There is a lack of evidence regarding the use of betel quid (BQ) and its potential contribution to oral cancer. Limited attention has been directed towards investigating the involvement of BQ-derived organic acids in the modulation of metabolic-epigenomic pathways associated with oral cancer initiation and progression. We employed novel protocol for preparing saliva-amalgamated BQ filtrate (SABFI) that mimics the oral cavity environment. SABFI and saliva control were further purified by an in-house developed vertical tube gel electrophoresis tool. The purified SABFI was then subjected to liquid chromatography-high resolution mass spectrometry analysis to identify the presence of organic acids. Profiling of SABFI showed a pool of prominent organic acids such as citric acid. malic acid, fumaric acid, 2-methylcitric acid, 2-hydroxyglutarate, cis-aconitic acid, succinic acid, 2-hydroxyglutaric acid lactone, tartaric acid and β-ketoglutaric acid. SABFI showed anti-proliferative and early apoptosis effects in oral cancer cells. Molecular docking and molecular dynamics simulations predicted that SABFI-derived organic acids as potential inhibitors of the epigenetic demethylase enzyme, Ten-Eleven Translocation-2 (TET2). By binding to the active site of α-ketoglutarate, a known substrate of TET2, these organic acids are likely to act as competitive inhibitors. This study reports a novel approach to study SABFI-derived organic acids that could mimic the chemical composition of BQ in the oral cavity. These SABFI-derived organic acids projected as inhibitors of TET2 and could be explored for their role oral cancer.
{"title":"Organic Acids Derived from Saliva-amalgamated Betel Quid Filtrate Are Predicted as a Ten-eleven Translocation-2 Inhibitor.","authors":"Devyani Bhatkar, Nistha Ananda, Kiran Bharat Lokhande, Kratika Khunteta, Priyadarshini Jain, Ameya Hebale, Sachin C Sarode, Nilesh Kumar Sharma","doi":"10.15430/JCP.2023.28.3.115","DOIUrl":"10.15430/JCP.2023.28.3.115","url":null,"abstract":"<p><p>There is a lack of evidence regarding the use of betel quid (BQ) and its potential contribution to oral cancer. Limited attention has been directed towards investigating the involvement of BQ-derived organic acids in the modulation of metabolic-epigenomic pathways associated with oral cancer initiation and progression. We employed novel protocol for preparing saliva-amalgamated BQ filtrate (SABFI) that mimics the oral cavity environment. SABFI and saliva control were further purified by an in-house developed vertical tube gel electrophoresis tool. The purified SABFI was then subjected to liquid chromatography-high resolution mass spectrometry analysis to identify the presence of organic acids. Profiling of SABFI showed a pool of prominent organic acids such as citric acid. malic acid, fumaric acid, 2-methylcitric acid, 2-hydroxyglutarate, <i>cis-</i>aconitic acid, succinic acid, 2-hydroxyglutaric acid lactone, tartaric acid and β-ketoglutaric acid. SABFI showed anti-proliferative and early apoptosis effects in oral cancer cells. Molecular docking and molecular dynamics simulations predicted that SABFI-derived organic acids as potential inhibitors of the epigenetic demethylase enzyme, Ten-Eleven Translocation-2 (TET2). By binding to the active site of α-ketoglutarate, a known substrate of TET2, these organic acids are likely to act as competitive inhibitors. This study reports a novel approach to study SABFI-derived organic acids that could mimic the chemical composition of BQ in the oral cavity. These SABFI-derived organic acids projected as inhibitors of TET2 and could be explored for their role oral cancer.</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"28 3","pages":"115-130"},"PeriodicalIF":2.5,"publicationDate":"2023-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/7b/09/jcp-28-3-115.PMC10564634.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41201911","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A category of diseases known as cancer includes abnormal cell development and the ability to infiltrate or spread to other regions of the body, making them a major cause of mortality worldwide. Chemotherapy, radiation, the use of cytotoxic medicines, and surgery are the mainstays of cancer treatment today. Plants or products produced from them hold promise as a source of anti-cancer medications that have fewer adverse effects. Due to the presence of numerous phytochemicals that have been isolated from various parts of the Hibiscus sabdariffa (HS) plant, including anthocyanin, flavonoids, saponins, tannins, polyphenols, organic acids, caffeic acids, citric acids, protocatechuic acid, and others, extracts of this plant have been reported to have anti-cancer effects. These compounds have been shown to reduce cancer cell proliferation, induce apoptosis, and cause cell cycle arrest. They also increase the expression levels of the cell cycle inhibitors (p53, p21, and p27) and the pro-apoptotic proteins (BAD, Bax, caspase 3, caspase 7, caspase 8, and caspase 9). This review highlights various intracellular signalling pathways involved in cancer preventive potential of HS.
