Journal of Cancer Prevention最新文献

{"title":"The 50-Year War on Cancer Revisited: Should We Continue to Fight the Enemy Within?","authors":"Young-Joon Surh","doi":"10.15430/JCP.2021.26.4.219","DOIUrl":"https://doi.org/10.15430/JCP.2021.26.4.219","url":null,"abstract":"This year marks the 50th anniversary of the “War on Cancer” declared by Richard Nixon, a former President of the United States of America. By signing into law the National Cancer Act on December 23, 1971, Nixon hoped this action to be the landmark legislation taken by his administration. Nixon apparently had confidence that cancer would be conquered in 5 years. This was indeed a surprisingly wonderful X-mas present to the nation. The act represented an important turning point in cancer research as well as treatment. As a result of enthusiasm in US Congress for eradicating cancer, there was a remarkable increase in the budget of National Cancer Institute (NCI) of which substantial portions were spent in supporting the basic research to reduce the incidence, morbidity and mortality from cancer. According to Vincent Devita who served as Director of US NCI from July 9, 1980 to September 1, 1988 and later directed Yale Cancer Center, the results have been explosive, leading to the revolution in molecular biology of cancer [1]. Though the ‘War on Cancer’ was officially declared in 1971, it actually had begun in about two years ago. On December 9, 1969, full-page advertisements were appeared in Washington Post and New York Times, entitled: “Mr. Nixon: you can cure cancer”. These ads were planned and initiated by the Citizens’ Committee for the Conquest of Cancer in which Marry Lasker played a prominent role. She was the widow of Chicago advertising executive Albert Lasker, and was a socialite, a philanthropist, and an activist. As a longtime supporter of public health causes, including national health insurance, Mrs. Lasker used her influential power and political network to rally support for cancer research [2]. The ad was effective. President Nixon heard the voice of the people who expressed their concern and wish to cure cancer. In his famous State of the Union address in January 1971, Nixon made a special request for an extra $100 million (equivalent approximately to $690,000,000 in 2021) to launch an intensive campaign to find a cure for cancer, and also for whatever additional funds later, if necessary, that can effectively be used. Marry Lasker, together with other individuals including policymakers and investment bankers, developed the framework of the National Cancer Act, which the President endorsed by the end of that year [3].","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"26 4","pages":"219-223"},"PeriodicalIF":2.5,"publicationDate":"2021-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/b0/28/jcp-26-4-219.PMC8749321.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39834082","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}

{"title":"Fecal Microbial Enterotypes Differentially Respond to a High-fat Diet Based on Sex in Fischer-344 Rats.","authors":"Soo In Choi,&nbsp;Nayoung Kim,&nbsp;Ryoung Hee Nam,&nbsp;Ji Hyun Park,&nbsp;Heewon Nho,&nbsp;Jeong Eun Yu,&nbsp;Chin-Hee Song,&nbsp;Sun Min Lee,&nbsp;Dong Ho Lee","doi":"10.15430/JCP.2021.26.4.277","DOIUrl":"https://doi.org/10.15430/JCP.2021.26.4.277","url":null,"abstract":"<p><p>The gut microbiota interacts with the host gut environment, which is influenced by such factors as sex, age, and host diet. These factors induce changes in the microbial composition. The aim of this study was to identify differences in the gut microbiome of Fisher-344 (F344) rats fed a high-fat diet (HFD), depending on their age and sex. Fecal microbiomes from 6-, 31-, and 74-week-old, and 2-year-old both male and female rats (corresponding to 5-, 30-, 60-, and 80-year-old humans) were analyzed using 16S rRNA gene sequencing, phylogenetic investigation of communities by reconstruction of unobserved states, and enterotype (E) assessment. Moreover, the effect of an HFD on colonic epithelial cells was measured using real-time quantitative PCR. Alpha diversity decreased in the HFD group regardless of age and sex. Based on the enterotype clustering of the whole fecal microbiome, clusters from male rats were divided into E1 and E2 enterotypes, while clusters from female rats were divided into E1, E2, and E3 enterotypes. The female E3 group showed a significantly high abundance in the <i>Ruminococcus</i> genus and expression of <i>Tlr2</i> mRNA, which may reflect compensation to the HFD. Moreover, the female E3 group showed a lower ratio of opportunistic pathogenic strains to commensal strains compared to the female E2 group. Administration of an HFD influenced the rat fecal microbiota in all assessed age groups, which could be further differentiated by sex. In particular, female rats showed a compensatory enterotype response to an HFD compared to male rats.</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"26 4","pages":"277-288"},"PeriodicalIF":2.5,"publicationDate":"2021-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/23/14/jcp-26-4-277.PMC8749319.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39834089","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}

