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Goto S, Hamano T, Fujii H, Taniguchi M, Abe M, Nitta K, Nishi S. The benefit of reduced serum phosphate levels depends on patient characteristics: a nationwide prospective cohort study. Clin Kidney J 2024; 17:sfae263. [PMID: 39385948 PMCID: PMC11462437 DOI: 10.1093/ckj/sfae263] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/12/2024] [Indexed: 10/12/2024] Open
Abstract
Background In cohort studies of hyperphosphatemic hemodialysis patients, reduced serum phosphate levels have been linked to a lower mortality risk. To investigate whether this benefit is influenced by patient characteristics, we calculated the number needed to be exposed (NNE), stratified by patient characteristics. Methods In this 9-year prospective cohort study using the nationwide Japanese registry, we enrolled 78 256 hemodialysis patients aged 18 years or older. We investigated the relationship between time-averaged (TA) phosphate levels and mortality due to cardiovascular disease (CVD) using Cox proportional models. We estimated the 1-year NNE for CVD death in patients with baseline serum phosphate levels ≥6.0 mg/dL and exposure to TA phosphate levels decreasing to 3.5-<5.0 mg/dL using mixed-effects Poisson models. Results The hazard ratio of CVD mortality decreased linearly with lower serum TA phosphate levels in those with prior atherosclerotic CVD (ACVD) or diabetic nephropathy (DN) but plateaued with serum phosphate <5.0 mg/dL in those without. The hazard ratios (95% confidence interval) for phosphate ≥7.0 mg/dL compared with 3.5-<3.9 mg/dL were 1.58 (1.38-1.81) in those with prior ACVD, 1.91 (1.68-2.17) in those without, 1.87 (1.63-2.16) in those with DN and 1.65 (1.46-1.87) in those without. However, the NNE for one more person to benefit (NNEB) for CVD death was lower in patients with a history of ACVD than in those without (61 vs 118). Patients with DN had lower NNEB than those without (69 vs 113). In patients with TA albumin ≥3.8 g/dL, older patients had lower NNEB, while patients with TA albumin <3.45 g/dL showed no benefit in some groups, including the elderly. Conclusions The benefit of intensive phosphate management may be pronounced in patients with a history of ACVD or DN. A comprehensive approach that considers both age and nutritional status may be necessary when managing serum phosphate levels.
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Affiliation(s)
- Shunsuke Goto
- Committee of the Renal Data Registry, Japanese Society for Dialysis Therapy, Tokyo, Japan
- Division of Nephrology and Kidney Center, Kobe University Graduate School of Medicine, Kobe, Japan
| | - Takayuki Hamano
- Department of Nephrology, Nagoya City University, Graduate School of Medical Sciences, Nagoya, Japan
- Department of Nephrology, Osaka University Graduate School of Medicine, Suita, Japan
| | - Hideki Fujii
- Division of Nephrology and Kidney Center, Kobe University Graduate School of Medicine, Kobe, Japan
| | - Masatomo Taniguchi
- Committee of the Renal Data Registry, Japanese Society for Dialysis Therapy, Tokyo, Japan
- Fukuoka Renal Clinic, Fukuoka, Japan
| | - Masanori Abe
- Committee of the Renal Data Registry, Japanese Society for Dialysis Therapy, Tokyo, Japan
- Division of Nephrology, Hypertension and Endocrinology, Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan
| | - Kosaku Nitta
- Committee of the Renal Data Registry, Japanese Society for Dialysis Therapy, Tokyo, Japan
- Department of Medicine, Kidney Center, Tokyo Women's Medical University, Tokyo, Japan
| | - Shinichi Nishi
- Division of Nephrology and Kidney Center, Kobe University Graduate School of Medicine, Kobe, Japan
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Pliszka M, Szablewski L. Associations between Diabetes Mellitus and Selected Cancers. Int J Mol Sci 2024; 25:7476. [PMID: 39000583 PMCID: PMC11242587 DOI: 10.3390/ijms25137476] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/05/2024] [Revised: 06/15/2024] [Accepted: 06/24/2024] [Indexed: 07/16/2024] Open
Abstract
Cancer is one of the major causes of mortality and is the second leading cause of death. Diabetes mellitus is a serious and growing problem worldwide, and its prevalence continues to grow; it is the 12th leading cause of death. An association between diabetes mellitus and cancer has been suggested for more than 100 years. Diabetes is a common disease diagnosed among patients with cancer, and evidence indicates that approximately 8-18% of patients with cancer have diabetes, with investigations suggesting an association between diabetes and some particular cancers, increasing the risk for developing cancers such as pancreatic, liver, colon, breast, stomach, and a few others. Breast and colorectal cancers have increased from 20% to 30% and there is a 97% increased risk of intrahepatic cholangiocarcinoma or endometrial cancer. On the other hand, a number of cancers and cancer therapies increase the risk of diabetes mellitus. Complications due to diabetes in patients with cancer may influence the choice of cancer therapy. Unfortunately, the mechanisms of the associations between diabetes mellitus and cancer are still unknown. The aim of this review is to summarize the association of diabetes mellitus with selected cancers and update the evidence on the underlying mechanisms of this association.
