While a rising prevalence of anemia in the United States was reported in older studies, recent data are lacking. To estimate the prevalence and time trends of anemia in the United States and to examine how these estimates differ by gender, age, race, and household income to poverty threshold ratio (HIPR), we used the National Health and Nutrition Examination Surveys from 1999 to 2020. The presence of anemia was determined using the World Health Organization criteria. Survey-weighted raw and adjusted prevalence ratios (PRs) were determined using generalized linear models for the overall population and by gender, age, race, and HIPR. In addition, an interaction between gender and race was explored. Complete data on anemia, age, gender, and race were available on 87,554 participants (mean age = 34.6 years, women = 49.8%, Whites = 37.3%). Anemia prevalence increased from 4.03% during the 1999–2000 survey cycle to 6.49% during 2017–2020. In adjusted analyses, anemia prevalence was higher in >65 than in 26–45 years old (PR = 2.14, 95% confidence interval (CI) = 1.95, 2.35), in Blacks than Whites (PR = 3.97, 95% CI = 3.63, 4.35), in women than men (PR = 1.98, 95% CI = 1.83, 2.13), and in those with HIPR ≤ 1 than >4 (PR = 0.68, 95% CI = 0.61, 0.75). Gender modified the relationship between anemia and race; when compared to their male counterparts, Black, Hispanic, and other women had higher anemia prevalence than White women (all interaction p values <0.05). The anemia prevalence in the United States has risen from 1999 to 2020 and remains high among the elderly, minorities, and women. The difference in anemia prevalence between men and women is larger in non-Whites.

e20022 Background: Cancer testis antigens (CTAs) are highly immunogenic, tissue-restricted proteins that may be over expressed in hematological malignancies. In this study, an in silico analysis of CTA-derived peptide presentation on HLA class I molecules is reported with an aim to identify putative CTA peptides with a high estimated binding affinity to known HLA class I molecules. Methods: Eighty unique HLA Class I alleles (HLA-A, B, and C), across 78 hematopoietic cell transplant recipients were computationally studied for their ability to bind peptides derived from three CTAs. The amino acid sequences of all three CTA proteins were obtained from UniProtKB. NetMHCPan-4.1 was utilized for in silico prediction of HLA class I binding affinities of the 9-mer peptides generated from these CTAs. Results: The CTA MAGE-A1 had 1202 unique peptides predicted to bind at least one HLA class I allele and 176 of these peptides were classified as strong binders (Rank <0.5 and IC50<500nM). Conversely, 71 unique HLA class 1 alleles were predicted to bind strongly to at least one MAGE-A1 derived peptide. The ability of different MAGE-A1 peptides to bind HLA varied considerably, e.g., peptide TSYVKVLEY, was predicted to bind strongly to 22 different HLA class I alleles. Similarly, 41 CTAG-1B-derived and 164 MAGE-A2-derived peptides were predicted to generate strong binders with at least one HLA class 1 allele. Conversely, 37 and 71 unique HLA class I alleles were predicted to bind strongly to at least one CTAG1B peptide and one MAGE-A1 peptide, respectively. CTAG1-B derived peptide FATPMEAEL and MAGE-A2-derived peptide FAHPRKLLM were predicted to bind strongly to 17 and 22 HLA class 1 alleles, respectively. In aggregate most patients presented multiple peptides across the 6 HLA class I molecules studied (Table). The number of strongly binding MAGE-A1 and CTAG-1B peptides from unique patients. Strong binding defined by Rank <0.5 and IC50<500nM. Conclusions: Most patients presented several CTA derived peptides, suggesting that the aggregate HLA presentation across the 6 classical HLA class I molecules will yield high odds of presentation of CTA expressed by target tissues. These HLA genotype-informed quantitative analyses raise the possibility that agents such as checkpoint inhibitors and immunomodulatory drugs may synergize with hypomethylating agents and augment CTA-directed T-cell responses.[Table: see text]