{"title":"Double-edged Sword Role of Iron-loaded Ferritin in Extracellular Vesicles.","authors":"Shinya Toyokuni,&nbsp;Yingyi Kong,&nbsp;Hao Zheng,&nbsp;Danyang Mi,&nbsp;Misako Katabuchi,&nbsp;Yashiro Motooka,&nbsp;Fumiya Ito","doi":"10.15430/JCP.2021.26.4.244","DOIUrl":"https://doi.org/10.15430/JCP.2021.26.4.244","url":null,"abstract":"<p><p>Human epidemiological and animal studies have demonstrated that excess iron is a risk for cancer. The responsible mechanisms are: 1) increased intracellular iron catalyzes the Fenton reaction to generate hydroxyl radicals, leading to mutagenic oxidative DNA lesions; 2) iron is necessary for cellular proliferation as cofactors of many enzymes. Thus, iron-excess milieu promotes selecting cellular evolution to ferroptosis-resistance, a major basis for carcinogenesis. Ferritin is a 24-subunit nanocage protein required for iron storage under the regulation of the iron-regulatory protein (IRP)/iron-responsive element (IRE) system. Ferritin is a serum marker, representing total body iron storage. However, how ferritin is secreted extracellularly has been unelucidated. We recently discovered that an exosomal marker CD63 is regulated by the IRP/IRE system and that iron-loaded ferritin is secreted as extracellular vesicles under the guidance of nuclear receptor coactivator 4 (NCOA4). On the other hand, we found that macrophages under asbestos-induced ferroptosis emit ferroptosis-dependent extracellular vesicles (FedEVs), which are received by nearby mesothelial cells, resulting in significant mutagenic DNA damage. Therefore, cells, including macrophages, can share excess iron with other cells, via iron-loaded ferritin packaged in extracellular vesicles as safe non-catalytic iron. However, similar process, such as one involving FedEVs, may cause accumulation of excess iron in other specific cells, which may eventually promote carcinogenesis.</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"26 4","pages":"244-249"},"PeriodicalIF":2.5,"publicationDate":"2021-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/37/e8/jcp-26-4-244.PMC8749322.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39834085","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}

