Pub Date : 2016-12-12DOI: 10.4172/2324-9110.1000170
Noriaki Hayashibara, Toshihisa Ogawa, E. Tsuji, Mariko Oya, A. Fujii
Neurofibromatosis type 1 is a genetic disorder resulting from a mutation in the NF1 gene, and is known to have an association with hyperparathyroidism that is caused by parathyroid adenoma in almost all cases. Parathyroid carcinoma in neurofibromatosis type 1 is extremely rare. Among the reports of neurofibromatosis type 1 with comorbid hyperparathyroidism have been a patient with coincident pheochromocytoma and medullary thyroid cancer, and a patient with a mutation of the RET gene, the causative gene of multiple endocrine neoplasia (MEN). These cases suggest an association between neurofibromatosis type 1 and multiple endocrine tumors, but the detailed mechanism is still unknown. Moreover, a mutation in the HRPT2 gene has been noted as a genetic cause of parathyroid carcinoma, but at presents no genetic link between neurofibromatosis type 1 and a mutation in the HRPT2 gene has been demonstrated, and the association between neurofibromatosis type 1 and parathyroid cancer remains unclear. We have reported an extremely rare case of neurofibromatosis type 1 with coincident hyperparathyroidism that is caused by parathyroid carcinoma.
{"title":"Parathyroid Carcinoma Coincident With Neurofibromatosis Type 1","authors":"Noriaki Hayashibara, Toshihisa Ogawa, E. Tsuji, Mariko Oya, A. Fujii","doi":"10.4172/2324-9110.1000170","DOIUrl":"https://doi.org/10.4172/2324-9110.1000170","url":null,"abstract":"Neurofibromatosis type 1 is a genetic disorder resulting from a mutation in the NF1 gene, and is known to have an association with hyperparathyroidism that is caused by parathyroid adenoma in almost all cases. Parathyroid carcinoma in neurofibromatosis type 1 is extremely rare. Among the reports of neurofibromatosis type 1 with comorbid hyperparathyroidism have been a patient with coincident pheochromocytoma and medullary thyroid cancer, and a patient with a mutation of the RET gene, the causative gene of multiple endocrine neoplasia (MEN). These cases suggest an association between neurofibromatosis type 1 and multiple endocrine tumors, but the detailed mechanism is still unknown. Moreover, a mutation in the HRPT2 gene has been noted as a genetic cause of parathyroid carcinoma, but at presents no genetic link between neurofibromatosis type 1 and a mutation in the HRPT2 gene has been demonstrated, and the association between neurofibromatosis type 1 and parathyroid cancer remains unclear. We have reported an extremely rare case of neurofibromatosis type 1 with coincident hyperparathyroidism that is caused by parathyroid carcinoma.","PeriodicalId":73658,"journal":{"name":"Journal of clinical & experimental oncology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70249906","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 : 2016-12-05DOI: 10.4172/2324-9110.1000165
B. Poljšak
Abstract Oxidized form of cellular nicotinamide adenine dinucleotide (NAD+) is currently intensively investigated topic in longevity science. However, if ageing is considered a defense mechanism against cancer, caution should be implemented regarding the use of NAD+ and its precursors. In the hypothesis presented NAD+ is shown as an important factor related to cancer formation and prevention. NAD+ depletion with age may play a major role in the process of cancer formation by limiting (1) energy production, (2) DNA repair, (3) genomic stability and signaling. Disruption of any of these processes could increase the cancer risk due to impaired genomic stability. NAD+ content is a critical protective factor in early carcinogenesis and can become detrimental factor later in cancer progression and promotion phase. Namely, NAD+ restoration could prevent or reverse the phenotype of malignant cells at early stages by inducing cellular repair and stress adaptive response as well as regulate cell cycle arrest and apoptotic removal of damaged cells. Contrary, during cancer promotion, progression and treatment increased NAD+ levels could have deleterious effects on the malignancy process due to growth advantage, increased resistance and greater cell survival. NAD+ levels can be increased with exercise, caloric restriction and ingestion of NAD+ precursors and intermediates or could be increased by using PARP and CD 38 inhibitors. The evidence indicating that modulation of NAD+ levels could be important in cancer prevention, initiation and progression phase is presented.