{"title":"Novel Insight into the Cellular and Molecular Signalling Pathways on Cancer Preventing Effects of <i>Hibiscus sabdariffa</i>: A Review.","authors":"Raihana Yasmin, Sangeeta Gogoi, Jumi Bora, Arijit Chakraborty, Susmita Dey, Ghazal Ghaziri, Surajit Bhattacharjee, Laishram Hemchandra Singh","doi":"10.15430/JCP.2023.28.3.77","DOIUrl":"10.15430/JCP.2023.28.3.77","url":null,"abstract":"<p><p>A category of diseases known as cancer includes abnormal cell development and the ability to infiltrate or spread to other regions of the body, making them a major cause of mortality worldwide. Chemotherapy, radiation, the use of cytotoxic medicines, and surgery are the mainstays of cancer treatment today. Plants or products produced from them hold promise as a source of anti-cancer medications that have fewer adverse effects. Due to the presence of numerous phytochemicals that have been isolated from various parts of the <i>Hibiscus sabdariffa</i> (HS) plant, including anthocyanin, flavonoids, saponins, tannins, polyphenols, organic acids, caffeic acids, citric acids, protocatechuic acid, and others, extracts of this plant have been reported to have anti-cancer effects. These compounds have been shown to reduce cancer cell proliferation, induce apoptosis, and cause cell cycle arrest. They also increase the expression levels of the cell cycle inhibitors (p53, p21, and p27) and the pro-apoptotic proteins (BAD, Bax, caspase 3, caspase 7, caspase 8, and caspase 9). This review highlights various intracellular signalling pathways involved in cancer preventive potential of HS.</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"28 3","pages":"77-92"},"PeriodicalIF":2.5,"publicationDate":"2023-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/2c/05/jcp-28-3-77.PMC10564632.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41201910","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-09-30DOI: 10.15430/JCP.2023.28.3.93
Soo In Choi, Nayoung Kim, Ryoung Hee Nam, Jae Young Jang, Eun Hye Kim, SungChan Ha, Kisung Kang, Wonseok Lee, HyeLim Choi, Yeon-Ran Kim, Yeong-Jae Seok, Cheol Min Shin, Dong Ho Lee
Roseburia faecis, a butyrate-producing, gram-positive anaerobic bacterium, was evaluated for its usefulness against repeated water avoidance stress (WAS)-induced irritable bowel syndrome (IBS) in a rat model, and the underlying mechanism was explored. We divided the subjects into three groups: one without stress exposure, another subjected to daily 1-hour WAS for 10 days, and a third exposed to the same WAS regimen while also receiving two different R. faecis strains (BBH024 or R22-12-24) via oral gavage for the same 10-day duration. Fecal pellet output (FPO), a toluidine blue assay for mast cell infiltration, and fecal microbiota analyses were conducted using 16S rRNA metagenomic sequencing. Predictive functional profiling of microbial communities in metabolism was also conducted. FPO and colonic mucosal mast cell counts were significantly higher in the WAS group than in the control group (male, P = 0.004; female, P = 0.027). The administration of both BBH024 (male, P = 0.015; female, P = 0.022) and R22-12-24 (male, P = 0.003; female, P = 0.040) significantly reduced FPO. Submucosal mast cell infiltration in the colon showed a similar pattern in males. In case of fecal microbiota, the WAS with R. faecis group showed increased abundance of the Roseburia genus compared to WAS alone. Moreover, the expression of a gene encoding a D-methionine transport system substrate-binding protein was significantly elevated in the WAS with R. faecis group compared to that in the WAS (male, P = 0.028; female, P = 0.025) group. These results indicate that R. faecis is a useful probiotic for treating IBS and colonic microinflammation.