{"title":"Association of High Expression of Mitochondrial Fission Regulator 2 with Poor Survival of Patients with Esophageal Squamous Cell Carcinoma.","authors":"Hongwei Li,&nbsp;Xingzhuang Zhu,&nbsp;Wei Zhang,&nbsp;Wenjie Lu,&nbsp;Chuan Liu,&nbsp;Jinbo Ma,&nbsp;Rukun Zang,&nbsp;Yipeng Song","doi":"10.15430/JCP.2021.26.4.250","DOIUrl":"https://doi.org/10.15430/JCP.2021.26.4.250","url":null,"abstract":"<p><p>Mitochondrial fission regulator 2 (MTFR2) is associated with mitochondrial fission, while few studies have assessed the associations between MTFR2 expression and clinical characteristics or prognosis of esophageal squamous cell carcinoma (ESCC). In this study, we compared the expression of MTFR2 in 6 ESCC tumors and relative normal tissues by immunohistochemistry (IHC). To assess the effect of MTFR2 expression on clinicopathologic characteristics and survival, 115 paraffin embedded ESCC tissue samples were assessed by IHC staining. Furthermore, the association between clinicopathological properties and MTFR2 expression in patients with ESCC was examined. The survival analysis was performed using the Cox regression models. We found that MTFR2 expression was significantly increased in ESCC tumors compared with normal esophageal epithelial cells. IHC analysis of 115 paraffin embedded ESCC tumor specimens of the patients showed that the expression of MTFR2 was significantly associated with clinical stage (<i>P</i> < 0.001), tumor classification (<i>P</i> < 0.001), histological grade (<i>P</i> < 0.001), and other clinicopathological characteristics. Both univariate and multivariate analyses showed that MTFR2 expression was inversely correlated with the survival of ESCC patients. In conclusion, the expression of MTFR2 is significantly associated with clinicopathologic characteristics and prognosis of ESCC. Thus, MTFR2 expression could serve as a potentially important prognostic biomarker and clinical target for patients with ESCC.</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"26 4","pages":"250-257"},"PeriodicalIF":2.5,"publicationDate":"2021-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/34/67/jcp-26-4-250.PMC8749323.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39834086","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}

{"title":"Erratum: Dioscin Decreases Breast Cancer Stem-like Cell Proliferation via Cell Cycle Arrest by Modulating p38 Mitogen-activated Protein Kinase and AKT/mTOR Signaling Pathways.","authors":"Chae Won Ock,&nbsp;Gi Dae Kim","doi":"10.15430/JCP.2021.26.4.318","DOIUrl":"https://doi.org/10.15430/JCP.2021.26.4.318","url":null,"abstract":"<p><p>[This corrects the article on p. 183 in vol. 26, PMID: 34703821.].</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"26 4","pages":"318"},"PeriodicalIF":2.5,"publicationDate":"2021-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/78/7a/jcp-26-4-318.PMC8749324.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39834492","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}

{"title":"Calorie Restriction for Cancer Prevention and Therapy: Mechanisms, Expectations, and Efficacy.","authors":"Chiara Vidoni,&nbsp;Alessandra Ferraresi,&nbsp;Andrea Esposito,&nbsp;Chinmay Maheshwari,&nbsp;Danny N Dhanasekaran,&nbsp;Vincenzo Mollace,&nbsp;Ciro Isidoro","doi":"10.15430/JCP.2021.26.4.224","DOIUrl":"https://doi.org/10.15430/JCP.2021.26.4.224","url":null,"abstract":"<p><p>Cancer is one of the most frequently diagnosed diseases, and despite the continuous efforts in searching for new and more effective treatments, its morbidity and mortality remain a significant health problem worldwide. Calorie restriction, a dietary manipulation that consists in a reduction of the calorie intake, is gaining attention as a potential adjuvant intervention for preventing and/or fighting cancer. Several forms of energy reduction intake, which includes caloric restriction tout-court, dietary restrictions, and intermittent fasting, are being explored for their ability to prevent or slow down cancer progression. Additionally, another anti-cancer approach being under investigation relies on the use of nutraceuticals known as \"Caloric Restriction Mimetics\" that can provide caloric restriction-mediated benefits without subjecting the patients to a strict diet. Preclinical in vitro and in vivo studies consistently show that diet modifiers reducing the calorie have impact on tumor microenvironment and cancer metabolism, resulting in reduced growth and progression of cancer. Preliminary clinical studies show that patients subjected to a reduced nutrient/energy intake experience improved outcomes from chemo- and radiotherapy while better tolerating the side effects. Here, we review the state of the art on the therapeutic potential of calorie restriction and of caloric restriction mimetics in preventing or retarding tumor development by modulating a subset of cellular processes. The most recent clinical progresses with caloric restriction mimetics in the clinical practice are also discussed.</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"26 4","pages":"224-236"},"PeriodicalIF":2.5,"publicationDate":"2021-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/a8/9c/jcp-26-4-224.PMC8749320.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39834083","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}