{"title":"NAD+ in Cancer Prevention and Treatment: Pros and Cons","authors":"B. Poljšak","doi":"10.4172/2324-9110.1000165","DOIUrl":"https://doi.org/10.4172/2324-9110.1000165","url":null,"abstract":"Abstract \u0000Oxidized form of cellular nicotinamide adenine dinucleotide (NAD+) is currently intensively investigated topic in longevity science. However, if ageing is considered a defense mechanism against cancer, caution should be implemented regarding the use of NAD+ and its precursors. In the hypothesis presented NAD+ is shown as an important factor related to cancer formation and prevention. NAD+ depletion with age may play a major role in the process of cancer formation by limiting (1) energy production, (2) DNA repair, (3) genomic stability and signaling. Disruption of any of these processes could increase the cancer risk due to impaired genomic stability. NAD+ content is a critical protective factor in early carcinogenesis and can become detrimental factor later in cancer progression and promotion phase. Namely, NAD+ restoration could prevent or reverse the phenotype of malignant cells at early stages by inducing cellular repair and stress adaptive response as well as regulate cell cycle arrest and apoptotic removal of damaged cells. Contrary, during cancer promotion, progression and treatment increased NAD+ levels could have deleterious effects on the malignancy process due to growth advantage, increased resistance and greater cell survival. NAD+ levels can be increased with exercise, caloric restriction and ingestion of NAD+ precursors and intermediates or could be increased by using PARP and CD 38 inhibitors. The evidence indicating that modulation of NAD+ levels could be important in cancer prevention, initiation and progression phase is presented.","PeriodicalId":73658,"journal":{"name":"Journal of clinical & experimental oncology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70249746","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 : 2016-12-05DOI: 10.4172/2324-9110.1000158
Tsvetkov Ch, G. Gorchev, S. Tomov, M. Nikolova, G. Genchev
Objective: The aim of the study was to evaluate overall survival and recurrence-free survival rate in patients with squamous cell vulvar cancer after applying an individualized therapeutic approach. Methods: The concept of individualized therapeutic approach in the treatment of squamous cell vulvar cancer was defined and 113 patients with the diagnosis were studied. All these patients were diagnosed, operated on and followed up at the Clinic of Gynecologic Oncology of the University Hospital Pleven, Bulgaria. Treatment was individualized and more conservative surgical techniques were applied when possible. The Kaplan-Meier method was used to estimate overall survival and disease-free survival rates. Results: Application of individualized approach resulting in: The 5-year survival rate was 73%, and the 10-year survival rate was about 67%. The five-year disease-free survival rate was about 57%, and ten-year disease-free survival rate was about 43%. Conclusion: High rates can be achieved through applying more conservative surgical techniques and individualized therapeutic approach in patients with vulvar cancer.
