Cancer recording and mortality in the General Practice Research Database and linked cancer registries

Boggon, Rachael; Staa, Tjeerd van; Chapman, Michael; Gallagher, Arlene M.; Hammad, Tarek A.; Richards, Mike

doi:10.1002/pds.3374

Cited by 130 publications

(121 citation statements)

References 13 publications

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“…Third, we did not validate our study outcome (e.g., through linkage with other databases). However, CPRD morbidity records can be regarded as a valid measure to capture colorectal cancer occurrence (35). Fourth, left truncation of our data hindered our ability to determine past duration of obesity at baseline, as well as time since the initiation of antidiabetic treatment.…”

Section: Discussionmentioning

confidence: 99%

The Risk of Colorectal Cancer in Patients With Type 2 Diabetes: Associations With Treatment Stage and Obesity

et al. 2014

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OBJECTIVETo assess the risk of colorectal cancer associated with type 2 diabetes, as compared with a nondiabetic reference population, and to study additional associations between treatment stage and duration of obesity and colorectal cancer risk. RESEARCH DESIGN AND METHODSWe conducted an observational population-based cohort study within the Clinical Practice Research Datalink (1987Datalink ( -2012. All patients ( ‡18 years) with at least one prescription for an antidiabetic drug (n = 300,039) were matched (1:1) by birth year, sex, and practice to a comparison cohort without diabetes. Cox proportional hazards models were used to derive adjusted hazard ratios (HRs) for colorectal cancer associated with type 2 diabetes. Within the diabetic cohort, associations of colorectal cancer with treatment stages and duration of obesity (BMI ‡30 kg/m 2 ) were studied. RESULTSAfter a median follow-up of 4.5 years, 2,759 cases of colorectal cancer were observed among the diabetic study population. Type 2 diabetes was associated with a 1.3-fold increased risk of colorectal cancer (HR 1.26 [95% CI 1.18-1.33]). Among diabetic patients, no association was found with treatment stages. A trend of increased colorectal cancer risk was observed with longer duration of obesity. Risk of colorectal cancer was significantly increased for patients with recorded duration of obesity of 4-8 years ) and >8 years (1.28 [1.11-1.49]). CONCLUSIONSType 2 diabetes is associated with a moderately increased risk of colorectal cancer. Among diabetic patients, an increased risk was observed for patients who suffered from obesity for a total duration of 4 years or more.Colorectal cancer is the third most common cancer in men and the second in women (1). Individuals with type 2 diabetes appear to have an increased risk of developing colorectal cancer compared with their nondiabetic counterparts (2). The global increase in incidence of type 2 diabetes, with an estimated total of 347 million adults suffering from type 2 diabetes in 2008 (3), warrants further examination of the potential link between type 2 diabetes and colorectal cancer.Observational cohort studies have found that colorectal cancer is more common in people with metabolic disturbances (4,5). Shared risk factors for colorectal cancer

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Section: Discussionmentioning

confidence: 99%

The Risk of Colorectal Cancer in Patients With Type 2 Diabetes: Associations With Treatment Stage and Obesity

et al. 2014

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“…21,22 The GPRD has been shown to collect valid and reliable prescription data. [14][15][16] A limitation is that the information recorded is for prescriptions, not whether the HT was used. Not all women prescribed HT will use it, but it is likely that those with several prescriptions did use the HT.…”

Section: Discussionmentioning

confidence: 99%

“…Information on prescriptions and clinical diagnosis has been shown to be reliable. [14][15][16] Site-specific cancers, but not tumor histology, have been validated. Patients are recorded as entering the GPRD when they are registered with a participating GP (and the research-active start date is this date or, if later, the date at which the participating practice is declared up to standard), and leave the database when they move to a nonparticipating GP, leave the NHS (e.g., emigrate) or die.…”

Section: The General Practice Research Databasementioning

confidence: 99%

Menopausal hormone therapy and central nervous system tumor risk: Large UK prospective study and meta‐analysis