{"title":"The Protective Effect of <i>Roseburia faecis</i> Against Repeated Water Avoidance Stress-induced Irritable Bowel Syndrome in a Wister Rat Model.","authors":"Soo In Choi, Nayoung Kim, Ryoung Hee Nam, Jae Young Jang, Eun Hye Kim, SungChan Ha, Kisung Kang, Wonseok Lee, HyeLim Choi, Yeon-Ran Kim, Yeong-Jae Seok, Cheol Min Shin, Dong Ho Lee","doi":"10.15430/JCP.2023.28.3.93","DOIUrl":"10.15430/JCP.2023.28.3.93","url":null,"abstract":"<p><p><i>Roseburia faecis,</i> a butyrate-producing, gram-positive anaerobic bacterium, was evaluated for its usefulness against repeated water avoidance stress (WAS)-induced irritable bowel syndrome (IBS) in a rat model, and the underlying mechanism was explored. We divided the subjects into three groups: one without stress exposure, another subjected to daily 1-hour WAS for 10 days, and a third exposed to the same WAS regimen while also receiving two different <i>R. faecis</i> strains (BBH024 or R22-12-24) via oral gavage for the same 10-day duration. Fecal pellet output (FPO), a toluidine blue assay for mast cell infiltration, and fecal microbiota analyses were conducted using 16S rRNA metagenomic sequencing. Predictive functional profiling of microbial communities in metabolism was also conducted. FPO and colonic mucosal mast cell counts were significantly higher in the WAS group than in the control group (male, <i>P</i> = 0.004; female, <i>P</i> = 0.027). The administration of both BBH024 (male, <i>P</i> = 0.015; female, <i>P</i> = 0.022) and R22-12-24 (male, <i>P</i> = 0.003; female, <i>P</i> = 0.040) significantly reduced FPO. Submucosal mast cell infiltration in the colon showed a similar pattern in males. In case of fecal microbiota, the WAS with <i>R. faecis</i> group showed increased abundance of the <i>Roseburia</i> genus compared to WAS alone. Moreover, the expression of a gene encoding a D-methionine transport system substrate-binding protein was significantly elevated in the WAS with <i>R. faecis</i> group compared to that in the WAS (male, <i>P</i> = 0.028; female, <i>P</i> = 0.025) group. These results indicate that <i>R. faecis</i> is a useful probiotic for treating IBS and colonic microinflammation.</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"28 3","pages":"93-105"},"PeriodicalIF":2.5,"publicationDate":"2023-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/3f/76/jcp-28-3-93.PMC10564633.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41201912","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-06-30DOI: 10.15430/JCP.2023.28.2.53
Yoonyoung Jang, Taehwa Kim, Brian H S Kim, Jung Ho Kim, Hye Seong, Youn Jeong Kim, Boyoung Park
This study aimed to estimate the medical cost of cancer in the first five years of diagnosis and in the final six months before death in people who developed cancer after human immunodeficiency virus (HIV) infection in Korea. The study utilized the Korea National Health Insurance Service-National Health Information Database (NHIS-NHID). Among 16,671 patients diagnosed with HIV infection from 2004 to 2020 in Korea, we identified 757 patients newly diagnosed with cancer after HIV diagnosis. The medical costs for 60 months after diagnosis and the last six months before death were calculated from 2006 to 2020. The mean annual medical cost due to cancer in HIV-infected people with cancer was higher for acquired immunodeficiency syndrome (AIDS)-defining cancers (48,242 USD) than for non-AIDS-defining cancers (24,338 USD), particularly non-Hodgkin's lymphoma (53,007 USD), for the first year of cancer diagnosis. Approximately 25% of the cost for the first year was disbursed during the first month of cancer diagnosis. From the second year, the mean annual medical cost due to cancer was significantly reduced. The total medical cost was higher for non-AIDS-defining cancers, reflecting their higher incidence rates despite lower mean medical costs. The mean monthly total medical cost per HIV-infected person who died after cancer diagnosis increased closer to the time of death. The estimated burden of medical costs in patients with HIV in the present study may be an important index for defining healthcare policies in HIV patients in whom the cancer-related burden is expected to increase.