{"title":"Primary Care Provider Knowledge and Practice in Risk Assessment for Early Age Onset Colorectal Cancer: Opportunities for Improvement.","authors":"Anjali Parekh,&nbsp;Camille J Hochheimer,&nbsp;Jeannine M Espinoza,&nbsp;Jordan J Karlitz,&nbsp;Carmen L Lewis,&nbsp;Sachin Wani,&nbsp;Swati G Patel","doi":"10.15430/JCP.2021.26.4.298","DOIUrl":"https://doi.org/10.15430/JCP.2021.26.4.298","url":null,"abstract":"<p><p>Colorectal cancer (CRC) incidence and mortality are rising in individuals under age 50, termed early age onset (EAO) CRC. Lower endoscopy is recommended for all patients with unexplained iron deficiency anemia (IDA) or hematochezia to assess the EAO-CRC. For those without symptoms, professional societies recommend decreasing the age to start screening from 50 to 45. Primary care provider (PCP) knowledge and practices around EAO-CRC risk assessment and screening are unknown. We conducted a survey study in May, 2020 of multi-specialty PCPs from three large medical systems to assess PCP knowledge, risk stratification practices and barriers/facilitators they face to offer CRC screening in patients < 50. We conducted univariate analysis to assess factors associated with knowledge and diagnostic practices. Response rate was 27.7% (196/708). Although 77.6% of respondents were aware that EAO-CRC incidence is increasing, only 42.9% knew that EAO-CRC mortality is also increasing. Of note, 91.8% recommend starting average risk screening at age 50. For 40- to 49-year-old patients present with unexplained IDA or hematochezia, 71.9% and 50.5% of respondents, respectively, recommend a diagnostic colonoscopy. Trainees were less likely to be aware of rising EAO-CRC mortality (odds ratio, 0.42; 95% CI, 0.21 to 0.82) and non-internal medicine providers were less likely to recommend CRC screening in those with a first-degree relative with CRC (odds ratio, 0.82; 95% CI, 0.72 to 0.93). Ongoing education efforts will be required to improve recognition and management of high-risk symptoms, particularly among non-internists and trainees.</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"26 4","pages":"298-303"},"PeriodicalIF":2.5,"publicationDate":"2021-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/7a/80/jcp-26-4-298.PMC8749316.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39834489","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}

{"title":"Translational Advances in Cancer Prevention Agent Development (TACPAD) Virtual Workshop on Immunomodulatory Agents: Report.","authors":"Altaf Mohammed, Roderick H Dashwood, Sally Dickinson, Mary L Disis, Elizabeth M Jaffee, Bryon D Johnson, Samir N Khleif, Michael N Pollak, Jeffrey Schlom, Robert H Shoemaker, Sasha E Stanton, Georg T Wondrak, Ming You, Hao Zhu, Mark Steven Miller","doi":"10.15430/JCP.2021.26.4.309","DOIUrl":"10.15430/JCP.2021.26.4.309","url":null,"abstract":"<p><p>The National Cancer Institute (NCI) Division of Cancer Prevention (DCP) convened the \"Translational Advances in Cancer Prevention Agent Development (TACPAD) Workshop on Immunomodulatory Agents\" as a virtual 2-day workshop on September 13 to 14, 2021. The main goals of this workshop were to foster the exchange of ideas and potentially new collaborative interactions among leading cancer immunoprevention researchers from basic and clinical research and highlight new and emerging trends in immunoprevention. The workshop included an overview of the mechanistic classes of immunomodulatory agents and three sessions covering the gamut from preclinical to clinical studies. The workshop convened individuals working in immunology and cancer prevention to discuss trends in discovery and development of immunomodulatory agents individually and in combination with other chemopreventive agents or vaccines.</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"26 4","pages":"309-317"},"PeriodicalIF":2.5,"publicationDate":"2021-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/2a/f9/jcp-26-4-309.PMC8749317.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39834491","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}