Benson

Kirichek

Beral³

et al. 2014

Intl Journal of Cancer

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Female sex hormones are thought to affect women's risk of developing central nervous system (CNS) tumors. Some have reported an increased risk in users of menopausal hormone therapy (HT) but evidence is limited. In the UK General Practice Research Database we compared prospectively collected information on HT prescriptions in women aged 50-79 years with CNS tumors diagnosed in 1987-2011 with that in matched controls (four per case). Relative risks (RRs) in relation to prescribed HT were calculated overall and by CNS tumor subtype. Statistical tests are two-sided. For all CNS tumors (n 5 3,500), glioma (n 5 689), meningioma (n 5 1,197), acoustic neuroma (n 5 439), and pituitary tumors (n 5 273) adjusted RRs for women prescribed HT versus not were, respectively, 1.21 (95% confidence intervals (CI) 5 1.10-1.32, p < 0.0001), 1.14 (0.93-1.40, p 5 0.2), 1.30 (1.11-1.51, p 5 0.001), 1.37 (1.06-1.75, p 5 0.01), and 1.35 (0.99-1.85, p 5 0.06). There was no significant difference in risk by tumor subtype (p heterogeneity 5 0.6). A meta-analysis was conducted, combining our results with those from other published studies with prospectively collected exposure information. The meta-analyses yielded significantly increased risks for all CNS tumors, glioma and meningioma in users of estrogen-only [1.35 (1.22-1.49), 1.23 (1.06-1.42) and 1.31 (1.20-1.43), respectively] but not estrogen-progestin HT [1.09 (0.99-1.19), 0.92 (0.78-1.08) and 1.05 (0.95-1.16), respectively]; these differences were statistically significant (p < 0.005 for each tumor type). There was no significant difference between glioma and meningioma risk in users of estrogen-only HT. The totality of the available evidence suggests an increased risk of all CNS tumors (and of glioma and meningioma separately) in users of estrogen-only HT. Absolute excess risk (2 per 10,000 users over 5 years) is small.Use of some types of hormone therapy (HT) for the menopause has been associated with an increased risk of cancers of the breast, ovary, and endometrium and decreased risk of cancers of the gastrointestinal tract.1,2 Some, but not all, have reported an increase in the risk of certain central nervous system (CNS) tumors in HT users. [3][4][5][6][7][8][9][10][11][12][13] Evidence is limited by the lack of systematic reporting of findings for all CNS tumors combined, as well as by different tumor subtypes and by specific HT preparations. The findings for all CNS tumors combined are of public health relevance. Reliable assessment of the association between HT use and CNS tumors requires careful control of potential sources of appreciable bias, such as from selective participation or recall of HT use within studies. Differential reporting of HT use in studies where information was recorded retrospectively, i.e., after women had been diagnosed with CNS tumors, is an important source of such bias.To study the association between use of different types of HT and the risk of CNS tumors we used prospectively recorded prescribing information for HT in a case-control study nested ...

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“…It contains high quality, individual patient-level information on demographics, clinical diagnoses and prescriptions issued. 18,19 ONS death registrations provide details on date and cause of death up to January 2012. Ethical approval for all observational studies conducted using CPRD data has been obtained from a multicenter research ethics committee.…”

Section: Data Sourcesmentioning

confidence: 99%

Metformin use and survival after colorectal cancer: A population‐based cohort study

McMenamin¹,

Murray²,

Hughes

et al. 2015

Intl Journal of Cancer

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Preclinical evidence suggests that metformin could delay cancer progression. Previous epidemiological studies however have been limited by small sample sizes and certain time-related biases. This study aimed to investigate whether colorectal cancer patients with type 2 diabetes who were exposed to metformin had reduced cancer-specific mortality. We conducted a retrospective cohort study of 1,197 colorectal cancer patients newly diagnosed from 1998 to 2009 (identified from English cancer registries) with type 2 diabetes (based upon Clinical Practice Research Datalink, CPRD, prescription and diagnosis records). In this cohort 382 colorectal cancer-specific deaths occurred up to 2012 from the Office of National Statistics (ONS) mortality data. Metformin use was identified from CPRD prescription records. Using time-dependent Cox regression models, unadjusted and adjusted hazard ratios (HR) and 95% CIs were calculated for the association between post-diagnostic exposure to metformin and colorectal cancer-specific mortality. Overall, there was no evidence of an association between metformin use and cancer-specific death before or after adjustment for potential confounders (adjusted HR 1.06, 95% CI 0.80, 1.40). In addition, after adjustment for confounders, there was also no evidence of associations between other diabetic medications and cancerspecific mortality including sulfonylureas (HR 1.14, 95% CI 0.86, 1.51), insulin use (HR 1.35, 95% CI 0.95, 1.93) or other antidiabetic medications including thiazolidinediones (HR 0.73, 95% CI 0.46, 1.14). Similar associations were observed by duration of use and for all-cause mortality. This population-based study, the largest to date, does not support a protective association between metformin and survival in colorectal cancer patients.Despite advances in surgical techniques and adjuvant therapies, colorectal cancer remains the third leading cause of cancer death. 1 Preclinical evidence suggests a beneficial role for metformin, a first-line oral anti-diabetic agent, in colorectal cancer progression. [2][3][4] Although not fully elucidated, the potential anti-tumour effects of metformin are thought to be due to inhibition of the mammalian target of rapamycin (mTOR) signalling pathway, resulting in suppression of cellular proliferation 5 tumour cell migration and invasion 6 as well as an increase in apoptosis. 7 Despite mounting preclinical evidence supporting a possible therapeutic role for metformin in colorectal cancer, only two epidemiological studies have evaluated the impact of post-diagnostic metformin exposure on cancer outcomes in colorectal cancer patients with type 2 diabetes. A Korean study of 595 colorectal cancer patients with type 2 diabetes reported substantial reductions in risk of colorectal cancerspecific and all-cause mortality among metformin users after diagnosis. 8 However, individuals in this study were improperly classified as exposed to metformin in the period from cohort entry to first metformin prescription and therefore these findings have been attri...

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Cancer recording and mortality in the General Practice Research Database and linked cancer registries

Abstract: Although concordance levels were reasonably high, the findings from this study can be used to direct efforts for better recording in both datasets.

Cited by 130 publications

References 13 publications

The Risk of Colorectal Cancer in Patients With Type 2 Diabetes: Associations With Treatment Stage and Obesity

The Risk of Colorectal Cancer in Patients With Type 2 Diabetes: Associations With Treatment Stage and Obesity

Menopausal hormone therapy and central nervous system tumor risk: Large UK prospective study and meta‐analysis

Metformin use and survival after colorectal cancer: A population‐based cohort study

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