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Hematopoietic Stem Cell Transplantation

Introduction

Hematopoietic stem cell transplantation (HSCT) is a potentially curative therapeutic modality for a broad range of malignant and non-malignant hematologic diseases, representing one of the most complex and consequential interventions in modern medicine. Approximately 50,000 HSCTs are performed annually worldwide, with roughly 22,000 in the United States. The field is divided into two fundamentally different categories: autologous transplantation, in which the patient's own stem cells are collected, cryopreserved, and reinfused after high-dose chemotherapy to rescue the bone marrow from otherwise lethal myeloablation; and allogeneic transplantation, in which donor-derived stem cells are infused to replace the recipient's hematopoietic system, providing both marrow reconstitution and an immunologic graft-versus-leukemia (GVL) effect. Transplant outcomes have improved dramatically over the past two decades through advances in conditioning regimen design, graft-versus-host disease (GVHD) prevention, donor selection, infection prophylaxis, and supportive care.

Indications

Autologous HSCT

Autologous HSCT is most commonly performed for multiple myeloma, where it serves as consolidation therapy following initial induction chemotherapy. The conditioning regimen employing high-dose melphalan at 200 mg/m2 remains the standard of care and provides deepened responses and prolonged progression-free survival. Lymphomas represent the second major indication, particularly relapsed or refractory diffuse large B-cell lymphoma that demonstrates chemosensitivity to salvage therapy (though this indication has diminished somewhat with the advent of CAR T-cell therapy for primary refractory disease), relapsed Hodgkin lymphoma, and mantle cell lymphoma as consolidation after induction. Systemic AL amyloidosis is treated with autologous HSCT in selected patients with limited organ involvement who can tolerate the procedure. An expanding frontier for autologous HSCT includes severe autoimmune diseases, with compelling trial data supporting its use in severe systemic sclerosis (the SCOT trial demonstrating superiority over cyclophosphamide) and refractory multiple sclerosis (the MIST trial).

Allogeneic HSCT

Allogeneic HSCT derives its therapeutic power from two mechanisms: the cytoreductive effect of the conditioning regimen and the immunologic GVL effect mediated by donor-derived immune cells. It is the only curative therapy for many hematologic malignancies and non-malignant conditions. In acute myeloid leukemia, allogeneic transplant is indicated for patients with intermediate- and adverse-risk disease in first complete remission and for relapsed or refractory disease. Acute lymphoblastic leukemia patients with high-risk features in first remission, Ph-positive ALL (though this indication has evolved with TKI and immunotherapy combinations), and relapsed disease are candidates. Myelodysplastic syndromes of intermediate-2 or high-risk by IPSS-R, or lower-risk disease harboring adverse molecular features, are indications for transplant. Myeloproliferative neoplasms, specifically myelofibrosis of intermediate-2 or high-risk, represent an important indication as HSCT is the only curative option. Chronic myeloid leukemia that is refractory to tyrosine kinase inhibitors or has progressed to blast crisis may warrant transplant. Among non-malignant diseases, aplastic anemia in young patients with a matched sibling donor, thalassemia major (with best outcomes achieved before the development of significant iron overload), sickle cell disease (with expanding access through haploidentical platforms), and primary immunodeficiency states including severe combined immunodeficiency (SCID), Wiskott-Aldrich syndrome, and chronic granulomatous disease are established indications.

Stem Cell Sources

Bone Marrow (BM)

Bone marrow harvest involves the aspiration of marrow from the posterior iliac crests under general anesthesia, with a target volume of approximately 10 to 20 mL per kilogram of recipient body weight, providing a minimum nucleated cell dose of 2 x 10^8 per kilogram of recipient weight. Bone marrow as a graft source offers the important advantage of a lower rate of chronic GVHD compared to peripheral blood stem cells, a difference that translates into meaningful reductions in long-term morbidity and the duration of immunosuppressive therapy. For this reason, bone marrow is the preferred stem cell source for non-malignant diseases including aplastic anemia, sickle cell disease, and thalassemia, for pediatric donors, and in transplant strategies that prioritize GVHD reduction.

