be integrated into a repetitive area of the mouse genome, specifically on Chr2qF1 within the intron of the FAM227B gene. Tandem integration of the transgene was observed with enumeration of an estimated 30 copies. Initial results suggested that a nearby gene, fibroblast growth factor 7 (Fgf7), could be affected by the gene insertion. Conclusions: Whole genome sequencing of this thymoma mouse model identified the region of tandem integration of a transgene on Chr2qF1 that may have potential translational implications in helping to understand the genomic etiology of thymoma in humans.
{"title":"Whole-Genome Sequencing to Identify the Genetic Etiology of a Spontaneous Thymoma Mouse Model","authors":"M. Radovich","doi":"10.31579/2640-1053/075","DOIUrl":"https://doi.org/10.31579/2640-1053/075","url":null,"abstract":"Background: A mouse model for thymoma was previously created serendipitously by the random introduction of a transgene consisting of a mouse α-cardiac promoter, a constitutively active human transforming growth factor-β, and a simian virus 40 integration sequence into C3HeB/FeJ mice. Previous data demonstrated that the likely cause of thymomas in the thymoma mouse model was due to insertional mutagenesis by the transgene. At the time, fluorescence in situ hybridization was used to localize the transgene to the short arm of chromosome 2 (Chr2qF2-G region). In this exploratory study, we aimed to identify the exact insertion site of the transgene as this could provide clues to the genetic causation of thymomas in humans. Materials and Methods: To identify the insertion site of the transgene, germline DNA from the thymoma mouse model was sequenced using low-pass, fragment-library, whole genome sequencing. Long-insert mate pair whole genome sequencing was employed to traverse the repetitive regions of the mouse’s genome and identify the integration site. Results: The transgene was found to be integrated into a repetitive area of the mouse genome, specifically on Chr2qF1 within the intron of the FAM227B gene. Tandem integration of the transgene was observed with enumeration of an estimated 30 copies. Initial results suggested that a nearby gene, fibroblast growth factor 7 (Fgf7), could be affected by the gene insertion. Conclusions: Whole genome sequencing of this thymoma mouse model identified the region of tandem integration of a transgene on Chr2qF1 that may have potential translational implications in helping to understand the genomic etiology of thymoma in humans.","PeriodicalId":93018,"journal":{"name":"Journal of cancer research and cellular therapeutics","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48743351","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}
Sphingomonas paucimobilis represents an aerobic Gram-negative bacillus that is gaining recognition as an important human pathogen. These species are widely distributed in both natural environment and hospitals. They appear as opportunistic pathogen that take advantage of underlying conditions and diseases. Regardless of the clinical significance, pathogenic mechanism varies throughout current bibliography. Aim of our study, reflects presentation of a rare case of an out-patient clinical asymptomatic, with vaginal culture positive for this rare microorganism, S. paucimobilis. Assiduous diagnosis and therapeutic mapping consist necessary conditions of effective treatment.
{"title":"Sphingomonas paucimobilis complicating vaginal fluid cultivation. A rare case","authors":"C. Sofoudis","doi":"10.31579/2640-1053/071","DOIUrl":"https://doi.org/10.31579/2640-1053/071","url":null,"abstract":"Sphingomonas paucimobilis represents an aerobic Gram-negative bacillus that is gaining recognition as an important human pathogen. These species are widely distributed in both natural environment and hospitals. They appear as opportunistic pathogen that take advantage of underlying conditions and diseases. Regardless of the clinical significance, pathogenic mechanism varies throughout current bibliography. Aim of our study, reflects presentation of a rare case of an out-patient clinical asymptomatic, with vaginal culture positive for this rare microorganism, S. paucimobilis. Assiduous diagnosis and therapeutic mapping consist necessary conditions of effective treatment.","PeriodicalId":93018,"journal":{"name":"Journal of cancer research and cellular therapeutics","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44073203","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}
Prieto Gratacós E, García Oliver P, Alvarez Rp, Redal Ma, Sosa I, Laguzzi M
The present report describes our clinical findings regarding the use of high dose intravenous insulin in cancer patients, as a means to deplete the blood compartment of glucose molecules. The purpose of this intervention is to create a favorable physiological state for the competitive inhibition of several rate-limiting enzymes within cancer cells, with structural analogues that behave as antimetabolites. Regardless of their histological origin, virtually all solid tumors reported on to date (February 2020) are found to be hypercaptant in PET-CT scans following the intravenous injection of 2-¹⁸fluoro-deoxy-D-glucose. Most solid tumors display a hypermetabolic phenotype (SUVmax ≥ 3), with marked overexpression of glucose transporters (GLUTs) in the outer membrane of their anaplastic cells subpopulations. The fact that neoplastic cells also overexpress glycolytic, fermentative and glutaminolytic enzymes up to an order of magnitude relative to healthy cells further strengthens the argument for a competitive inhibition with antimetabolites. The rationale for a deep, systemic deprivation of glucose was suggested by classical enzymological work concerning competitive inhibition (the Woods principle), and our group has shown that a metabolic intervention with structural analogues of glucose and pyruvate is strongly enhanced by a systemic suppression of the natural substrates of hexokinase 2 (HK-2) and lactic dehydrogenase isozyme A (LDH-A), followed by the timely introduction of several non- metabolizable analogues. Sustained, deep hypoglycemia (<10mg/dl) under physiological ketosis provides an advantageous context for antitumor treatment with structural analogues of glucose, pyruvate and glutamine. Data provided in this report demonstrates the feasibility and safety of the procedure.
