Assessing the interrelationship between stigma, social influence, and cervical cancer prevention in an urban underserved setting: An exploratory study.

In the US, incidence and mortality from cervical cancer disproportionately affects racial/ethnic minorities and low-income women. Despite affordable access to primary and secondary prevention measures at Federally Qualified Health Centers (FQHCs), Human Papillomavirus (HPV) vaccination and screening rates are low, suggesting the presence of non-financial barriers to uptake in this population. This explanatory sequential mixed-methods study sought to explore factors that influence the acceptability of cervical cancer prevention services among parents and legal guardians of vaccine-eligible girls attending an urban FQHC and to assess social influences related to cervical cancer prevention. Participants included eight mothers, one father, and two grandparents/legal guardians. Nine participants self-identified as Black/Afro-Caribbean, or African American, two as Latinx, and one as Native American. The quantitative data suggested discordance between participants' cervical cancer prevention knowledge and their practices. Most indicated that their daughters had received the HPV vaccine but were unsure about HPV transmission modes. Qualitative data revealed that participants were comfortable disclosing information on HPV infection and vaccination status, and most women were likely to share information related to cervical cancer testing and diagnosis. Few comments indicated personal stigma on the part of participants, but there was frequent expression of perceived public stigma (shaming and blaming women), gender differences (men are indifferent to risk), and distrust of the healthcare system. Findings highlight several concepts including the disharmony between knowledge and practice, prevalent perceived public stigma, cumbersome attitudes on the part of men regarding HPV and cervical cancer, and distrust of the healthcare system.

Altered chromosomal positioning, compaction, and gene expression with a lamin A/C gene mutation.

BACKGROUND: Lamins A and C, encoded by the LMNA gene, are filamentous proteins that form the core scaffold of the nuclear lamina. Dominant LMNA gene mutations cause multiple human diseases including cardiac and skeletal myopathies. The nuclear lamina is thought to regulate gene expression by its direct interaction with chromatin. LMNA gene mutations may mediate disease by disrupting normal gene expression. METHODS/FINDINGS: To investigate the hypothesis that mutant lamin A/C changes the lamina's ability to interact with chromatin, we studied gene misexpression resulting from the cardiomyopathic LMNA E161K mutation and correlated this with changes in chromosome positioning. We identified clusters of misexpressed genes and examined the nuclear positioning of two such genomic clusters, each harboring genes relevant to striated muscle disease including LMO7 and MBNL2. Both gene clusters were found to be more centrally positioned in LMNA-mutant nuclei. Additionally, these loci were less compacted. In LMNA mutant heart and fibroblasts, we found that chromosome 13 had a disproportionately high fraction of misexpressed genes. Using three-dimensional fluorescence in situ hybridization we found that the entire territory of chromosome 13 was displaced towards the center of the nucleus in LMNA mutant fibroblasts. Additional cardiomyopathic LMNA gene mutations were also shown to have abnormal positioning of chromosome 13, although in the opposite direction. CONCLUSIONS: These data support a model in which LMNA mutations perturb the intranuclear positioning and compaction of chromosomal domains and provide a mechanism by which gene expression may be altered.