Peripheral Blood Stem Cells (PBSC)

Peripheral blood stem cell collection involves mobilization of CD34-positive hematopoietic progenitors from the marrow into the peripheral blood through administration of granulocyte colony-stimulating factor (G-CSF) at 10 mcg/kg/day subcutaneously for 4 to 5 days, followed by leukapheresis. PBSC has become the most commonly used stem cell source for both adult allogeneic and autologous HSCT. Its principal advantage is faster engraftment, with neutrophil recovery typically occurring by day 12 to 14 compared to day 18 to 21 for bone marrow, and a higher CD34-positive cell yield. The significant disadvantage is a substantially higher rate of chronic GVHD, estimated at 60 to 70% compared to 40 to 50% with bone marrow in the matched sibling donor setting, driven by the higher T-cell content of the PBSC graft.

Umbilical Cord Blood (UCB)

Umbilical cord blood is collected from the placenta and umbilical cord at the time of delivery and cryopreserved in public cord blood banks. It offers several unique advantages: rapid availability without the need for donor scheduling, lower HLA-matching stringency (with acceptable outcomes at 4 of 6 HLA match rather than the 8 of 8 required for unrelated bone marrow or PBSC), a lower rate of GVHD, and reduced risk of viral transmission. However, the limited cell dose contained in a single cord blood unit is a significant limitation, particularly for adult recipients, and may necessitate the use of double cord blood transplants. Engraftment is slower than with other sources, with neutrophil recovery typically occurring around day 24 to 28, and graft failure rates are higher. The use of cord blood has declined substantially in recent years with the expansion of haploidentical HSCT platforms, which provide virtually universal donor availability while generally offering faster engraftment and more robust immune reconstitution.

Conditioning Regimens

Myeloablative Conditioning (MAC)

Myeloablative conditioning regimens are designed to achieve three objectives: eradicate residual malignant cells, create marrow space for donor cell engraftment, and provide sufficient immunosuppression to prevent graft rejection. Total body irradiation (TBI)-based regimens, typically employing 12 to 13.2 Gy delivered in fractionated doses combined with cyclophosphamide, are the standard conditioning for ALL. Busulfan-based regimens represent the primary chemotherapy-only alternative. Contemporary practice strongly favors pharmacokinetically (PK) targeted busulfan dosing, with a target area under the curve of 3,600 to 5,000 micromolar per liter per minute, to optimize efficacy while minimizing hepatotoxicity. Busulfan combined with cyclophosphamide (BuCy) is a well-established regimen, while busulfan with fludarabine (BuFlu) has gained favor due to its more favorable toxicity profile. Thiotepa-based combinations are employed in selected settings. Myeloablative conditioning carries higher transplant-related mortality due to its greater organ toxicity but offers a lower relapse rate through more intensive tumor eradication.

Reduced-Intensity Conditioning (RIC)

Reduced-intensity conditioning regimens provide sufficient immunosuppression to permit donor cell engraftment while relying predominantly on the immunologic graft-versus-leukemia effect rather than chemotherapeutic cytotoxicity for disease control. This approach fundamentally changed the landscape of transplant eligibility by extending the option of allogeneic HSCT to patients in their seventh and even eighth decades of life and to those with comorbidities that would preclude myeloablative conditioning. Common RIC regimens include fludarabine combined with melphalan at 140 mg/m2, which is widely used for MDS and AML in older patients, fludarabine with reduced-dose busulfan, and the non-myeloablative Seattle platform of fludarabine with 2 Gy TBI, which provides minimal direct cytotoxicity and places maximum reliance on the GVL effect. The trade-offs of reduced-intensity conditioning include a higher relapse rate and a greater likelihood of initial mixed chimerism, where both donor and recipient hematopoiesis coexist before full donor engraftment is established.

<image>A comprehensive HSCT overview diagram. At the top, show the three stem cell sources (bone marrow, peripheral blood, cord blood) with their key characteristics (cell dose, engraftment time, GVHD risk). Below, display the conditioning intensity spectrum as a horizontal gradient from non-myeloablative (left, Flu/TBI 2Gy) through reduced-intensity (center, Flu/Mel140, Flu/Bu) to myeloablative (right, Bu/Cy, TBI/Cy), with notes on TRM and relapse risk at each end. In the center, show the donor type options: matched sibling donor (best outcomes), matched unrelated donor (MUD, larger registry), haploidentical (virtually universal availability, PT-Cy platform), and cord blood. For each donor type, include: HLA matching requirement, GVHD prophylaxis platform, approximate OS range, and advantages/disadvantages. At the bottom, show the transplant timeline: conditioning → Day 0 (infusion) → engraftment (Day +12-28) → immune reconstitution (months-years) → long-term follow-up. Medical education poster format.</image>

