Analyzing establishment nonresponse using an interpretable regression tree model with linked administrative data

To gain insight into how characteristics of an establishment are associated with nonresponse, a recursive partitioning algorithm is applied to the Occupational Employment Statistics May 2006 survey data to build a regression tree. The tree models an establishment's propensity to respond to the survey given certain establishment characteristics. It provides mutually exclusive cells based on the characteristics with homogeneous response propensities. This makes it easy to identify interpretable associations between the characteristic variables and an establishment's propensity to respond, something not easily done using a logistic regression propensity model. We test the model obtained using the May data against data from the November 2006 Occupational Employment Statistics survey. Testing the model on a disjoint set of establishment data with a very large sample size $(n=179,360)$ offers evidence that the regression tree model accurately describes the association between the establishment characteristics and the response propensity for the OES survey. The accuracy of this modeling approach is compared to that of logistic regression through simulation. This representation is then used along with frame-level administrative wage data linked to sample data to investigate the possibility of nonresponse bias. We show that without proper adjustments the nonresponse does pose a risk of bias and is possibly nonignorable.Comment: Published in at http://dx.doi.org/10.1214/11-AOAS521 the Annals of Applied Statistics (http://www.imstat.org/aoas/) by the Institute of Mathematical Statistics (http://www.imstat.org

Prediagnostic smoking history, alcohol consumption, and colorectal cancer survival: The Seattle Colon Cancer Family Registry

Smoking and alcohol consumption are associated with an increased risk of developing colorectal cancer. However, it is unclear whether these exposures are associated with survival after colorectal cancer diagnosis

Association between molecular subtypes of colorectal cancer and patient survival

BACKGROUND and AIMS: Colorectal cancer (CRC) is a heterogeneous disease that can develop via several pathways. Different CRC subtypes, identified based on tumor markers, have been proposed to reflect these pathways. We evaluated the significance of these previously proposed classifications to survival. METHODS: Participants in the population-based Seattle Colon Cancer Family Registry were diagnosed with invasive CRC from 1998 through 2007 in western Washington State (N = 2706), and followed for survival through 2012. Tumor samples were collected from 2050 participants and classified into 5 subtypes based on combinations of tumor markers: type 1 (microsatellite instability [MSI]-high, CpG island methylator phenotype [CIMP] -positive, positive for BRAF mutation, negative for KRAS mutation); type 2 (microsatellite stable [MSS] or MSI-low, CIMP-positive, positive for BRAF mutation, negative for KRAS mutation); type 3 (MSS or MSI low, non-CIMP, negative for BRAF mutation, positive for KRAS mutation); type 4 (MSS or MSI-low, non-CIMP, negative for mutations in BRAF and KRAS); and type 5 (MSI-high, non-CIMP, negative for mutations in BRAF and KRAS). Multiple imputation was used to impute tumor markers for those missing data on 1-3 markers. We used Cox regression to estimate hazard ratios (HR) and 95% confidence intervals (CI) for associations of subtypes with disease-specific and overall mortality, adjusting for age, sex, body mass, diagnosis year, and smoking history. RESULTS: Compared with participants with type 4 tumors (the most predominant), participants with type 2 tumors had the highest disease-specific mortality (HR = 2.20, 95% CI: 1.47-3.31); subjects with type 3 tumors also had higher disease-specific mortality (HR = 1.32, 95% CI: 1.07-1.63). Subjects with type 5 tumors had the lowest disease-specific mortality (HR = 0.30, 95% CI: 0.14-0.66). Associations with overall mortality were similar to those with disease-specific mortality. CONCLUSIONS: Based on a large, population-based study, CRC subtypes, defined by proposed etiologic pathways, are associated with marked differences in survival. These findings indicate the clinical importance of studies into the molecular heterogeneity of CRC

Clinicopathologic Risk Factor Distributions for MLH1 Promoter Region Methylation in CIMP-Positive Tumors

The CpG Island Methylator Phenotype (CIMP) is a major molecular pathway in colorectal cancer (CRC). Approximately 25% to 60% of CIMP tumors are microsatellite unstable (MSI-H) due to DNA hypermethylation of the MLH1 gene promoter. Our aim was to determine if the distributions of clinicopathologic factors in CIMP-positive tumors with MLH1 DNA methylation differed from those in CIMP-positive tumors without DNA methylation of MLH1

Colon and Rectal Cancer Survival by Tumor Location and Microsatellite Instability: The Colon Cancer Family Registry

Cancers in the proximal colon, distal colon, and rectum are frequently studied together; however, there are biological differences in cancers across these sites, particularly in the prevalence of microsatellite instability

Association Between Molecular Subtypes of Colorectal Cancer and Patient Survival

Colorectal cancer (CRC) is a heterogeneous disease that can develop via several pathways. Different CRC subtypes, identified based on tumor markers, have been proposed to reflect these pathways. We evaluated the significance of these previously proposed classifications to survival

BRAF Mutation Status and Survival after Colorectal Cancer Diagnosis According to Patient and Tumor Characteristics

BRAF mutations in colorectal cancer (CRC) are disproportionately observed in tumors exhibiting microsatellite instability (MSI), and are associated with other prognostic factors. The independent association between BRAF-mutation status and CRC survival, however, remains unclear

Association between germline variants and somatic mutations in colorectal cancer

Colorectal cancer (CRC) is a heterogeneous disease with evidence of distinct tumor types that develop through different somatically altered pathways. To better understand the impact of the host genome on somatically mutated genes and pathways, we assessed associations of germline variations with somatic events via two complementary approaches. We first analyzed the association between individual germline genetic variants and the presence of non-silent somatic mutations in genes in 1375 CRC cases with genome-wide SNPs data and a tumor sequencing panel targeting 205 genes. In the second analysis, we tested if germline variants located within previously identified regions of somatic allelic imbalance were associated with overall CRC risk using summary statistics from a recent large scale GWAS (n similar or equal to 125 k CRC cases and controls). The first analysis revealed that a variant (rs78963230) located within a CNA region associated with TLR3 was also associated with a non-silent mutation within gene FBXW7. In the secondary analysis, the variant rs2302274 located in CDX1/PDGFRB frequently gained/lost in colorectal tumors was associated with overall CRC risk (OR = 0.96, p = 7.50e-7). In summary, we demonstrate that an integrative analysis of somatic and germline variation can lead to new insights about CRC

Post-postfeminism? New feminist visibilities in postfeminist times

This article contributes to debates about the value and utility of the notion of postfeminism for a seemingly “new” moment marked by a resurgence of interest in feminism in the media and among young women. The paper reviews current understandings of postfeminism and criticisms of the term’s failure to speak to or connect with contemporary feminism. It offers a defence of the continued importance of a critical notion of postfeminism, used as an analytical category to capture a distinctive contradictory-but-patterned sensibility intimately connected to neoliberalism. The paper raises questions about the meaning of the apparent new visibility of feminism and highlights the multiplicity of different feminisms currently circulating in mainstream media culture – which exist in tension with each other. I argue for the importance of being able to “think together” the rise of popular feminism alongside and in tandem with intensified misogyny. I further show how a postfeminist sensibility informs even those media productions that ostensibly celebrate the new feminism. Ultimately, the paper argues that claims that we have moved “beyond” postfeminism are (sadly) premature, and the notion still has much to offer feminist cultural critics