{"title":"Survival Rate after Individualized Approach in Treatment of Vulvar Cancer: A Ten-Year Single Institution Experience","authors":"Tsvetkov Ch, G. Gorchev, S. Tomov, M. Nikolova, G. Genchev","doi":"10.4172/2324-9110.1000158","DOIUrl":"https://doi.org/10.4172/2324-9110.1000158","url":null,"abstract":"Objective: The aim of the study was to evaluate overall survival and recurrence-free survival rate in patients with squamous cell vulvar cancer after applying an individualized therapeutic approach. \u0000Methods: The concept of individualized therapeutic approach in the treatment of squamous cell vulvar cancer was defined and 113 patients with the diagnosis were studied. All these patients were diagnosed, operated on and followed up at the Clinic of Gynecologic Oncology of the University Hospital Pleven, Bulgaria. Treatment was individualized and more conservative surgical techniques were applied when possible. The Kaplan-Meier method was used to estimate overall survival and disease-free survival rates. \u0000Results: Application of individualized approach resulting in: The 5-year survival rate was 73%, and the 10-year survival rate was about 67%. The five-year disease-free survival rate was about 57%, and ten-year disease-free survival rate was about 43%. \u0000Conclusion: High rates can be achieved through applying more conservative surgical techniques and individualized therapeutic approach in patients with vulvar cancer.","PeriodicalId":73658,"journal":{"name":"Journal of clinical & experimental oncology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70249364","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 : 2016-12-05DOI: 10.4172/2324-9110.1000156
Ranjit Kumar, M. Augustus, A. Nair, R. Ebner, G. Nayar, Rajah Vijay Kumar
Background: Radical paradigm shifts in traditional thinking is paramount to winning the war on cancer and understanding why this disease survives even the most brutal of toxic therapies. There is mounting evidence that biophysical signals are integral to the cycle of initiation, progression and death of cancer cells. Innovative technologies that manipulate this vulnerability in solid tumors could effectively be used to perturb only diseased cells and tissues. Not compromising normally functioning cells while controlling tumor progression, is the ultimate goal for evolving cancer therapeutics like Quantum Magnetic Resonance Therapy, headed promisingly in that direction. Methods: A patented, CE marked device, the CYTOTRON® delivers rotating, target-specific, modulated, safe Radio Frequencies in the presence of an integrated, instantaneous magnetic field. The presumed modulation of the transmembrane potential of tumor cells and downstream cellular signalling by RF for tissue degeneration in cancer underlies Rotational Field Quantum Magnetic Resonance platform technology. Whole body MRI for tissue proton density determinations was used to compute individualized dosimetry to target solitary or multiple regions of interest in the whole body, simultaneously. Exposure to QMRT was for 1 hour daily for 28 consecutive days. Quality of Life assessments, overall survival and tumor stability using RECIST v1.1 were followed up for 12 months. Results: Significant increase in life expectancy from the predicted to the actual mean (p=2.13 E-12), and improvements in Karnofsky Performance Scale scores (p=7.25 E-06) and Quality of Life scores (p=1.71 E-08 and p=1.91 E-06) were noted. Thirty six of 51 (71 %) terminally ill patients had stable disease one month after completion of QMRT or longer. Conclusions: Exposure to radiofrequency-mediated QMRT improved life expectancy and quality of life, along with arrest of tumor progression. This therapy can be safely positioned in a palliative care setting, transitioning to mainstream cancer care with more rigorous clinical validation.
{"title":"Quantum Magnetic Resonance Therapy: Targeting Biophysical Cancer Vulnerabilities to Effectively Treat and Palliate","authors":"Ranjit Kumar, M. Augustus, A. Nair, R. Ebner, G. Nayar, Rajah Vijay Kumar","doi":"10.4172/2324-9110.1000156","DOIUrl":"https://doi.org/10.4172/2324-9110.1000156","url":null,"abstract":"Background: Radical paradigm shifts in traditional thinking is paramount to winning the war on cancer and understanding why this disease survives even the most brutal of toxic therapies. There is mounting evidence that biophysical signals are integral to the cycle of initiation, progression and death of cancer cells. Innovative technologies that manipulate this vulnerability in solid tumors could effectively be used to perturb only diseased cells and tissues. Not compromising normally functioning cells while controlling tumor progression, is the ultimate goal for evolving cancer therapeutics like Quantum Magnetic Resonance Therapy, headed promisingly in that direction. \u0000Methods: A patented, CE marked device, the CYTOTRON® delivers rotating, target-specific, modulated, safe Radio Frequencies in the presence of an integrated, instantaneous magnetic field. The presumed modulation of the transmembrane potential of tumor cells and downstream cellular