Donor Selection and HLA Matching

HLA System

The human leukocyte antigen (HLA) system, encoded by the major histocompatibility complex on chromosome 6p21, is the principal determinant of immunologic compatibility between donor and recipient. HLA Class I molecules (HLA-A, HLA-B, and HLA-C) are expressed on virtually all nucleated cells and present intracellular peptides to CD8-positive cytotoxic T lymphocytes, while HLA Class II molecules (HLA-DRB1, HLA-DQB1, and HLA-DPB1) are expressed primarily on antigen-presenting cells and present extracellular peptides to CD4-positive helper T lymphocytes.

A matched sibling donor (MSD) who shares 8 of 8 HLA alleles at the A, B, C, and DRB1 loci remains the optimal donor for most transplant settings. The probability of any given sibling being an 8/8 match is 25%, reflecting the inheritance of one HLA haplotype from each parent. When no matched sibling is available, a matched unrelated donor (MUD) is sought through the National Marrow Donor Program (NMDP/Be The Match) registry, with an 8/8 or 7/8 match considered acceptable. The likelihood of finding a matched unrelated donor varies significantly by ethnic background, with approximately 80% of Caucasian patients finding a suitable match compared to substantially lower rates for patients of minority ethnic backgrounds, reflecting the underrepresentation of these populations in donor registries.

Haploidentical HSCT

The development of haploidentical HSCT has been one of the most transformative advances in the field, providing transplant access to virtually every patient, as nearly all individuals have at least one haploidentical donor among their parents, children, or siblings who shares one complete HLA haplotype. The post-transplant cyclophosphamide (PT-Cy) platform, pioneered at Johns Hopkins, has been the key innovation enabling safe haploidentical transplantation. Cyclophosphamide administered at 50 mg/kg intravenously on days +3 and +4 after stem cell infusion selectively eliminates alloreactive T cells that have been activated by the HLA-mismatched antigens in the early post-transplant period, while sparing quiescent T cells and hematopoietic progenitors. GVHD prophylaxis with the PT-Cy platform typically includes post-transplant cyclophosphamide combined with a calcineurin inhibitor (tacrolimus or sirolimus) and mycophenolate mofetil. GVHD rates with this platform are comparable to those seen with matched unrelated donor transplant, and transplant-related mortality has proven acceptable.

The BMT CTN 1703 trial, comparing haploidentical bone marrow with PT-Cy to matched unrelated donor PBSC, has produced data suggesting non-inferior overall survival for the haploidentical approach, with the added advantage of lower chronic GVHD rates. These results, while requiring further maturation, have accelerated the adoption of haploidentical HSCT as a first-line donor option at many centers and have expanded indications to include AML, MDS, MPN, aplastic anemia, sickle cell disease, and thalassemia.

Graft-Versus-Host Disease (GVHD)

Acute GVHD (aGVHD)

Acute GVHD classically occurs within the first 100 days following allogeneic transplantation, though late-onset acute GVHD can present beyond this timeframe and is classified based on clinical features rather than timing alone. The pathogenesis involves donor-derived alloreactive CD4-positive and CD8-positive T lymphocytes recognizing recipient tissue antigens as foreign and mounting a cytotoxic immune attack. The three principal target organs are the skin, presenting as a maculopapular erythematous rash that may progress to bullous disease or desquamation; the liver, manifesting as cholestatic hepatitis with elevated bilirubin; and the gastrointestinal tract, producing nausea, abdominal cramping, secretory diarrhea, and in severe cases, gastrointestinal hemorrhage.

Acute GVHD is graded on a scale of I to IV based on the extent and severity of organ involvement. Grade I disease involves skin only with less than 50% body surface area affected. Grade II includes skin involvement of 50% or more body surface area, liver involvement with bilirubin between 3 and 6 mg/dL, or GI involvement with diarrhea volumes of 500 to 1,000 mL per day. Grades III and IV represent severe multiorgan disease, with Grade IV being life-threatening. The incidence of clinically significant acute GVHD ranges from 30 to 50% with matched sibling donors, 40 to 60% with matched unrelated donors, and is lower with PT-Cy-based haploidentical platforms.

