Cancer in an Historic Washington DC African American Population and Its Geospatial Distribution

Background: Cancer continues to be a major cause of morbidity and mortality in the African American community but insights into the types and incidence of cancer 85 years ago have been virtually non-existent and little is known of its geospatial distribution. Historical information on cancer can shed light on current health disparities, particularly among African Americans.Objective: The aims of this study were to: (1) assess the frequencies of the cancer types present among Cobb Collection individuals; (2) compare these data with current research on cancer in African Americans; and (3) evaluate the pattern of cancer expression, including its geospatial distributions, as a cause of death between 1931 and 1969 in an historic African American subgroup and compare this pattern with the historic and contemporary patterns of cancer etiology and incidence.Methods: Systematic assessments of the existing clinical, demographic, and anatomical records in the Cobb Research Laboratory were made of individuals identified as dying from specific cancers from 1931 to 1969. These were compared with the national profiles of cancer during the historic time an individual died as well as the contemporary patterns of cancer deaths. Analysis of their residential addresses just prior to death were assessed using a commercial geographic information system. Each location was assigned a geospatial location and proximity between each site and clusters of sites were investigated.Results: Seventeen different cancer types were found within 28 individuals of the Cobb Collection between 1931 and 1969. The cancer types with the highest frequencies were carcinoma of stomach, lung, esophagus, larynx and bronchogenic carcinoma. Eighty-four percent of all cancer incidents occurred in males and 76% were among individuals identified as African American. Seventy-one percent of the highest incidence cancers were among African American males. Geospatial clustering was observed most noticeably in the redistribution of carcinoma of the esophagus.Conclusion: Our results provide historical depth to our knowledge of the common cancer causes of morbidity among African Americans of Washington DC from 1931 to 1969. We contrast these findings with national historical data on cancer etiology and ethnic disparities in incidence. Our study suggests that historic data can provide longitudinal depth to our understanding of the persistence of cancer susceptibilities in a vulnerable subgroup

Hypoxia disrupt tight junctions and promote metastasis of oral squamous cell carcinoma via loss of par3

Abstract Background Oral squamous cell carcinoma (OSCC) is a highly malignant tumor that is frequently associated with lymph node metastasis, resulting in poor prognosis and survival in patients. In the tumor microenvironment, hypoxia plays an important role in regulating cellular responses such as progressive and rapid growth and metastasis. In these processes, tumor cells autonomously undergo diverse transitions and acquire functions. However, hypoxia-induced transition of OSCC and the involvement of hypoxia in OSCC metastasis remain unclear. Therefore, in this study, we aimed to elucidate the mechanism of hypoxia-induced OSCC metastasis and particularly, its impact on tight junctions (TJs). Methods The expression of hypoxia-inducible factor 1-alpha (HIF-1α) was detected in tumor tissues and adjacent normal tissues from 29 patients with OSCC using reverse transcription quantitative real-time polymerase chain reaction (qRT-PCR), western blotting, and immunohistochemistry (IHC). The migration and invasion abilities of OSCC cell lines treated with small interfering (si)RNA targeting HIF-1α or cultured in hypoxic conditions were analyzed using Transwell assays. The effect of HIF-1α expression on in vivo tumor metastasis of OSCC cells was evaluated using lung metastasis model. Results HIF-1α was overexpressed in patients with OSCC. OSCC metastasis was correlated with HIF-1α expression in OSCC tissues. Hypoxia increased the migration and invasion abilities of OSCC cell lines by regulating the expression and localization of partitioning-defective protein 3 (Par3) and TJs. Furthermore, HIF-1α silencing effectively decreased the invasion and migration abilities of OSCC cell lines and restored TJ expression and localization via Par3. The expression of HIF-1α was positively regulated the OSCC metastasis in vivo. Conclusions Hypoxia promotes OSCC metastasis by regulating the expression and localization of Par3 and TJ proteins. HIF-1α positively correlates to OSCC metastasis. Lastly, HIF-1α expression could regulate the expression of Par3 and TJs in OSCC. This finding may aid in elucidating the molecular mechanisms of OSCC metastasis and progression and developing new diagnostic and therapeutic approaches for OSCC metastasis