signalling by RF for tissue degeneration in cancer underlies Rotational Field Quantum Magnetic Resonance platform technology. Whole body MRI for tissue proton density determinations was used to compute individualized dosimetry to target solitary or multiple regions of interest in the whole body, simultaneously. Exposure to QMRT was for 1 hour daily for 28 consecutive days. Quality of Life assessments, overall survival and tumor stability using RECIST v1.1 were followed up for 12 months. \u0000Results: Significant increase in life expectancy from the predicted to the actual mean (p=2.13 E-12), and improvements in Karnofsky Performance Scale scores (p=7.25 E-06) and Quality of Life scores (p=1.71 E-08 and p=1.91 E-06) were noted. Thirty six of 51 (71 %) terminally ill patients had stable disease one month after completion of QMRT or longer. \u0000Conclusions: Exposure to radiofrequency-mediated QMRT improved life expectancy and quality of life, along with arrest of tumor progression. This therapy can be safely positioned in a palliative care setting, transitioning to mainstream cancer care with more rigorous clinical validation.","PeriodicalId":73658,"journal":{"name":"Journal of clinical & experimental oncology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70249549","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 : 2016-12-05DOI: 10.4172/2324-9110.1000161
Ricardo Kenji Iguchi Panucci, Alex, re Mellitto, C. R. Oliveira, Welker de Mello Marin, C. Bincoletto
This study aims to assess the possible antitumor effects of the Ursolic Acid through cell death studies. Hence, Jurkat cell lines related to leukemia were subjected to treatment with different concentrations of the Ursolic Acid in order to identify their likely mechanism of death. After completion of cell viability tests, we suggest that this acid used in this study have antiproliferative/ cytotoxic activity in a dose-dependent manner. The results obtained indicate that the Ursolic Acid assessed in this study have cytotoxic activity with IC50% value of 10 μM. In addition, we observed that the IC50% value tested on the same cell line revealed a significant percentage of stagnant cells in cell cycle sub-G1 phase, a finding that allows us to infer the cytotoxic ability of the acid assessed.
{"title":"In vitro Study of Anti-Leukemic Potential of Ursolic Acid in Jurkat Cell Line","authors":"Ricardo Kenji Iguchi Panucci, Alex, re Mellitto, C. R. Oliveira, Welker de Mello Marin, C. Bincoletto","doi":"10.4172/2324-9110.1000161","DOIUrl":"https://doi.org/10.4172/2324-9110.1000161","url":null,"abstract":"This study aims to assess the possible antitumor effects of the Ursolic Acid through cell death studies. Hence, Jurkat cell lines related to leukemia were subjected to treatment with different concentrations of the Ursolic Acid in order to identify their likely mechanism of death. After completion of cell viability tests, we suggest that this acid used in this study have antiproliferative/ cytotoxic activity in a dose-dependent manner. The results obtained indicate that the Ursolic Acid assessed in this study have cytotoxic activity with IC50% value of 10 μM. In addition, we observed that the IC50% value tested on the same cell line revealed a significant percentage of stagnant cells in cell cycle sub-G1 phase, a finding that allows us to infer the cytotoxic ability of the acid assessed.","PeriodicalId":73658,"journal":{"name":"Journal of clinical & experimental oncology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70250059","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 : 2016-12-05DOI: 10.4172/2324-9110.1000150
Malshe Ag
Background: Current research is towards proton dynamics across the cell membrane with a view to make intra-cellular space acidic. Different proton migration inhibitors are being tried, need for developing appropriate transporter with lesser side effects is being felt. These efforts have ignored realising acid-base variations and variant pH leading to impaired glycolysis rate. Aim:Use of proton rich chemical like hydrochloric acid would rebalance acid-base proportion and bring pH back into accepted range avoiding malignant cell formation. Normalising glycolysis rate would obviate need of developing anti-porter inhibitor compounds. Design:Hypothesizing; malignancy developed following imbalance between acid-base proportions of intra and extra cellular environment. Proton dynamics via use of proton rich chemical like hydrochloric acid rebalances and bring pH back in the prescribed range, avoiding formation of a cancerous cell. Method: Hypothesis based on available published work. Results: Hydrochloric acid restores acid-base proportions, increases oxygen contents of RBCs, CTLs besides acidifying cytosolic environment thus bringing about apoptosis of a malignant cell. Conclusion: Malignancy is pH dependent. Increasing intracellular alkalinity is the beginning of cancerous development. Adequate availability of proton rich chemical like HCl is essential in maintaining acid-base balance and alkaline pH throughout in the prescribed range, thus avoiding formation of malignancy.