GVHD Prophylaxis

Standard GVHD prophylaxis has traditionally employed a calcineurin inhibitor (tacrolimus or cyclosporine) combined with short-course methotrexate. The PT-Cy-based platform (post-transplant cyclophosphamide plus tacrolimus plus mycophenolate) has emerged as a superior prophylactic strategy, initially validated in haploidentical transplantation and now expanding to matched unrelated donor transplants. The BMT CTN 1703 trial demonstrated that PT-Cy-based prophylaxis significantly reduced chronic GVHD compared to standard calcineurin inhibitor plus methotrexate in MUD transplants, a finding that is reshaping clinical practice. Abatacept (CTLA-4-Ig), a T-cell costimulation blocker, has shown benefit when added to standard prophylaxis in MUD and mismatched transplants, with the GVHD-1 trial demonstrating reduced severe acute GVHD. Rabbit anti-thymocyte globulin (ATG) incorporated into the conditioning regimen reduces GVHD incidence but at the cost of delayed immune reconstitution, increased infections, and potentially increased relapse risk.

Acute GVHD Treatment

First-line treatment for acute GVHD consists of systemic corticosteroids, typically methylprednisolone at 2 mg/kg/day or its equivalent in prednisone at 1 mg/kg twice daily. Complete response is achieved in approximately 50% of patients, with an additional 25% achieving a partial response. Once a response is established, steroids should be tapered gradually over 8 to 12 weeks to minimize both the immunologic consequences of rapid withdrawal and the substantial morbidity of prolonged corticosteroid exposure.

Steroid-refractory acute GVHD, defined as failure to improve by day 5 of treatment or progression by day 3, carries a poor prognosis and requires second-line therapy. Ruxolitinib (Jakafi), a JAK1/JAK2 inhibitor, is the FDA-approved standard second-line agent based on the REACH2 trial, which demonstrated an overall response rate of 62% compared to 39% for best available therapy. The anti-inflammatory and immunomodulatory effects of JAK pathway inhibition make ruxolitinib a mechanistically rational agent in this setting. Additional options for steroid-refractory disease include extracorporeal photopheresis (ECP), anti-thymocyte globulin, and vedolizumab (an anti-alpha-4-beta-7 integrin antibody) for GI-specific GVHD.

Chronic GVHD (cGVHD)

Chronic GVHD typically develops beyond 100 days after transplantation, usually between 3 and 18 months, and presents as a multisystem autoimmune-like syndrome that is the leading cause of late non-relapse mortality and long-term morbidity following allogeneic HSCT. Unlike acute GVHD, which targets predominantly three organs, chronic GVHD can involve virtually any organ system. Skin manifestations range from lichenoid papules to widespread sclerotic changes resembling systemic sclerosis. Oral involvement includes mucosal erosions, lichenoid lesions, and sicca syndrome. Ocular disease presents as keratoconjunctivitis sicca. Hepatic involvement manifests as cholestatic liver disease. Pulmonary involvement, manifesting as bronchiolitis obliterans, is one of the most feared complications due to its progressive and often irreversible nature. Joint contractures, fascial sclerosis, and gastrointestinal involvement are additional manifestations. The NIH consensus criteria grade chronic GVHD as mild, moderate, or severe based on organ-specific scoring. Incidence ranges from 40 to 70% after PBSC transplants and is lower with bone marrow grafts and PT-Cy-based prophylaxis.

Chronic GVHD Treatment

First-line treatment consists of systemic corticosteroids, typically prednisone at 1 mg/kg/day, with or without continued calcineurin inhibitor therapy. The second-line therapeutic landscape for steroid-refractory chronic GVHD has expanded substantially in recent years with multiple FDA-approved agents. Ruxolitinib received approval based on the REACH3 trial, which demonstrated an overall response rate of 76% compared to 60% for best available therapy. Ibrutinib, a Bruton tyrosine kinase inhibitor, was the first FDA-approved agent for chronic GVHD, targeting both B-cell and T-cell signaling pathways relevant to GVHD pathogenesis, though its use is limited by toxicity. Belumosudil (Rezurock), a selective ROCK2 inhibitor, demonstrated an overall response rate of 75% in heavily pretreated steroid-refractory chronic GVHD in the ROCKstar trial and is generally well tolerated. Axatilimab, a monoclonal antibody targeting colony-stimulating factor 1 receptor (CSF1R), received FDA approval in 2024 based on the AGAVE-201 trial showing an overall response rate of 74% in heavily pretreated chronic GVHD. Additional options include extracorporeal photopheresis, rituximab, and imatinib (particularly for sclerotic manifestations).