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Affiliation(s)
- Monika Pliszka
- Chair and Department of General Biology and Parasitology, Medical University of Warsaw, Chałubińskiego Str. 5, 02-004 Warsaw, Poland
| | - Leszek Szablewski
- Chair and Department of General Biology and Parasitology, Medical University of Warsaw, Chałubińskiego Str. 5, 02-004 Warsaw, Poland
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Khan S, Chang SH, Seyerle AA, Wang M, Hicks V, Drake BF. Post-diagnostic metformin and statin use and risk of biochemical recurrence in Veterans diagnosed with prostate cancer. Prostate 2023; 83:1150-1157. [PMID: 37191401 DOI: 10.1002/pros.24557] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/20/2022] [Revised: 03/03/2023] [Accepted: 05/01/2023] [Indexed: 05/17/2023]
Abstract
OBJECTIVE To evaluate the impact of post-diagnostic metformin or statin use and duration on risk of biochemical recurrence in a racially-diverse cohort of Veterans. METHODS The population consisted of men diagnosed with prostate cancer in the Veterans Health Administration and treated with either radical prostatectomy or radiation (Full cohort n = 65,759, Black men n = 18,817, White men n = 46,631, Other = 311). The association between post-diagnostic (1) metformin and (2) statin use with biochemical recurrence was assessed using multivariable, time-varying Cox Proportional Hazard Models for the overall cohort and by race. In a secondary analysis, metformin and statin duration were evaluated. RESULTS Post-diagnostic metformin use was not associated with biochemical recurrence (multivariable-adjusted hazard ratio [aHR]: 1.01; 95% confidence interval [CI]: 0.94, 1.09), with similar results observed for both Black and White men. However, duration of metformin use was associated with a reduced risk of biochemical recurrence in the cohort overall (HR: 0.94; 95% CI: 0.92, 0.95) as well as both Black and White men. By contrast, statin use was associated with a reduced risk of biochemical recurrence (HR: 0.83; 95% CI: 0.79, 0.88) in the overall cohort as well as both White and Black men. Duration of statin use was also inversely associated with biochemical recurrence in all groups. CONCLUSION Post-diagnostic metformin and statin use have the potential to prevent biochemical recurrence in men diagnosed with prostate cancer.
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Affiliation(s)
- Saira Khan
- Research Service, St. Louis Veterans Affairs Medical Center, St. Louis, Missouri, USA
- Department of Surgery, Division of Public Health Sciences, School of Medicine, Washington University in St. Louis, St. Louis, Missouri, USA
- Epidemiology Program, College of Heath Sciences, University of Delaware, Newark, Delaware, USA
| | - Su-Hsin Chang
- Research Service, St. Louis Veterans Affairs Medical Center, St. Louis, Missouri, USA
- Department of Surgery, Division of Public Health Sciences, School of Medicine, Washington University in St. Louis, St. Louis, Missouri, USA
| | - Amanda A Seyerle
- Division of Pharmaceutical Outcomes and Policy, Eshelman School of Pharmacy, Chapel Hill, North Carolina, USA
| | - Mei Wang
- Research Service, St. Louis Veterans Affairs Medical Center, St. Louis, Missouri, USA
- Department of Surgery, Division of Public Health Sciences, School of Medicine, Washington University in St. Louis, St. Louis, Missouri, USA
| | - Veronica Hicks
- Research Service, St. Louis Veterans Affairs Medical Center, St. Louis, Missouri, USA
- Department of Surgery, Division of Public Health Sciences, School of Medicine, Washington University in St. Louis, St. Louis, Missouri, USA
| | - Bettina F Drake
- Research Service, St. Louis Veterans Affairs Medical Center, St. Louis, Missouri, USA
- Department of Surgery, Division of Public Health Sciences, School of Medicine, Washington University in St. Louis, St. Louis, Missouri, USA
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Yang X, Chen H, Zhang S, Chen X, Sheng Y, Pang J. Association of cigarette smoking habits with the risk of prostate cancer: a systematic review and meta-analysis. BMC Public Health 2023; 23:1150. [PMID: 37316851 DOI: 10.1186/s12889-023-16085-w] [Citation(s) in RCA: 5] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/21/2022] [Accepted: 06/09/2023] [Indexed: 06/16/2023] Open
Abstract
BACKGROUND Association of cigarette smoking habits with the risk of prostate cancer is still a matter of debate. This systematic review and meta-analysis aimed to assess the association between cigarette smoking and prostate cancer risk. METHODS We conducted a systematic search on PubMed, Embase, Cochrane Library, and Web of Science without language or time restrictions on June 11, 2022. Literature search and study screening were performed according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses statement. Prospective cohort studies that assessed the association between cigarette smoking habits and the risk of prostate cancer were included. Quality assessment was conducted using the Newcastle-Ottawa Scale. We used random-effects models to obtain pooled estimates and the corresponding 95% confidence intervals. RESULTS A total of 7296 publications were screened, of which 44 cohort studies were identified for qualitative analysis; 39 articles comprising 3 296 398 participants and 130 924 cases were selected for further meta-analysis. Current smoking had a significantly reduced risk of prostate cancer (RR, 0.74; 95% CI, 0.68-0.80; P < 0.001), especially in studies completed in the prostate-specific antigen screening era. Compared to former smokers, current smokers had a significant lower risk of PCa (RR, 0.70; 95% CI, 0.65-0.75; P < 0.001). Ever smoking showed no association with prostate cancer risk in overall analyses (RR, 0.96; 95% CI, 0.93-1.00; P = 0.074), but an increased risk of prostate cancer in the pre-prostate-specific antigen screening era (RR, 1.05; 95% CI, 1.00-1.10; P = 0.046) and a lower risk of prostate cancer in the prostate-specific antigen screening era (RR, 0.95; 95% CI, 0.91-0.99; P = 0.011) were observed. Former smoking did not show any association with the risk of prostate cancer. CONCLUSIONS The findings suggest that the lower risk of prostate cancer in smokers can probably be attributed to their poor adherence to cancer screening and the occurrence of deadly smoking-related diseases, and we should take measures to help smokers to be more compliant with early cancer screening and to quit smoking. TRIAL REGISTRATION This study was registered on PROSPERO (CRD42022326464).