{"title":"Hydrogen ion/Proton Dynamics: A Possible Therapeutic Approach in MalignancyTreatment","authors":"Malshe Ag","doi":"10.4172/2324-9110.1000150","DOIUrl":"https://doi.org/10.4172/2324-9110.1000150","url":null,"abstract":"Background: Current research is towards proton dynamics across the cell membrane with a view to make intra-cellular space acidic. Different proton migration inhibitors are being tried, need for developing appropriate transporter with lesser side effects is being felt. These efforts have ignored realising acid-base variations and variant pH leading to impaired glycolysis rate. \u0000Aim:Use of proton rich chemical like hydrochloric acid would rebalance acid-base proportion and bring pH back into accepted range avoiding malignant cell formation. Normalising glycolysis rate would obviate need of developing anti-porter inhibitor compounds. \u0000Design:Hypothesizing; malignancy developed following imbalance between acid-base proportions of intra and extra cellular environment. Proton dynamics via use of proton rich chemical like hydrochloric acid rebalances and bring pH back in the prescribed range, avoiding formation of a cancerous cell. \u0000Method: Hypothesis based on available published work. \u0000Results: Hydrochloric acid restores acid-base proportions, increases oxygen contents of RBCs, CTLs besides acidifying cytosolic environment thus bringing about apoptosis of a malignant cell. \u0000Conclusion: Malignancy is pH dependent. Increasing intracellular alkalinity is the beginning of cancerous development. Adequate availability of proton rich chemical like HCl is essential in maintaining acid-base balance and alkaline pH throughout in the prescribed range, thus avoiding formation of malignancy.","PeriodicalId":73658,"journal":{"name":"Journal of clinical & experimental oncology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70249327","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 : 2016-12-05DOI: 10.4172/2324-9110.1000160
Josua A. Decker, Garima Jain, Tina Kießling, S. Philip, er, M. Rid, Thomas Barth, P. Möller, M. Cronauer, R. Marienfeld
Objective: Prostate carcinoma (PCa) is the leading causes of cancer-related death in elderly men. Although several risk factors for the development of prostate cancer have been identified, the impact of chronic prostatitis is still a matter of debate. A key event of prostate cancer pathogenesis is the decrease of the homeo box protein NKX3.1 in the luminal epithelial cells of the prostate observed in early pre-cancerous lesions. Furthermore, inactivation of Nkx3.1 in a mouse model led to high incidence of prostatic intraepithelial neoplasia (PIN) formation underscoring the importance of NKX3.1 loss. In this study, we aimed to define the impact of diverse cytokines and growth factors known to be expressed during chronic prostatitis on NKX3.1 expression. Methods: We determined the NKX3.1 expression in inflamed areas of prostatectomy specimens by immunohistochemistry. NKX3.1 protein and mRNA levels in cytokine and growth factor stimulated PCa cell lines were determined by western blot and RTqPCR. Transcriptional activity of the androgen receptor (AR) was determined by luciferase reporter assays and impact of the AR on NKX3.1 expression by siRNA mediated AR knock down. Results: Treatment of prostate carcinoma cell lines with epidermal growth factor (EGF) dramatically reduced NKX3.1 protein and mRNA levels, while TNFα or IL-1α had only a moderate effect. Moreover, EGF or a combination of PMA and ionomycin (P+I) also caused diminished levels of the AR. However, while NKX3.1 reduction is observed as early as one hour after stimulation the decrease of AR occurred with a delayed kinetic. We show that P+I-induced NKX3.1 proteolysis is proteasome-dependent and influenced by protein kinase C. Conclusion: In summary, we provide evidences for a crucial role of inflammatory mitogenic factors leading to reduced NKX3.1 and AR levels which might contribute to the initiation of pre-cancerous PIN lesions.