Graft-Versus-Leukemia (GVL) Effect

The graft-versus-leukemia effect is the immunologic foundation upon which the curative potential of allogeneic HSCT for malignant disease rests. Donor-derived T cells and NK cells recognize and eliminate residual malignant cells in the recipient through alloreactive and tumor antigen-specific mechanisms. The evidence for GVL is compelling: relapse risk is higher in patients who receive T-cell-depleted grafts, in those who undergo syngeneic (identical twin) transplantation, and in those who develop less GVHD, each observation demonstrating the contribution of donor immune cells to disease control.

Donor lymphocyte infusion (DLI) is a therapeutic application of the GVL principle in which additional donor T cells are infused after transplantation to augment the anti-tumor immune response, most commonly in the setting of relapse. DLI is most effective in CML, where it can induce durable molecular remissions, and has also shown activity in relapsed AML and MDS, though with lower response rates and a higher risk of GVHD. The central challenge in transplant immunology remains the dissociation of GVL from GVHD, as the two phenomena share overlapping immunologic mechanisms but are not identical. Strategies to selectively enhance GVL while minimizing GVHD represent one of the most active areas of research in the field.

Post-Transplant Complications

Infections (By Timeline)

The infectious complications following HSCT follow a predictable temporal pattern that reflects the sequential phases of immune reconstitution. During the pre-engraftment period (day 0 through approximately day 30), profound neutropenia and mucosal barrier disruption from the conditioning regimen predispose to bacterial infections (both gram-positive organisms, particularly coagulase-negative staphylococci from central lines, and gram-negative organisms), invasive fungal infections (Candida species and Aspergillus), and reactivation of herpes simplex virus.

The early post-engraftment period (day 30 through 100) is characterized by defective cell-mediated immunity and is the period of highest risk for CMV reactivation, which is monitored through weekly PCR surveillance. Preemptive therapy with ganciclovir or valganciclovir is initiated upon detection of viremia above institutional thresholds. Pneumocystis jirovecii pneumonia is prevented through prophylaxis with trimethoprim-sulfamethoxazole, continued until the patient is off immunosuppressive therapy. Adenovirus reactivation and BK virus-associated hemorrhagic cystitis are additional risks during this period.

The late post-transplant period (beyond day 100) is dominated by infections reflecting the incomplete reconstitution of humoral and cellular immunity, particularly in patients with ongoing GVHD. Varicella-zoster virus reactivation is common and is prevented by acyclovir prophylaxis continued for at least 1 year. Encapsulated organisms pose a risk due to functional asplenia and hypogammaglobulinemia, particularly in patients with active GVHD. EBV-driven post-transplant lymphoproliferative disorder (PTLD) and community-acquired respiratory viruses are additional late infectious concerns.

Letermovir (Prevymis)

Letermovir represents a major advance in CMV prevention following allogeneic HSCT. It inhibits the CMV terminase complex, a mechanism of action distinct from existing antivirals, and is indicated for primary CMV prophylaxis in CMV-seropositive allogeneic HSCT recipients. The pivotal phase 3 trial demonstrated a reduction in clinically significant CMV infection from 37% in the placebo group to 18% in the letermovir group through day 100. Prophylaxis should be maintained through at least day +100 and extended longer in patients with ongoing immunosuppression for GVHD. Letermovir has a favorable side effect profile compared to ganciclovir and does not cause myelosuppression, an important advantage during the engraftment period.

Veno-Occlusive Disease / Sinusoidal Obstruction Syndrome (VOD/SOS)

Veno-occlusive disease, now more accurately termed sinusoidal obstruction syndrome, results from direct toxic injury to the hepatic sinusoidal endothelium by the conditioning regimen. The damaged endothelial cells swell and detach, obstructing sinusoidal blood flow and leading to sinusoidal congestion, hepatocyte necrosis, and progressive hepatic dysfunction. The clinical presentation includes tender hepatomegaly, unexplained weight gain from fluid retention, jaundice with rising bilirubin, and ascites, typically developing within the first 21 days after transplant. Risk factors include myeloablative busulfan conditioning (particularly when busulfan is not pharmacokinetically targeted), pre-existing liver disease, and prior exposure to gemtuzumab ozogamicin.