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Affiliation(s)
- Xiangwei Yang
- Department of Urology, Kidney and Urology Center, Pelvic Floor Disorders Center, The Seventh Affiliated Hospital, Sun Yat-Sen University, No.628 Zhenyuan Road, Shenzhen, 518107, China
| | - Hong Chen
- School of Nursing, LKS Faculty of Medicine, University of Hong Kong, Hong Kong, China
| | - Shiqiang Zhang
- Department of Urology, Kidney and Urology Center, Pelvic Floor Disorders Center, The Seventh Affiliated Hospital, Sun Yat-Sen University, No.628 Zhenyuan Road, Shenzhen, 518107, China
| | - Xianju Chen
- Department of Urology, Kidney and Urology Center, Pelvic Floor Disorders Center, The Seventh Affiliated Hospital, Sun Yat-Sen University, No.628 Zhenyuan Road, Shenzhen, 518107, China
| | - Yiyu Sheng
- Department of Urology, Kidney and Urology Center, Pelvic Floor Disorders Center, The Seventh Affiliated Hospital, Sun Yat-Sen University, No.628 Zhenyuan Road, Shenzhen, 518107, China
| | - Jun Pang
- Department of Urology, Kidney and Urology Center, Pelvic Floor Disorders Center, The Seventh Affiliated Hospital, Sun Yat-Sen University, No.628 Zhenyuan Road, Shenzhen, 518107, China.
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Hormonal patterns in men with prediabetes and diabetes in NHANES III: possible links with prostate cancer. Cancer Causes Control 2022; 33:429-440. [PMID: 35059918 PMCID: PMC9066414 DOI: 10.1007/s10552-021-01538-7] [Citation(s) in RCA: 3] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/01/2021] [Accepted: 12/10/2021] [Indexed: 10/19/2022]
Abstract
PURPOSE Pathways involving sex hormones and insulin-like growth factors (IGFs) have been proposed to explain, in part, the lower risk of prostate cancer among men with diabetes. To gain insights into potential biological mechanisms we explored differences in serum concentrations of sex hormones and IGFs across the trajectory from normoglycemia to prediabetes to poorly controlled diabetes. METHODS Using cross-sectional data from the National Health and Nutrition Examination Survey III we examined differences in levels of circulating sex hormones, sex hormone-binding globulin (SHBG), IGF-1, and IFG-binding protein 3 (IGFBP-3), according to diabetes status: no diabetes [n = 648], prediabetes [n = 578], undiagnosed diabetes [n = 106], well-controlled diabetes [n = 42], and poorly controlled diabetes [n = 56]. Adjusted geometric mean concentrations were derived using multivariable linear regression, adjusted for age, race, and other lifestyle factors. RESULTS Total testosterone concentrations were lower among prediabetics (4.89 ng/mL, 95% confidence interval (CI) 4.95-5.21) than men without prediabetes/diabetes (5.29 ng/mL, 95% CI 5.06-5.53) but did not reduce further across diabetes groups. Concentrations of estradiol, estimated free testosterone, SHGB, IGF-1, and IGFBP-3 did not differ. While the ratio of IGF-1 to IGFBP-3 was lower among men with prediabetics and undiagnosed diabetes than men without prediabetes/diabetes, there was no trend across groups. A positive trend for the ratio of estradiol-to-testosterone levels was observed across groups (p trend = 0.045). CONCLUSION Our findings do not provide clear support for either an androgen driven or IGF-driven pathway for the inverse association between diabetes and prostate cancer risk.
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Hatami Marbini M, Amiri F, Sajadi Hezaveh Z. Dietary glycemic index, glycemic load, insulin index, insulin load and risk of diabetes-related cancers: A systematic review of cohort studies. Clin Nutr ESPEN 2021; 42:22-31. [PMID: 33745582 DOI: 10.1016/j.clnesp.2021.02.008] [Citation(s) in RCA: 13] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/06/2021] [Accepted: 02/05/2021] [Indexed: 11/19/2022]
Abstract
BACKGROUND & AIMS It is believed that diets high in glycemic index (GI), glycemic load (GL), Insulin index (II), and Insulin load (IL) are associated with the increased risks of certain cancers through increasing serum glucose or insulin levels. METHODS We conducted this systematic review of cohort studies to evaluate the possible relation between GI, GL, II, and IL with diabetes-related cancers, including colorectal, bladder, breast, endometrium, liver, pancreas, and prostate cancers. Two separate investigators conducted a literature search through PubMed/Medline, Scopus, and Web of Science databases up to February 2020, plus reference lists of relevant articles. RESULTS Fifty-three cohort studies with a total of 100 098 cancer cases were included in this systematic review. Fifteen out of eighteen studies among breast cancer cases reported no significant association between GI/GL and cancer risk. These numbers were 4 out of 13 for colorectal cancer, 7 out of 9 for endometrial cancer, 2 out of 3 for liver cancer, 8 out of 10 for pancreatic cancer, and 3 out of 3 for prostate cancer. Only one cohort investigated this association in terms of bladder cancer and reported a significant association. Also, five studies reported this relation in terms of II/IL, and only one cohort among endometrial cancer patients observed a significant positive association between the risk of cancer and IL. CONCLUSION We concluded a weak association between dietary GI/GL and no association between II/IL with diabetes-related cancer risk. More cohort studies are required to be performed regarding II/IL and the risk of cancer.