{"title":"Economic Burden of Cancer for the First Five Years after Cancer Diagnosis in Patients with Human Immunodeficiency Virus in Korea.","authors":"Yoonyoung Jang, Taehwa Kim, Brian H S Kim, Jung Ho Kim, Hye Seong, Youn Jeong Kim, Boyoung Park","doi":"10.15430/JCP.2023.28.2.53","DOIUrl":"https://doi.org/10.15430/JCP.2023.28.2.53","url":null,"abstract":"<p><p>This study aimed to estimate the medical cost of cancer in the first five years of diagnosis and in the final six months before death in people who developed cancer after human immunodeficiency virus (HIV) infection in Korea. The study utilized the Korea National Health Insurance Service-National Health Information Database (NHIS-NHID). Among 16,671 patients diagnosed with HIV infection from 2004 to 2020 in Korea, we identified 757 patients newly diagnosed with cancer after HIV diagnosis. The medical costs for 60 months after diagnosis and the last six months before death were calculated from 2006 to 2020. The mean annual medical cost due to cancer in HIV-infected people with cancer was higher for acquired immunodeficiency syndrome (AIDS)-defining cancers (48,242 USD) than for non-AIDS-defining cancers (24,338 USD), particularly non-Hodgkin's lymphoma (53,007 USD), for the first year of cancer diagnosis. Approximately 25% of the cost for the first year was disbursed during the first month of cancer diagnosis. From the second year, the mean annual medical cost due to cancer was significantly reduced. The total medical cost was higher for non-AIDS-defining cancers, reflecting their higher incidence rates despite lower mean medical costs. The mean monthly total medical cost per HIV-infected person who died after cancer diagnosis increased closer to the time of death. The estimated burden of medical costs in patients with HIV in the present study may be an important index for defining healthcare policies in HIV patients in whom the cancer-related burden is expected to increase.</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"28 2","pages":"53-63"},"PeriodicalIF":2.5,"publicationDate":"2023-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10331032/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9814474","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-06-30DOI: 10.15430/JCP.2023.28.2.47
Yu Rim Kim, Ji Yoon Baek, Seung Hee Seo, Hyeree Park, Sooyoung Cho, Aesun Shin, Sup, Sup
Data from the Korean National Health Insurance Service (NHIS) have been widely used to provide real-world evidence. Due to the nature of claims data, researchers use operational definitions to define patients with specific diseases. This study aimed to conduct a systematic review of the operational definitions of liver cancer used in studies based on the NHIS database and to suggest the most appropriate operational definition. Literature search was completed on January 6, 2021, using PubMed and KoreaMed. We applied the most frequently used operational definitions of liver cancer to the NHIS-National Sample Cohort and calculated age-standardized incidence rates (ASRs) of liver cancer by year. The ASRs using each operational definition were compared with the ASR from the Korea Central Cancer (KCCR) data. Among 236 articles, 90 were selected for review, covering histologically various kinds of liver cancer and varied by study subjects. Most studies (n = 79) did not mention whether the codes for the operational definition were from only the main diagnosis or from both the main and sub-diagnosis. The most frequently used operational definition was C22 (n = 39); however, the most similar operational definition was the ASR using "C22.0 or C22.9" for men and "C22.0" for women as the main diagnosis to the ASR from the KCCR. Based on the comparison with KCCR data, we suggest using "C22.0 or C22.9" for men and "C22.0" for women as the main diagnosis for the operational definition of liver cancer when using the NHIS data.
