RESUMO
For cancer patients undergoing treatment who may be at higher risk of COVID-19, access to high-quality online health information (OHI) may be of particular importance amidst a plethora of harmful medical misinformation online. Therefore, we assessed the readability and quality of OHI available for various cancer types and treatment modalities. Search phrases included "cancer radiation COVID," "cancer surgery COVID," "cancer chemotherapy COVID," and "cancer type COVID," for the fourteen most common cancer types (e.g., "prostate cancer COVID" and "breast cancer COVID"), yielding a total of 17 search phrases. The first 20 sources were recorded and analyzed for each keyword, yielding a total of 340 unique sources. For each of these sources, the approximate grade level required to comprehend the text was calculated as a mean of five validated readability scores; subsequently, for the first ten results of each search, the DISCERN tool was manually used to assess quality. Search terms were translated into Spanish and French, and a quality assessment using the Health on the Net Code (HONcode) accreditation was conducted. The median grade level readability for all sources was 13 (IQR 11-14). Median DISCERN scores for the 170 sources assessed were 55 out of 75, suggesting good quality. OHI with quality scores below the median DISCERN score had a median readability of 12.5 (IQR 11-14) grade reading level vs 14 (IQR 12-17) for those above the median DISCERN score (T-test P < 0.0001). Percentages of HONcode-accredited websites were 34.9%, 39.9%, and 38.6% for English, Spanish, and French OHI, respectively. We conclude that efforts are needed to make high-quality OHI available at the appropriate reading level for patients with cancer; such efforts may contribute to the alleviation of disparities in access to healthcare information.
Assuntos
COVID-19 , Neoplasias , Masculino , Humanos , Compreensão , Reprodutibilidade dos Testes , Pandemias , Neoplasias/terapia , InternetRESUMO
Clonal hematopoiesis of indeterminate potential (CHIP) is defined by the presence of a cancer-associated somatic mutation in white blood cells in the absence of overt hematological malignancy. It arises most commonly from loss-of-function mutations in the epigenetic regulators DNMT3A and TET2. CHIP predisposes to both hematological malignancies and atherosclerotic cardiovascular disease in humans. Here we demonstrate that loss of Dnmt3a in myeloid cells increased murine atherosclerosis to a similar degree as previously seen with loss of Tet2. Loss of Dnmt3a enhanced inflammation in macrophages in vitro and generated a distinct adventitial macrophage population in vivo which merges a resident macrophage profile with an inflammatory cytokine signature. These changes surprisingly phenocopy the effect of loss of Tet2. Our results identify a common pathway promoting heightened innate immune cell activation with loss of either gene, providing a biological basis for the excess atherosclerotic disease burden in carriers of these two most prevalent CHIP mutations.