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Affiliation(s)
- Motahare Hatami Marbini
- Department of Nutrition, School of Public Health, Iran University of Medical Sciences, Tehran, Iran
| | - Fatemehsadat Amiri
- Department of Nutrition, School of Public Health, Iran University of Medical Sciences, Tehran, Iran.
| | - Zohreh Sajadi Hezaveh
- Cancer Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran
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Soltani S, Abdollahi S, Aune D, Jayedi A. Body mass index and cancer risk in patients with type 2 diabetes: a dose-response meta-analysis of cohort studies. Sci Rep 2021; 11:2479. [PMID: 33510262 PMCID: PMC7844243 DOI: 10.1038/s41598-021-81671-0] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/12/2020] [Accepted: 01/11/2021] [Indexed: 01/10/2023] Open
Abstract
Although obesity has been associated with an increased cancer risk in the general population, the association in patients with type 2 diabetes (T2D) remains controversial. We conducted a dose-response meta-analysis of cohort studies of body mass index (BMI) and the risk of total and site-specific cancers in patients with T2D. A systematic literature search was conducted in PubMed, Scopus, and Medline until September 2020 for cohort studies on the association between BMI and cancer risk in patients with T2D. Summary relative risks (RRs) and 95% confidence intervals (CIs) were calculated using random effects models. Ten prospective and three retrospective cohort studies (3,345,031 participants and 37,412 cases) were included in the meta-analysis. Each 5-unit increase in BMI (kg/m2) was associated with a 6% higher risk of total cancer (RR: 1.06, 95% CI 1.01, 1.10; I2 = 55.4%, n = 6), and with a 12% increased risk in the analysis of breast cancer (RR: 1.12, 95% CI 1.05, 1.20; I2 = 0%, n = 3). The pooled RRs showed no association with prostate cancer (RR: 1.02, 95% CI 0.92, 1.13; I2 = 64.6%, n = 4), pancreatic cancer (RR: 0.97, 95% CI 0.84, 1.11; I2 = 71%, n = 3), and colorectal cancer (RR: 1.05, 95% CI 0.98, 1.13; I2 = 65.9%, n = 2). There was no indication of nonlinearity for total cancer (Pnon-linearity = 0.99), however, there was evidence of a nonlinear association between BMI and breast cancer (Pnon-linearity = 0.004) with steeper increases in risk from a BMI around 35 and above respectively. Higher BMI was associated with a higher risk of total, and breast cancer but not with risk of other cancers, in patients with T2D, however, further studies are needed before firm conclusions can be drawn.
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Affiliation(s)
- Sepideh Soltani
- Yazd Cardiovascular Research Center, Shahid Sadoughi University of Medical Sciences, Yazd, Iran
| | - Shima Abdollahi
- Department of Nutrition and Public Health, School of Public Health, North Khorasan University of Medical Sciences, Bojnurd, Iran
| | - Dagfinn Aune
- Department of Epidemiology and Biostatistics, Imperial College London, London, UK
- Department of Nutrition, Bjørknes University College, Oslo, Norway
- Department of Endocrinology, Morbid Obesity and Preventive Medicine, Oslo University Hospital, Ullevål, Oslo, Norway
| | - Ahmad Jayedi
- Food Safety Research Center (Salt), Semnan University of Medical Sciences, Semnan, Iran.
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Wang M, Yang Y, Liao Z. Diabetes and cancer: Epidemiological and biological links. World J Diabetes 2020; 11:227-238. [PMID: 32547697 PMCID: PMC7284016 DOI: 10.4239/wjd.v11.i6.227] [Citation(s) in RCA: 85] [Impact Index Per Article: 17.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/12/2020] [Revised: 04/24/2020] [Accepted: 05/05/2020] [Indexed: 02/06/2023] Open
Abstract
The incidence of diabetes and cancer has increased significantly in recent years. Furthermore, there are many common risk factors for both diabetes and cancer, such as obesity, sedentary lifestyle, smoking, and ageing. A large body of epidemiological evidence has indicated that diabetes is considered as an independent risk factor for increased rates of heterogeneous types of cancer occurrence and death. The incidence and mortality of various types of cancer, such as pancreas, liver, colorectal, breast, endometrial, and bladder cancers, have a modest growth in diabetics. However, diabetes may work as a protective factor for prostate cancer. Although the underlying biological mechanisms have not been totally understood, studies have validated that insulin/insulin-like growth factor (IGF) axis (including insulin resistance, hyperinsulinemia, and IGF), hyperglycemia, inflammatory cytokines, and sex hormones provide good circumstances for cancer cell proliferation and metastasis. Insulin/IGF axis activates several metabolic and mitogenic signaling pathways; hyperglycemia provides energy for cancer cell growth; inflammatory cytokines influence cancer cell apoptosis. Thus, these three factors affect all types of cancer, while sex hormones only play important roles in breast cancer, endometrial cancer, and prostate cancer. This minireview consolidates and discusses the epidemiological and biological links between diabetes and various types of cancer.