{"title":"Operational Definition of Liver Cancer in Studies Using Data from the National Health Insurance Service: A Systematic Review.","authors":"Yu Rim Kim, Ji Yoon Baek, Seung Hee Seo, Hyeree Park, Sooyoung Cho, Aesun Shin, Sup, Sup","doi":"10.15430/JCP.2023.28.2.47","DOIUrl":"https://doi.org/10.15430/JCP.2023.28.2.47","url":null,"abstract":"<p><p>Data from the Korean National Health Insurance Service (NHIS) have been widely used to provide real-world evidence. Due to the nature of claims data, researchers use operational definitions to define patients with specific diseases. This study aimed to conduct a systematic review of the operational definitions of liver cancer used in studies based on the NHIS database and to suggest the most appropriate operational definition. Literature search was completed on January 6, 2021, using PubMed and KoreaMed. We applied the most frequently used operational definitions of liver cancer to the NHIS-National Sample Cohort and calculated age-standardized incidence rates (ASRs) of liver cancer by year. The ASRs using each operational definition were compared with the ASR from the Korea Central Cancer (KCCR) data. Among 236 articles, 90 were selected for review, covering histologically various kinds of liver cancer and varied by study subjects. Most studies (n = 79) did not mention whether the codes for the operational definition were from only the main diagnosis or from both the main and sub-diagnosis. The most frequently used operational definition was C22 (n = 39); however, the most similar operational definition was the ASR using \"C22.0 or C22.9\" for men and \"C22.0\" for women as the main diagnosis to the ASR from the KCCR. Based on the comparison with KCCR data, we suggest using \"C22.0 or C22.9\" for men and \"C22.0\" for women as the main diagnosis for the operational definition of liver cancer when using the NHIS data.</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"28 2","pages":"47-52"},"PeriodicalIF":2.5,"publicationDate":"2023-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10331033/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10191200","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-06-30DOI: 10.15430/JCP.2023.28.2.75
Soojung Jin, Jung-Ha Park, Hee Jung Yun, You Na Oh, Seunghye Oh, Yung Hyun Choi, Byung Woo Kim, Hyun Ju Kwon
[This corrects the article on p. 221 in vol. 27, PMID: 36713942.].
[这更正了第27卷221页的文章,PMID: 36713942]。
{"title":"Erratum: Cedrol, a Sesquiterpene Isolated from <i>Juniperus chinensis</i>, Inhibits Human Colorectal Tumor Growth associated through Downregulation of Minichromosome Maintenance Proteins.","authors":"Soojung Jin, Jung-Ha Park, Hee Jung Yun, You Na Oh, Seunghye Oh, Yung Hyun Choi, Byung Woo Kim, Hyun Ju Kwon","doi":"10.15430/JCP.2023.28.2.75","DOIUrl":"https://doi.org/10.15430/JCP.2023.28.2.75","url":null,"abstract":"<p><p>[This corrects the article on p. 221 in vol. 27, PMID: 36713942.].</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"28 2","pages":"75"},"PeriodicalIF":2.5,"publicationDate":"2023-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10331034/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10172010","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-06-30DOI: 10.15430/JCP.2023.28.2.64
Dessiet Oma, Maria Teklemariam, Daniel Seifu, Zelalem Desalegn, Endale Anberbir, Tamrat Abebe, Solomon Mequannent, Solomon Tebeje, Wajana Lako Labisso
The application of immunohistochemistry (IHC) for molecular characterization of breast cancer (BC) is of paramount importance; however, it is not universally standardized, subject to observer variability and quantifying is a challenge. An alternative molecular technology, such as endpoint reverse transcription (RT)-PCR gene expression analysis, may improve observer variability and diagnostic accuracy. This study was intended to compare IHC with the RT-PCR based technique and assess the potential of RT-PCR for molecular subtyping of BC. In this comparative cross-sectional study, 54 BC tissues were collected from three public hospitals in Addis Ababa and shipped to Gynaecology department at Martin-Luther University (Germany) for laboratory analysis. Only 41 samples were qualified for IHC and RT-PCR investigation of estrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor receptor 2 (HER2), and Ki-67 protein expression analysis. Kappa statistics was used to assess the concordance between the two techniques. The overall percent agreement between RT-PCR and IHC was 68.3% for ER (positive percent agreement [PPA] 71.1%; negative percent agreement [NPA] 33.3%), 39.0% for PR (PPA 14.3%; NPA 92.3%), and 82.9% for HER2 (PPA 62.5%; NPA 87.9%). Cohen's κ-values of 0.018 (< 0.20), 0.045 (< 0.200), and 0.481 (0.41-0.60) were generated for ER, PR, and HER2, respectively. Concordance for molecular subtypes was only 56.1% (23/41) and 0.20 kappa value. IHC and endpoint RT-PCR techniques have shown to be discordant for 43% samples. Molecular subtyping using endpoint RT-PCR was fairly concordant with IHC. Thus, endpoint RT-PCR may give an objective result, and can be applied for BC subtyping.
