# (PQ2) Donor socioeconomic status as a predictor of altered immune function and treatment response following hematopoietic cell transplantation for hematologic malignancy

> **NIH NIH R01** · MEDICAL COLLEGE OF WISCONSIN · 2021 · $354,037

## Abstract

ABSTRACT
Patients with high risk or relapsed hematological malignancies may be cured using allogeneic hematopoietic
cell transplantation (HCT); however, HCT carries a significant risk of mortality. Our group has identified that
this risk is disproportionately worse among recipients of low socioeconomic status (SES). HCT is increasingly
used to treat a variety of malignancies and hematologic disorders, yet social adversity continues to account for
higher rates of morbidity and mortality from this cancer treatment. We have previously identified a recipient-
level SES-related immunobiologic factor implicated in adverse allogeneic HCT patient outcomes - a gene
expression pattern termed the “conserved transcriptional response to adversity” (CTRA). A significant
component of the CTRA profile is pro-inflammatory. Reciprocally, several donor-level characteristics are
important in predicting allogeneic HCT outcomes. Further, donor cells engraft in the recipient, such that
subsequent hematopoiesis is donor-derived. Despite this, it is not known whether donor immunobiologic
disparities associated with SES confer additional prognostic risk to HCT recipients. The goal of this research
project is to identify SES-related donor-level immunobiologic risk factors for adverse HCT outcomes. The
primary aims of this proposal are to: 1) quantify how donor SES alters recipient HCT outcomes; 2) determine
the relationship between donor SES and gene expression and the effect of donor gene expression on recipient
HCT outcomes; and 3) evaluate the interaction of donor and recipient SES on clinical outcomes and quantify
the combined effects of donor and recipient gene expression on clinical outcomes. Our overarching
hypothesis is that SES-related pro-inflammatory gene expression patterns in donors will be associated with
inferior recipient HCT outcomes, and that this effect will be synergistic with recipient gene expression patterns
in influencing recipient outcomes. The research plan employs molecular biology and immunologic techniques
to investigate immunobiologic factors underlying health disparities by collaborating with the federally funded
Center for International Blood and Marrow Transplant Research (CIBMTR). We will leverage the expertise of a
multidisciplinary team of principal investigators, co-investigators, and consultants by using clinical (N=2840)
and biological (N=184) HCT donor data. We will examine the association between donor CTRA and related
transcriptome dynamics and recipient allogeneic transplant outcomes - including disease-free survival,
transplant-related mortality, relapse risk, graft-versus-host disease, and overall survival – as well as the
relationships between donor and recipient immunobiologic patterning on response to HCT. This translational
study builds upon our prior research, explores the transplantable nature of donor sociodemographic factors on
cancer biology, and lays the critical groundwork for interventions targeting SES-related donor...

## Key facts

- **NIH application ID:** 10239032
- **Project number:** 5R01CA238562-03
- **Recipient organization:** MEDICAL COLLEGE OF WISCONSIN
- **Principal Investigator:** Jennifer Mary KNIGHT
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $354,037
- **Award type:** 5
- **Project period:** 2019-09-11 → 2023-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10239032

## Citation

> US National Institutes of Health, RePORTER application 10239032, (PQ2) Donor socioeconomic status as a predictor of altered immune function and treatment response following hematopoietic cell transplantation for hematologic malignancy (5R01CA238562-03). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10239032. Licensed CC0.

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