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Affiliation(s)
- Mina Wang
- School of Biological Sciences, Nanyang Technological University, Singapore 637551, Singapore
- The Department of Acupuncture and Moxibustion, Beijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing Key Laboratory of Acupuncture Neuromodulation, Beijing 100010, China
- Graduate School, Beijing University of Chinese Medicine, Beijing 100029, China
| | - Yingying Yang
- Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna 17177, Sweden
- Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai 200065, China
| | - Zehuan Liao
- School of Biological Sciences, Nanyang Technological University, Singapore 637551, Singapore
- Department of Microbiology, Tumor and Cell Biology (MTC), Karolinska Institutet, Solna 17177, Sweden
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Ying D, Gianfrancesco MA, Trupin L, Yazdany J, Greidinger EL, Schmajuk G. Increased Risk of Ischemic Stroke in Systemic Sclerosis: A National Cohort Study of US Veterans. J Rheumatol 2020; 47:82-88. [PMID: 30877213 PMCID: PMC7269199 DOI: 10.3899/jrheum.181311] [Citation(s) in RCA: 11] [Impact Index Per Article: 2.2] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 02/27/2019] [Indexed: 11/22/2022]
Abstract
OBJECTIVE Previously thought to involve primarily the microvasculature, systemic sclerosis (SSc) has been increasingly linked to macrovascular disease. Cardiovascular (CV) and cerebrovascular disease are responsible for 20-30% of mortality in SSc, but few studies have shown an independent association between SSc and stroke. We assessed whether SSc was an independent risk factor for ischemic stroke. METHODS We conducted a retrospective cohort study using the national Veterans Affairs (VA) administrative database containing records from 1999 to 2014. We obtained data for all patients with a diagnosis of SSc as well as 2 controls per SSc patient matched on sex, race, smoking status, and VA site. All patients were followed until development of ischemic stroke, death, or last encounter. We used a Cox proportional hazard regression model to estimate risk of ischemic stroke, with adjustments for CV comorbidities (hypertension, diabetes, atrial fibrillation, non-cerebrovascular atherosclerotic disease, hyperlipidemia), baseline medication use (aspirin, nonsteroidal antiinflammatory drugs), and Medicare enrollment. RESULTS Among 4545 individuals with SSc (83% male, mean age 60.9 yrs), the incidence rate of ischemic stroke was 15.3 per 1000 person-years (vs 12.2 in the control cohort), with an unadjusted HR 1.28 (95% CI 1.11-1.47). The adjusted HR was 1.21 (95% CI 1.05-1.40) after adjusting for baseline CV risk factors, medications, and Medicare enrollment. CONCLUSION SSc is independently associated with a higher risk of ischemic stroke among US veterans. Patients with SSc represent a population likely to benefit from targeted stroke screening or prevention therapies.
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Affiliation(s)
- David Ying
- From the San Francisco Veterans Affairs Medical Center, San Francisco; Division of Rheumatology, University of California, San Francisco, California; Miami Veterans Affairs Medical Center, Miami; Division of Rheumatology, University of Miami Miller School of Medicine, Miami, Florida, USA.
- D. Ying, MD, San Francisco Veterans Affairs Medical Center, and Division of Rheumatology, University of California, San Francisco; M.A. Gianfrancesco, PhD, MPH, Division of Rheumatology, University of California, San Francisco; L. Trupin, MPH, Division of Rheumatology, University of California, San Francisco; J. Yazdany, MD, MPH, Division of Rheumatology, University of California, San Francisco; E.L. Greidinger, MD, Miami Veterans Affairs Medical Center, and Division of Rheumatology, University of Miami Miller School of Medicine; G. Schmajuk, MD, MS, San Francisco Veterans Affairs Medical Center, and Division of Rheumatology, University of California, San Francisco. E.L. Greidinger and G. Schmajuk contributed equally to this work.
| | - Milena A Gianfrancesco
- From the San Francisco Veterans Affairs Medical Center, San Francisco; Division of Rheumatology, University of California, San Francisco, California; Miami Veterans Affairs Medical Center, Miami; Division of Rheumatology, University of Miami Miller School of Medicine, Miami, Florida, USA
- D. Ying, MD, San Francisco Veterans Affairs Medical Center, and Division of Rheumatology, University of California, San Francisco; M.A. Gianfrancesco, PhD, MPH, Division of Rheumatology, University of California, San Francisco; L. Trupin, MPH, Division of Rheumatology, University of California, San Francisco; J. Yazdany, MD, MPH, Division of Rheumatology, University of California, San Francisco; E.L. Greidinger, MD, Miami Veterans Affairs Medical Center, and Division of Rheumatology, University of Miami Miller School of Medicine; G. Schmajuk, MD, MS, San Francisco Veterans Affairs Medical Center, and Division of Rheumatology, University of California, San Francisco. E.L. Greidinger and G. Schmajuk contributed equally to this work
| | - Laura Trupin
- From the San Francisco Veterans Affairs Medical Center, San Francisco; Division of Rheumatology, University of California, San Francisco, California; Miami Veterans Affairs Medical Center, Miami; Division of Rheumatology, University of Miami Miller School of Medicine, Miami, Florida, USA
- D. Ying, MD, San Francisco Veterans Affairs Medical Center, and Division of Rheumatology, University of California, San Francisco; M.A. Gianfrancesco, PhD, MPH, Division of Rheumatology, University of California, San Francisco; L. Trupin, MPH, Division of Rheumatology, University of California, San Francisco; J. Yazdany, MD, MPH, Division of Rheumatology, University of California, San Francisco; E.L. Greidinger, MD, Miami Veterans Affairs Medical Center, and Division of Rheumatology, University of Miami Miller School of Medicine; G. Schmajuk, MD, MS, San Francisco Veterans Affairs Medical Center, and Division of Rheumatology, University of California, San Francisco. E.L. Greidinger and G. Schmajuk contributed equally to this work
| | - Jinoos Yazdany
- From the San Francisco Veterans Affairs Medical Center, San Francisco; Division of Rheumatology, University of California, San Francisco, California; Miami Veterans Affairs Medical Center, Miami; Division of Rheumatology, University of Miami Miller School of Medicine, Miami, Florida, USA