{"title":"Comparative Pre-clinical Efficacy of Chinese and Indian Cultivars of Bitter Melon (<i>Momordica charantia</i>) against Pancreatic Cancer.","authors":"Kushal Kandhari, Sandeep Paudel, Komal Raina, Chapla Agarwal, Rama Kant, Michael F Wempe, Cindy O'Bryant, Rajesh Agarwal","doi":"10.15430/JCP.2021.26.4.266","DOIUrl":"10.15430/JCP.2021.26.4.266","url":null,"abstract":"<p><p>Given the high rates of incidence and mortality associated with pancreatic cancer (PanC), there is a need to develop alternative strategies to target PanC. Recent studies have demonstrated that fruits of bitter melon (<i>Momordica charantia</i>) exhibit strong anticancer efficacy against PanC. However, the comparative effects of different bitter melon varieties have not been investigated. This has important implications, given that several bitter melon cultivars are geographically available but their differential effects are not known; and that on a global level, individuals could consume different bitter melon varieties sourced from different cultivars for anti-PanC benefits. Considering these shortcomings, in the present study, comparative pre-clinical anti-PanC studies have been conducted using lyophilized-juice and aqueous-methanolic extracts of the two most widely consumed but geographically diverse bitter melon varieties (Chinese [bitter melon juice; BMJ] and Indian [bitter melon extract; BME] variants). We observed that both BMJ and BME possess comparable efficacy against PanC growth and progression; specifically, these preparations have the potential to (a) inhibit PanC cell proliferation and induce cell death; (b) suppress PanC tumor growth, proliferation, and induce apoptosis; (c) restrict capillary tube formation by human umbilical vein endothelial cells, and decrease angiogenesis in PanC tumor xenografts. Thus, given the comparable pre-clinical anti-PanC efficacy of bitter melon cultivars, the geographical non-availability of a certain cultivar should not be a limiting factor in selecting a variant for moving forward for future clinical use/clinical trials either as a preventive or a therapeutic alternative for targeting PanC.</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"26 4","pages":"266-276"},"PeriodicalIF":2.5,"publicationDate":"2021-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/73/6c/jcp-26-4-266.PMC8749318.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39834088","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}

{"title":"Role of Branched-chain Amino Acid Metabolism in Tumor Development and Progression.","authors":"Min Kyu Jung,&nbsp;Akinkunmi Paul Okekunle,&nbsp;Jung Eun Lee,&nbsp;Mi Kyung Sung,&nbsp;Yun Jeong Lim","doi":"10.15430/JCP.2021.26.4.237","DOIUrl":"https://doi.org/10.15430/JCP.2021.26.4.237","url":null,"abstract":"<p><p>Branched-chain amino acids (BCAAs), isoleucine, leucine and valine, are essential amino acids with vital roles in protein synthesis and energy production. We reviewed the fundamentals of BCAA metabolism in advanced cancer patients. BCAAs and various catabolic products act as signalling molecules, which activate mechanisms ranging from protein synthesis to insulin secretion. Recently, BCAA metabolism has been suggested to contribute to cancer progression. Of particular interest is the modulation of the mTOR activity by BCAAs. There are likely multiple pathways involved in BCAA metabolism implicated in carcinogenesis. Understanding the mechanism(s) underlying altered BCAAs metabolism will significantly advance the current understanding of nutrient involvement in carcinogenesis and direct future studies to unravel the significance of BCCA metabolites in tumor development and progression.</p>","PeriodicalId":15120,"journal":{"name":"Journal of Cancer Prevention","volume":"26 4","pages":"237-243"},"PeriodicalIF":2.5,"publicationDate":"2021-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/d0/a9/jcp-26-4-237.PMC8749315.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39834084","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}