Background: The incidence of colorectal cancer (CRC) in the US has declined. The decreasing trend is observed in non-Hispanic Whites, Blacks, and Hispanics. However, close analysis of the trends demonstrates that the decline among Hispanics is less than other races/ethnicities. We investigate the burden of CRC in Hispanics living near the U.S.-Mexico border, a subpopulation of Hispanics composed primarily of individuals of Mexican origin. Objectives: The objective of this study was to investigate and compare incidence rates of CRC in non-Hispanic Whites and Hispanics living in counties along the U.S.-Mexico border. Methods: Data from the National Institutes of Health National Cancer Institute and State Cancer Profiles were analyzed to obtain CRC incidence rates (per 100,000 population) for persons ≥ 50 years of age residing in counties along the U.S.-Mexico border by race (non-Hispanic White and Hispanic) and gender from 2011 to 2015. Results: Incidence rates of CRC in Hispanic men ≥ 50 years of age, living in counties along the U.S.-Mexico border, were higher than the national average for Hispanic men of similar age. In contrast, the incidence of CRC declined or remained stable in non-Hispanic Whites and women. Conclusions: Our study unveils a significant disparity in CRC incidence among Hispanics living near the U.S.-Mexico border, disproportionally affecting men ≥ 50 years of age. Socioeconomic and cultural/lifestyle factors are likely contributing to these disparities.

We describe a patient with MDS/MPN with ring sideroblasts and thrombocytosis who had deletions of long arm of chromosome 5 (5q-) and chromosome 20 (20q-). Molecular studies showed an exon 9, frame shift mutation in the calreticulin (CALR) gene, and absence of mutations in JAK2, MPL, SETBP1 or SF3B1.Treatment with lenalidomide resulted in durable clinical remission which has lasted 2 years.

Introduction/Objective Chronic Myeloid Leukemia (CML) is a myeloproliferative neoplasm originating from malignant clonal proliferation of a pluripotent hematopoietic stem cell. CML is characterized by a reciprocal translocation between chromosomes 9 and 22, t(9;22)(q34;q11), that gives rise to an abnormal chromosome 22 called the Philadelphia (Ph) chromosome. The translocation results in the formation of a chimeric BCR-ABL1 fusion gene, which is the molecular hallmark of the disease. However, 5-10% of CML patients present with additional chromosomal abnormalities which is often considered a sign of clonal evolution, genetic instability, and is generally thought to portend a poor prognosis. Methods We present a case of CML with a rare 3- way translocation, t(3;9;22)(q21;q34;q11.2), who achieved a major molecular response on imatinib for 18 months. A review of the literature and Mitelman database search is presented focusing on the prognostic implications of this 3 way translocation in the era of tyrosine kinase inhibitors starting in 2001 till now. Results Twenty seven cases were reported, but the patient therapeutic response to imatinib and clinical outcome were only reported in 11 cases. Nine cases achieved a cytogenetic remission while the remaining two cases had an adverse outcome. Conclusion Taken in conjunction with the favorable outcome in our patient, we suggest that t(3;9;22) is not an adverse prognostic factor in the era of tyrosine kinase inhibitors.

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