- D. Ying, MD, San Francisco Veterans Affairs Medical Center, and Division of Rheumatology, University of California, San Francisco; M.A. Gianfrancesco, PhD, MPH, Division of Rheumatology, University of California, San Francisco; L. Trupin, MPH, Division of Rheumatology, University of California, San Francisco; J. Yazdany, MD, MPH, Division of Rheumatology, University of California, San Francisco; E.L. Greidinger, MD, Miami Veterans Affairs Medical Center, and Division of Rheumatology, University of Miami Miller School of Medicine; G. Schmajuk, MD, MS, San Francisco Veterans Affairs Medical Center, and Division of Rheumatology, University of California, San Francisco. E.L. Greidinger and G. Schmajuk contributed equally to this work
| | - Eric L Greidinger
- From the San Francisco Veterans Affairs Medical Center, San Francisco; Division of Rheumatology, University of California, San Francisco, California; Miami Veterans Affairs Medical Center, Miami; Division of Rheumatology, University of Miami Miller School of Medicine, Miami, Florida, USA
- D. Ying, MD, San Francisco Veterans Affairs Medical Center, and Division of Rheumatology, University of California, San Francisco; M.A. Gianfrancesco, PhD, MPH, Division of Rheumatology, University of California, San Francisco; L. Trupin, MPH, Division of Rheumatology, University of California, San Francisco; J. Yazdany, MD, MPH, Division of Rheumatology, University of California, San Francisco; E.L. Greidinger, MD, Miami Veterans Affairs Medical Center, and Division of Rheumatology, University of Miami Miller School of Medicine; G. Schmajuk, MD, MS, San Francisco Veterans Affairs Medical Center, and Division of Rheumatology, University of California, San Francisco. E.L. Greidinger and G. Schmajuk contributed equally to this work
| | - Gabriela Schmajuk
- From the San Francisco Veterans Affairs Medical Center, San Francisco; Division of Rheumatology, University of California, San Francisco, California; Miami Veterans Affairs Medical Center, Miami; Division of Rheumatology, University of Miami Miller School of Medicine, Miami, Florida, USA
- D. Ying, MD, San Francisco Veterans Affairs Medical Center, and Division of Rheumatology, University of California, San Francisco; M.A. Gianfrancesco, PhD, MPH, Division of Rheumatology, University of California, San Francisco; L. Trupin, MPH, Division of Rheumatology, University of California, San Francisco; J. Yazdany, MD, MPH, Division of Rheumatology, University of California, San Francisco; E.L. Greidinger, MD, Miami Veterans Affairs Medical Center, and Division of Rheumatology, University of Miami Miller School of Medicine; G. Schmajuk, MD, MS, San Francisco Veterans Affairs Medical Center, and Division of Rheumatology, University of California, San Francisco. E.L. Greidinger and G. Schmajuk contributed equally to this work
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10
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Brookman-May SD, Campi R, Henríquez JDS, Klatte T, Langenhuijsen JF, Brausi M, Linares-Espinós E, Volpe A, Marszalek M, Akdogan B, Roll C, Stief CG, Rodriguez-Faba O, Minervini A. Latest Evidence on the Impact of Smoking, Sports, and Sexual Activity as Modifiable Lifestyle Risk Factors for Prostate Cancer Incidence, Recurrence, and Progression: A Systematic Review of the Literature by the European Association of Urology Section of Oncological Urology (ESOU). Eur Urol Focus 2018; 5:756-787. [PMID: 29576530 DOI: 10.1016/j.euf.2018.02.007] [Citation(s) in RCA: 51] [Impact Index Per Article: 7.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/14/2018] [Revised: 02/05/2018] [Accepted: 02/19/2018] [Indexed: 12/19/2022]
Abstract
CONTEXT Smoking, sexual activity, and physical activity (PA) are discussed as modifiable lifestyle factors associated with prostate cancer (PCa) development and progression. OBJECTIVE To evaluate the available evidence concerning the association of smoking, sexual activity, and sports and exercise on PCa risk, treatment outcome, progression, and cancer-specific mortality. EVIDENCE ACQUISITION A systematic review of studies published between 2007 and 2017 using MEDLINE (via PubMed), Cochrane Central Register of Controlled Trials, and Web of Science databases according to the Preferred Reporting Items for Systematic Reviews and Meta-Analysis statement criteria was conducted. EVIDENCE SYNTHESIS While data concerning the impact of smoking on PCa development remain conflicting, there is robust evidence that smoking is associated with aggressive tumor features and worse cancer-related outcome, which seems to be maintained for 10 yr after smoking cessation. Less convincing and limited evidence exists for the association of sexual activity with PCa risk. The findings related to PA and PCa support the inference that exercise might be a useful factor in the prevention of PCa and tumor progression, while it is not finally proved under which specific conditions PA might be protective against disease development. CONCLUSIONS Smoking is associated with aggressive tumor features and worse cancer-related prognosis; as this negative impact seems to be maintained for 10yr after smoking cessation, urologists should advise men to quit smoking latest at PCa diagnosis to improve their prognosis. As several studies indicate a positive impact of exercise on tumor development, progression, and treatment outcome, it is certainly reasonable to advocate an active lifestyle. Least convincing evidence is available for the interaction of sexual activity and PCa, and well-conducted and longitudinal studies are clearly necessary to evaluate whether the suggested associations between PCa risk and sexual behavior are real or spurious. PATIENT SUMMARY In this systematic review, we looked at the impact of smoking, sexual activity, and sports and exercise on prostate cancer risk and outcome after treatment. While the evidence for sexual activity is not overall clear, we found that smoking might lead to more aggressive cancers and result in worse treatment outcome. Physical activity might prevent prostate cancer and improve cancer-related outcomes as well. Hence, it is certainly reasonable to advocate an active lifestyle and advise men to quit smoking.