{"title":"Loss of the Tumor Suppressor NKX3.1 in Prostate Cancer Cells is Induced by Prostatitis Related Mitogens","authors":"Josua A. Decker, Garima Jain, Tina Kießling, S. Philip, er, M. Rid, Thomas Barth, P. Möller, M. Cronauer, R. Marienfeld","doi":"10.4172/2324-9110.1000160","DOIUrl":"https://doi.org/10.4172/2324-9110.1000160","url":null,"abstract":"Objective: Prostate carcinoma (PCa) is the leading causes of cancer-related death in elderly men. Although several risk factors for the development of prostate cancer have been identified, the impact of chronic prostatitis is still a matter of debate. A key event of prostate cancer pathogenesis is the decrease of the homeo box protein NKX3.1 in the luminal epithelial cells of the prostate observed in early pre-cancerous lesions. Furthermore, inactivation of Nkx3.1 in a mouse model led to high incidence of prostatic intraepithelial neoplasia (PIN) formation underscoring the importance of NKX3.1 loss. In this study, we aimed to define the impact of diverse cytokines and growth factors known to be expressed during chronic prostatitis on NKX3.1 expression. \u0000Methods: We determined the NKX3.1 expression in inflamed areas of prostatectomy specimens by immunohistochemistry. NKX3.1 protein and mRNA levels in cytokine and growth factor stimulated PCa cell lines were determined by western blot and RTqPCR. Transcriptional activity of the androgen receptor (AR) was determined by luciferase reporter assays and impact of the AR on NKX3.1 expression by siRNA mediated AR knock down. \u0000Results: Treatment of prostate carcinoma cell lines with epidermal growth factor (EGF) dramatically reduced NKX3.1 protein and mRNA levels, while TNFα or IL-1α had only a moderate effect. Moreover, EGF or a combination of PMA and ionomycin (P+I) also caused diminished levels of the AR. However, while NKX3.1 reduction is observed as early as one hour after stimulation the decrease of AR occurred with a delayed kinetic. We show that P+I-induced NKX3.1 proteolysis is proteasome-dependent and influenced by protein kinase C. \u0000Conclusion: In summary, we provide evidences for a crucial role of inflammatory mitogenic factors leading to reduced NKX3.1 and AR levels which might contribute to the initiation of pre-cancerous PIN lesions.","PeriodicalId":73658,"journal":{"name":"Journal of clinical & experimental oncology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70249507","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 : 2016-12-05DOI: 10.4172/2324-9110.1000163
Lauren T. Kerivan, Michael Reintgen, Eric Reintgen, Jeff Smith, Julie Claar, D. Wenk, D. Reintgen
Male Breast Cancer Breast cancer is one of the most common malignancies in women but is relatively rare in men with an incidence rate of 0.5% compared to female breast cancer. The risk of breast cancer in male increases with age and men usually present with later stage of disease those results in a worse outcome.
{"title":"Male Breast Cancer","authors":"Lauren T. Kerivan, Michael Reintgen, Eric Reintgen, Jeff Smith, Julie Claar, D. Wenk, D. Reintgen","doi":"10.4172/2324-9110.1000163","DOIUrl":"https://doi.org/10.4172/2324-9110.1000163","url":null,"abstract":"Male Breast Cancer \u0000Breast cancer is one of the most common malignancies in women but is relatively rare in men with an incidence rate of 0.5% compared to female breast cancer. The risk of breast cancer in male increases with age and men usually present with later stage of disease those results in a worse outcome.","PeriodicalId":73658,"journal":{"name":"Journal of clinical & experimental oncology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70249692","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 : 2016-12-05DOI: 10.4172/2324-9110.1000159
Mahboubeh Ashourpour, A. Namdar, N. Kheshtchin, Morteza Hafezi, Najmeh Khosravianfar, M. Ajami, B. Delfan, Yaser Azizi, S. Arab, R. Mirzaei, A. Mirshafiey, J. Hadjati, A. Razavi
Background: Immunosuppression in melanoma is mediated by increased accumulation of Myeloid Derived Suppressor Cells (MDSCs). Olive Leaf Extract (OLE) has been developed as a natural anti-inflammatory, anti-oxidant, anti-proliferative and antiapoptotic agent on cancer immunotherapy. Objective: To investigate whether OLE could inhibit MDSCs, enhance anti-tumor activities and consequently increase the survival rate of the murine melanoma model. Methods: The C57BL/6 mice were inoculated subcutaneously with B16/F10 melanoma tumor cell lines. Induced mice were orally treated with 500 mgkg-1 of olive extract per kg of body weight for 8 consecutive days. The frequency and function of MDSCs and induction of inflammatory mediators as well as tumor growth and survival rate were assessed in treated and untreated mice. Results: The results of current study revealed that the optimal dose of OLE (500 mgkg-1) reduced the tumor growth (40%), and prolonged mice survival (25%) by significant decreasing (P<0.05) the number (over 50%), and suppressive function of MDSCs (over 60%) (P<0.05). OLE was also significantly (P<0.05) down regulated the induction of inflammatory agents in melanoma-bearing mice (over 50%) at the applied dose (500 mgkg-1). Conclusion: Therefore, these results altogether provided some evidence that regulation of immunosuppression were the possible therapeutic effects of OLE in tumor cells.