{"title":"Immunohistochemistry versus PCR Technology for Molecular Subtyping of Breast Cancer: Multicentered Expereinces from Addis Ababa, Ethiopia.","authors":"Dessiet Oma, Maria Teklemariam, Daniel Seifu, Zelalem Desalegn, Endale Anberbir, Tamrat Abebe, Solomon Mequannent, Solomon Tebeje, Wajana Lako Labisso","doi":"10.15430/JCP.2023.28.2.64","DOIUrl":"https://doi.org/10.15430/JCP.2023.28.2.64","url":null,"abstract":"<p><p>The application of immunohistochemistry (IHC) for molecular characterization of breast cancer (BC) is of paramount importance; however, it is not universally standardized, subject to observer variability and quantifying is a challenge. An alternative molecular technology, such as endpoint reverse transcription (RT)-PCR gene expression analysis, may improve observer variability and diagnostic accuracy. This study was intended to compare IHC with the RT-PCR based technique and assess the potential of RT-PCR for molecular subtyping of BC. In this comparative cross-sectional study, 54 BC tissues were collected from three public hospitals in Addis Ababa and shipped to Gynaecology department at Martin-Luther University (Germany) for laboratory analysis. Only 41 samples were qualified for IHC and RT-PCR investigation of estrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor receptor 2 (HER2), and Ki-67 protein expression analysis. Kappa statistics was used to assess the concordance between the two techniques. The overall percent agreement between RT-PCR and IHC was 68.3% for ER (positive percent agreement [PPA] 71.1%; negative percent agreement [NPA] 33.3%), 39.0% for PR (PPA 14.3%; NPA 92.3%), and 82.9% for HER2 (PPA 62.5%; NPA 87.9%). Cohen's κ-values of 0.018 (< 0.20), 0.045 (< 0.200), and 0.481 (0.41-0.60) were generated for ER, PR, and HER2, respectively. Concordance for molecular subtypes was only 56.1% (23/41) and 0.20 kappa value. IHC and endpoint RT-PCR techniques have shown to be discordant for 43% samples. Molecular subtyping using endpoint RT-PCR was fairly concordant with IHC. Thus, endpoint RT-PCR may give an objective result, and can be applied for BC subtyping.</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"28 2","pages":"64-74"},"PeriodicalIF":2.5,"publicationDate":"2023-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10331035/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9869887","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-06-30DOI: 10.15430/JCP.2023.28.2.40
Min Chang Oh, Pincha Devage Sameera Madushan Fernando, Mei Jing Piao, Kyoung Ah Kang, Herath Mudiyanselage Udari Lakmini Herath, Jin Won Hyun
Excessive UVB exposure causes development of both malignant and non-malignant melanoma via the secretion of α-melanocyte-stimulating hormone (α-MSH). We investigated whether baicalein (5,6,7-trihydroxyflavone) could inhibit α-MSH-stimulated melanogenesis. Baicalein prevented UVB- and α-MSH-induced melanin production and attenuated α-MSH-stimulated tyrosinase (monophenol monooxygenase) activity, and expression of tyrosinase and tyrosine-related protein-2. In addition, baicalein prevented melanogenesis and pigmentation via the p38 mitogen-activated protein kinases signaling pathway. These findings suggest that baicalein represents a natural compound for attenuating melanogenesis.