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Affiliation(s)
| | - Riccardo Campi
- Department of Urology, University of Florence, Careggi Hospital, Florence, Italy
| | - Jose D S Henríquez
- Unidad de Uro-Oncología, Servicio de Urología, Fundació Puigvert, Universitat Autònoma de Barcelona, Barcelona, Spain
| | - Tobias Klatte
- Department of Urology, Addenbrooke's Hospital, Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK
| | | | - Maurizio Brausi
- Department of Urology, B. Ramazzini Hospital, Carpi-Modena, Italy
| | | | - Alessandro Volpe
- Department of Urology, University of Eastern Piedmont, Maggiore della Carità Hospital, Novara, Italy
| | - Martin Marszalek
- Department of Urology and Andrology, Donauspital, Vienna, Austria
| | - Bulent Akdogan
- Department of Urology, Hacettepe University School of Medicine, Ankara, Turkey
| | - Christina Roll
- Department of Trauma and Reconstructive Surgery, University of Regensburg, Regensburg, Germany
| | - Christian G Stief
- Department of Urology, Ludwig-Maximilians University (LMU) Munich, Munich, Germany
| | - Oscar Rodriguez-Faba
- Unidad de Uro-Oncología, Servicio de Urología, Fundació Puigvert, Universitat Autònoma de Barcelona, Barcelona, Spain
| | - Andrea Minervini
- Department of Urology, University of Florence, Careggi Hospital, Florence, Italy
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11
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Haring A, Murtola TJ, Talala K, Taari K, Tammela TLJ, Auvinen A. Antidiabetic drug use and prostate cancer risk in the Finnish Randomized Study of Screening for Prostate Cancer. Scand J Urol 2017; 51:5-12. [DOI: 10.1080/21681805.2016.1271353] [Citation(s) in RCA: 27] [Impact Index Per Article: 3.4] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/08/2023]
Affiliation(s)
- Antti Haring
- School of Medicine, University of Tampere, Tampere, Finland
| | - Teemu J. Murtola
- School of Medicine, University of Tampere, Tampere, Finland
- Department of Urology, Tampere University Hospital, Tampere, Finland
| | | | - Kimmo Taari
- Department of Urology, University of Helsinki and Helsinki University Hospital, Helsinki, Finland
| | - Teuvo L. J. Tammela
- School of Medicine, University of Tampere, Tampere, Finland
- Department of Urology, Tampere University Hospital, Tampere, Finland
| | - Anssi Auvinen
- School of Health Sciences, University of Tampere, Tampere, Finland
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12
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Weh KM, Aiyer HS, Howell AB, Kresty LA. Cranberry proanthocyanidins modulate reactive oxygen species in Barrett's and esophageal adenocarcinoma cell lines. JOURNAL OF BERRY RESEARCH 2016; 6:125-136. [PMID: 27583064 PMCID: PMC5002987 DOI: 10.3233/jbr-160122] [Citation(s) in RCA: 19] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 12/23/2015] [Accepted: 01/31/2016] [Indexed: 06/06/2023]
Abstract
BACKGROUND We recently reported that a cranberry proanthocyanidin rich extract (C-PAC) induces autophagic cell death in apoptotic resistant esophageal adenocarcinoma (EAC) cells and necrosis in autophagy resistant cells. EAC is characterized by high morbidity and mortality rates supporting development of improved preventive interventions. OBJECTIVE The current investigation sought to investigate the role of reactive oxygen species (ROS) in the context of C-PAC induced cell death. METHODS A panel of human esophageal cell lines of EAC or BE (Barrett's esophagus) origin were treated with C-PAC and assessed for ROS modulation using CellROX® Green reagent and the Amplex Red assay to specifically measure hydrogen peroxide levels. RESULTS C-PAC significantly increased ROS levels in EAC cells, but significantly reduced ROS levels in CP-C BE cells. Increased hydrogen peroxide levels were also detected in C-PAC treated EAC cells and supernatant; however, hydrogen peroxide levels were significantly increased in medium alone, without cells, suggesting that C-PAC interferes or directly acts on the substrate. Hydrogen peroxide levels did not change in C-PAC treated CP-C BE cells. CONCLUSION These experiments provide additional mechanistic insight regarding C-PAC induced cancer cell death through modulation of ROS. Additional research is warranted to identify specific ROS species associated with C-PAC exposure.
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Affiliation(s)
- Katherine M. Weh
- Department of Medicine, Division of Hematology and Oncology, Medical College of Wisconsin, Milwaukee, WI, USA
| | - Harini S. Aiyer
- Department of Medicine, Division of Hematology and Oncology, Medical College of Wisconsin, Milwaukee, WI, USA
| | - Amy B. Howell
- Department of Plant Pathology and Biology, Marucci Center for Blueberry and Cranberry Research, Rutgers University, Chatsworth, NJ, USA
| | - Laura A. Kresty
- Department of Medicine, Division of Hematology and Oncology, Medical College of Wisconsin, Milwaukee, WI, USA
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13
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De Nunzio C, Andriole GL, Thompson IM, Freedland SJ. Smoking and Prostate Cancer: A Systematic Review. Eur Urol Focus 2015; 1:28-38. [DOI: 10.1016/j.euf.2014.10.002] [Citation(s) in RCA: 27] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/21/2014] [Accepted: 10/21/2014] [Indexed: 11/16/2022]
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14
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Sun A, Liu R, Sun G. Serum prostate-specific antigen levels in men with prediabetes: A cross-sectional study. Scandinavian Journal of Clinical and Laboratory Investigation 2015; 75:273-81. [DOI: 10.3109/00365513.2015.1010176] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 12/14/2022]
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15
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A systematic review and meta-analysis of tobacco use and prostate cancer mortality and incidence in prospective cohort studies. Eur Urol 2014; 66:1054-64. [PMID: 25242554 DOI: 10.1016/j.eururo.2014.08.059] [Citation(s) in RCA: 152] [Impact Index Per Article: 13.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/28/2014] [Accepted: 08/25/2014] [Indexed: 12/13/2022]
Abstract
CONTEXT An association between tobacco smoking and prostate cancer (PCa) incidence and mortality was suggested in an earlier meta-analysis of 24 prospective studies in which dose-response associations and risks per unit of tobacco use were not examined. OBJECTIVE We investigated the association between several measures of tobacco use and PCa mortality (primary outcome) and incidence (secondary outcome) including dose-response association. EVIDENCE ACQUISITION Relevant articles from prospective studies were identified by searching the PubMed and Web of Science databases (through January 21, 2014) and reference lists of relevant articles. Combined relative risks (RRs) and 95% confidence intervals (CIs) were calculated using random effects methods. We also calculated population attributable risk (PAR) for smoking and PCa mortality. EVIDENCE SYNTHESIS We included 51 articles in this meta-analysis (11823 PCa deaths, 50349 incident cases, and 4,082,606 cohort participants). Current cigarette smoking was associated with an increased risk of PCa death (RR: 1.24; 95% CI, 1.18-1.31), with little evidence for heterogeneity and publication bias. The number of cigarettes smoked per day had a dose-response association with PCa mortality (p=0.02; RR for 20 cigarettes per day: 1.20). The PAR for cigarette smoking and PCa deaths in the United States and Europe were 6.7% and 9.5%, respectively, corresponding to >10000 deaths/year in these two regions. Current cigarette smoking was inversely associated with incident PCa (RR: 0.90; 95% CI, 0.85-0.96), with high heterogeneity in the results. However, in studies completed in 1995 or earlier (considered as completed before the prostate-specific antigen screening era), ever smoking showed a positive association with incident PCa (RR: 1.06; 95% CI, 1.00-1.12) with little heterogeneity. CONCLUSIONS Combined evidence from observational studies shows a modest but statistically significant association between cigarette smoking and fatal PCa. Smoking appears to be a modifiable risk factor for PCa death. PATIENT SUMMARY Smoking increases the chance of prostate cancer death. Not smoking prevents this harm and many other tobacco-related diseases.