{"title":"Olive Leaf Extract Reduces Myeloid-Derived Suppressor Cells, and Modulates the Function of Residual Cells in Experimental Model of Melanoma","authors":"Mahboubeh Ashourpour, A. Namdar, N. Kheshtchin, Morteza Hafezi, Najmeh Khosravianfar, M. Ajami, B. Delfan, Yaser Azizi, S. Arab, R. Mirzaei, A. Mirshafiey, J. Hadjati, A. Razavi","doi":"10.4172/2324-9110.1000159","DOIUrl":"https://doi.org/10.4172/2324-9110.1000159","url":null,"abstract":"Background: Immunosuppression in melanoma is mediated by increased accumulation of Myeloid Derived Suppressor Cells (MDSCs). Olive Leaf Extract (OLE) has been developed as a natural anti-inflammatory, anti-oxidant, anti-proliferative and antiapoptotic agent on cancer immunotherapy. \u0000Objective: To investigate whether OLE could inhibit MDSCs, enhance anti-tumor activities and consequently increase the survival rate of the murine melanoma model. \u0000Methods: The C57BL/6 mice were inoculated subcutaneously with B16/F10 melanoma tumor cell lines. Induced mice were orally treated with 500 mgkg-1 of olive extract per kg of body weight for 8 consecutive days. The frequency and function of MDSCs and induction of inflammatory mediators as well as tumor growth and survival rate were assessed in treated and untreated mice. \u0000Results: The results of current study revealed that the optimal dose of OLE (500 mgkg-1) reduced the tumor growth (40%), and prolonged mice survival (25%) by significant decreasing (P<0.05) the number (over 50%), and suppressive function of MDSCs (over 60%) (P<0.05). OLE was also significantly (P<0.05) down regulated the induction of inflammatory agents in melanoma-bearing mice (over 50%) at the applied dose (500 mgkg-1). \u0000Conclusion: Therefore, these results altogether provided some evidence that regulation of immunosuppression were the possible therapeutic effects of OLE in tumor cells.","PeriodicalId":73658,"journal":{"name":"Journal of clinical & experimental oncology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70249447","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 : 2016-12-05DOI: 10.4172/2324-9110.1000164
Raman A Babayeuski, V. Ortega, C. Mendiola, I. Jatoi, G. Velagaleti
Colonic Adenocarcinoma in a Patient with Velo Cardio Facial Syndrome (VCFS) and 22q11.2 Microdeletion Colorectal cancer (CRC) is one of the most common cancers and second most common cause of cancer related mortality. Chromosomal instability and microsatellite instability have long been considered as major factors in the etiology of colon cancer. Chromosome 22q losses have been reported both in primary and metastatic CRC. Chromosome 22q11.2 microdeletion syndrome is an umbrella term that encompasses various phenotypes, and is the most common microdeletion syndrome in humans. We report an uncommon association of colon cancer in a patient with VCFS and 22q11.2 microdeletion. While this finding may be coincidental, it is important to further evaluate patients with CRC and 22q11.2 microdeletion to assess if this association is more frequent than has been reported.
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