{"title":"Baicalein Inhibits α-Melanocyte-stimulating Hormone-stimulated Melanogenesis via p38 Mitogen-activated Protein Kinase Pathway in B16F10 Mouse Melanoma Cells.","authors":"Min Chang Oh, Pincha Devage Sameera Madushan Fernando, Mei Jing Piao, Kyoung Ah Kang, Herath Mudiyanselage Udari Lakmini Herath, Jin Won Hyun","doi":"10.15430/JCP.2023.28.2.40","DOIUrl":"https://doi.org/10.15430/JCP.2023.28.2.40","url":null,"abstract":"<p><p>Excessive UVB exposure causes development of both malignant and non-malignant melanoma via the secretion of α-melanocyte-stimulating hormone (α-MSH). We investigated whether baicalein (5,6,7-trihydroxyflavone) could inhibit α-MSH-stimulated melanogenesis. Baicalein prevented UVB- and α-MSH-induced melanin production and attenuated α-MSH-stimulated tyrosinase (monophenol monooxygenase) activity, and expression of tyrosinase and tyrosine-related protein-2. In addition, baicalein prevented melanogenesis and pigmentation via the p38 mitogen-activated protein kinases signaling pathway. These findings suggest that baicalein represents a natural compound for attenuating melanogenesis.</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"28 2","pages":"40-46"},"PeriodicalIF":2.5,"publicationDate":"2023-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10331030/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10172582","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-06-30DOI: 10.15430/JCP.2023.28.2.31
Nazia Tarannum, Deepak Kumar, Ranu Agrawal
Herein, an instrument free facile acid-base titrimetric methodology is reported for lysophosphatidic acid (LPA) measurement in serum and plasma samples for ovarian cancer detection. The concept is based on the titrimetric method in which alkaline solution was titrated with free fatty acid. Free fatty acid is generated due to action of the lysophospholipase to LPA. A phospholipid derivative known as LPA can function as a signaling molecule. A glycerol backbone serves as the foundation for phosphatidic acid, which also has bonds to an unsaturated fatty acid at carbon-1, a hydroxyl group at carbon-2, and a phosphate molecule at carbon-3. Free fatty acid and glycerol-3-phosphate are formed when LPA reacts with lysophospholipase. The formation of free fatty acid depends on the concentration of LPA. The standard graph of known concentrations of LPA, LPA spiked serum and LPA spiked plasma was plotted. The concentration of LPA in unknown serum and plasma were calculated from the standard graph. The limit of detection of LPA in spiked serum and plasma samples via titrimetric assay was calculated as 0.156 μmol/L. A patient's chance of survival may be outweighed by an early diagnosis of ovarian cancer.
{"title":"Facile Titrimetric Assay of Lysophosphatidic Acid in Human Serum and Plasma for Ovarian Cancer Detection.","authors":"Nazia Tarannum, Deepak Kumar, Ranu Agrawal","doi":"10.15430/JCP.2023.28.2.31","DOIUrl":"https://doi.org/10.15430/JCP.2023.28.2.31","url":null,"abstract":"<p><p>Herein, an instrument free facile acid-base titrimetric methodology is reported for lysophosphatidic acid (LPA) measurement in serum and plasma samples for ovarian cancer detection. The concept is based on the titrimetric method in which alkaline solution was titrated with free fatty acid. Free fatty acid is generated due to action of the lysophospholipase to LPA. A phospholipid derivative known as LPA can function as a signaling molecule. A glycerol backbone serves as the foundation for phosphatidic acid, which also has bonds to an unsaturated fatty acid at carbon-1, a hydroxyl group at carbon-2, and a phosphate molecule at carbon-3. Free fatty acid and glycerol-3-phosphate are formed when LPA reacts with lysophospholipase. The formation of free fatty acid depends on the concentration of LPA. The standard graph of known concentrations of LPA, LPA spiked serum and LPA spiked plasma was plotted. The concentration of LPA in unknown serum and plasma were calculated from the standard graph. The limit of detection of LPA in spiked serum and plasma samples via titrimetric assay was calculated as 0.156 μmol/L. A patient's chance of survival may be outweighed by an early diagnosis of ovarian cancer.</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"28 2","pages":"31-39"},"PeriodicalIF":2.5,"publicationDate":"2023-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10331031/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10172009","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-03-30DOI: 10.15430/JCP.2023.28.1.29
JunPyo Han, Yujin Jang, Dong Yeop Shin, Jun Lee, Young Rok Seo
[This corrects the article on p. 199 in vol. 27, PMID: 36713944.].
[这更正了第27卷第199页的文章,PMID: 36713944]。
{"title":"Erratum: A Genomic Approach to Identify the Difference between Acute and Chronic UVB Exposures in the Causation of Inflammation and Cancer.","authors":"JunPyo Han, Yujin Jang, Dong Yeop Shin, Jun Lee, Young Rok Seo","doi":"10.15430/JCP.2023.28.1.29","DOIUrl":"https://doi.org/10.15430/JCP.2023.28.1.29","url":null,"abstract":"<p><p>[This corrects the article on p. 199 in vol. 27, PMID: 36713944.].</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"28 1","pages":"29"},"PeriodicalIF":2.5,"publicationDate":"2023-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/9b/74/jcp-28-1-29.PMC10080014.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9265222","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}