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Onitilo AA, Stankowski RV, Berg RL, Engel JM, Williams GM, Doi SA. A novel method for studying the temporal relationship between type 2 diabetes mellitus and cancer using the electronic medical record. BMC Med Inform Decis Mak 2014; 14:38. [PMID: 24886371 PMCID: PMC4022430 DOI: 10.1186/1472-6947-14-38] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/12/2013] [Accepted: 04/29/2014] [Indexed: 11/15/2022] Open
Abstract
Background We developed an algorithm for the identification of patients with type 2 diabetes and ascertainment of the date of diabetes onset for examination of the temporal relationship between diabetes and cancer using data in the electronic medical record (EMR). Methods The Marshfield Clinic EMR was searched for patients who developed type 2 diabetes between January 1, 1995 and December 31, 2009 using a combination of diagnostic codes and laboratory data. Subjects without diabetes were also identified and matched to subjects with diabetes by age, gender, smoking history, residence, and date of diabetes onset/reference date. Results The final cohort consisted of 11,236 subjects with and 54,365 subjects without diabetes. Stringent requirements for laboratory values resulted in a decrease in the number of potential subjects by nearly 70%. Mean observation time in the EMR was similar for both groups with 13—14 years before and 5–7 years after the reference date. The two cohorts were largely similar except that BMI and frequency of healthcare encounters were greater in subjects with diabetes. Conclusion The cohort described here will be useful for the examination of the temporal relationship between diabetes and cancer and is unique in that it allows for determination of the date of diabetes onset with reasonable accuracy.
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Affiliation(s)
- Adedayo A Onitilo
- Department of Hematology/Oncology, Marshfield Clinic Weston Center, 3501 Cranberry Boulevard, Weston, WI 54476, USA.
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Al-Zhoughbi W, Huang J, Paramasivan GS, Till H, Pichler M, Guertl-Lackner B, Hoefler G, Hoefler G. Tumor macroenvironment and metabolism. Semin Oncol 2014; 41:281-95. [PMID: 24787299 PMCID: PMC4012137 DOI: 10.1053/j.seminoncol.2014.02.005] [Citation(s) in RCA: 120] [Impact Index Per Article: 10.9] [Reference Citation Analysis] [Abstract] [Track Full Text] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/30/2022]
Abstract
In this review we introduce the concept of the tumor macroenvironment and explore it in the context of metabolism. Tumor cells interact with the tumor microenvironment including immune cells. Blood and lymph vessels are the critical components that deliver nutrients to the tumor and also connect the tumor to the macroenvironment. Several factors are then released from the tumor itself but potentially also from the tumor microenvironment, influencing the metabolism of distant tissues and organs. Amino acids, and distinct lipid and lipoprotein species can be essential for further tumor growth. The role of glucose in tumor metabolism has been studied extensively. Cancer-associated cachexia is the most important tumor-associated systemic syndrome and not only affects the quality of life of patients with various malignancies but is estimated to be the cause of death in 15%-20% of all cancer patients. On the other hand, systemic metabolic diseases such as obesity and diabetes are known to influence tumor development. Furthermore, the clinical implications of the tumor macroenvironment are explored in the context of the patient's outcome with special consideration for pediatric tumors. Finally, ways to target the tumor macroenvironment that will provide new approaches for therapeutic concepts are described.
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Affiliation(s)
- Wael Al-Zhoughbi
- Institute of Pathology, Medical University of Graz, Graz, Austria
| | - Jianfeng Huang
- Institute of Pathology, Medical University of Graz, Graz, Austria
| | | | - Holger Till
- Department of Paediatric and Adolescent Surgery, Medical University of Graz, Graz, Austria
| | - Martin Pichler
- Department of Internal Medicine, Medical University of Graz, Graz, Austria
| | | | - Gerald Hoefler
- Institute of Pathology, Medical University of Graz, Graz, Austria,Address correspondence to Gerald Hoefler, MD, Institute of Pathology, Medical University of Graz, Auenbruggerplatz 25, 8036 Graz, Austria
| | - Gerald Hoefler
- Institute of Pathology, Medical University of Graz, Graz, Austria.
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