{"title":"Nuliglucaemia Lucidae: Extreme Deprivation of Blood Glucose as Organic Context for Cancer Treatment with Antimetabolites","authors":"Prieto Gratacós E, García Oliver P, Alvarez Rp, Redal Ma, Sosa I, Laguzzi M","doi":"10.31579/2640-1053/068","DOIUrl":"https://doi.org/10.31579/2640-1053/068","url":null,"abstract":"The present report describes our clinical findings regarding the use of high dose intravenous insulin in cancer patients, as a means to deplete the blood compartment of glucose molecules. The purpose of this intervention is to create a favorable physiological state for the competitive inhibition of several rate-limiting enzymes within cancer cells, with structural analogues that behave as antimetabolites. Regardless of their histological origin, virtually all solid tumors reported on to date (February 2020) are found to be hypercaptant in PET-CT scans following the intravenous injection of 2-¹⁸fluoro-deoxy-D-glucose. Most solid tumors display a hypermetabolic phenotype (SUVmax ≥ 3), with marked overexpression of glucose transporters (GLUTs) in the outer membrane of their anaplastic cells subpopulations. The fact that neoplastic cells also overexpress glycolytic, fermentative and glutaminolytic enzymes up to an order of magnitude relative to healthy cells further strengthens the argument for a competitive inhibition with antimetabolites. The rationale for a deep, systemic deprivation of glucose was suggested by classical enzymological work concerning competitive inhibition (the Woods principle), and our group has shown that a metabolic intervention with structural analogues of glucose and pyruvate is strongly enhanced by a systemic suppression of the natural substrates of hexokinase 2 (HK-2) and lactic dehydrogenase isozyme A (LDH-A), followed by the timely introduction of several non- metabolizable analogues. Sustained, deep hypoglycemia (<10mg/dl) under physiological ketosis provides an advantageous context for antitumor treatment with structural analogues of glucose, pyruvate and glutamine. Data provided in this report demonstrates the feasibility and safety of the procedure.","PeriodicalId":93018,"journal":{"name":"Journal of cancer research and cellular therapeutics","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48064010","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}
Vaping associated pulmonary injury (VAPI), a group of respiratory symptoms, sometimes accompanied by non-specific symptoms like generalized fatigue, body ache, fever, nausea, diarrhea, vomiting and chills that has been previously categorized as a diagnosis of exclusion and best described as an exogenous lipoid pneumonia, or chemical pneumonitis. Here we describe the onset of an exogenous cause of lipoid pneumonia in an otherwise healthy patient using cannabis-containing products. We explore, similarities in the clinical case, identify common clinical features, characteristic radiologic findings along with cytological changes in the lungs.
{"title":"Vaping Induced Pathological Changes in the Lung-A Case Report Study","authors":"Rashmi R Bhuyan, Kumkum Vadera","doi":"10.31579/2640-1053/103","DOIUrl":"https://doi.org/10.31579/2640-1053/103","url":null,"abstract":"Vaping associated pulmonary injury (VAPI), a group of respiratory symptoms, sometimes accompanied by non-specific symptoms like generalized fatigue, body ache, fever, nausea, diarrhea, vomiting and chills that has been previously categorized as a diagnosis of exclusion and best described as an exogenous lipoid pneumonia, or chemical pneumonitis. Here we describe the onset of an exogenous cause of lipoid pneumonia in an otherwise healthy patient using cannabis-containing products. We explore, similarities in the clinical case, identify common clinical features, characteristic radiologic findings along with cytological changes in the lungs.","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":"70018048","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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