Diagnosis is established clinically using the Baltimore criteria (bilirubin of 2 mg/dL or more plus at least two of hepatomegaly, weight gain exceeding 5%, and ascites) or modified Seattle criteria. Doppler ultrasonography demonstrating reversed portal venous flow supports the diagnosis. Prevention relies on ursodiol prophylaxis and pharmacokinetically targeted busulfan dosing. Treatment of established VOD/SOS centers on defibrotide (Defitelio), a polydeoxyribonucleotide with profibrinolytic and endothelial-protective properties, administered at 6.25 mg/kg intravenously every 6 hours. Defibrotide has demonstrated an overall survival benefit in severe VOD/SOS and is the only approved treatment. Early initiation is critical; waiting for multi-organ failure to develop before starting treatment markedly worsens outcomes, as severe VOD/SOS with multi-organ failure carries a mortality exceeding 80% without treatment.

Post-Transplant Lymphoproliferative Disorder (PTLD)

Post-transplant lymphoproliferative disorder is an EBV-driven B-cell proliferative process that arises in the context of the profound T-cell immunosuppression following allogeneic HSCT. Without adequate T-cell surveillance, EBV-infected B cells proliferate unchecked, progressing from polyclonal proliferation to frank lymphoma. Monitoring of EBV viral load by quantitative PCR allows early detection of rising EBV titers, prompting preemptive therapy with rituximab (an anti-CD20 monoclonal antibody) to deplete the EBV-harboring B cells before PTLD becomes established. Treatment of confirmed PTLD involves reduction of immunosuppressive therapy to allow immune reconstitution, rituximab, and in cases of aggressive or refractory disease, systemic chemotherapy.

<image>A post-HSCT complication timeline showing the major complications organized by time after transplant. Create a horizontal timeline from Day 0 to Year 2+. Show three infection phases: pre-engraftment (bacterial, fungal, HSV), early post-engraftment (CMV, PCP, adenovirus, BK virus), and late (VZV, encapsulated organisms, EBV-PTLD). Overlay non-infectious complications on the same timeline: VOD/SOS (Day 0-21), acute GVHD (Day 14-100+), engraftment syndrome (Day 7-14), hemorrhagic cystitis (Day 14-60), chronic GVHD (Day 100 onward), and late effects (secondary malignancies, endocrine dysfunction, cataracts). Include prophylaxis strategies shown as colored bars along the bottom: letermovir for CMV (Day 0-100+), acyclovir for HSV/VZV (Day 0 through 1 year), fluconazole/voriconazole for fungal (duration varies), TMP-SMX for PCP (until off immunosuppression). Color-code by category: infections (red), GVHD (blue), organ toxicity (orange), late effects (purple). Medical education timeline format.</image>

Key Clinical Pearls

• Post-transplant cyclophosphamide has revolutionized haploidentical HSCT and is now being adopted for MUD transplants based on BMT CTN 1703 data; it reduces chronic GVHD without compromising GVL
• Ruxolitinib is now the standard second-line therapy for both steroid-refractory acute and chronic GVHD based on REACH2 and REACH3 trials
• Letermovir prophylaxis has significantly reduced CMV disease in seropositive allogeneic HSCT recipients; it should be continued through at least day +100 and longer if ongoing immunosuppression
• VOD/SOS risk is highest with myeloablative busulfan conditioning; PK-targeted dosing and ursodiol prophylaxis are essential preventive strategies
• Defibrotide is the only approved treatment for severe VOD/SOS; early initiation improves outcomes; do not wait for multi-organ failure
• The GVL effect is the therapeutic backbone of allogeneic HSCT for malignant disease; strategies to enhance GVL while minimizing GVHD are the central challenge in transplant immunology

References

1. Copelan EA. Hematopoietic Stem-Cell Transplantation. N Engl J Med. 2006;354(17):1813-1826.
2. Zeiser R, Blazar BR. Acute Graft-versus-Host Disease — Biologic Process, Prevention, and Therapy. N Engl J Med. 2017;377(22):2167-2179.
3. Jagasia M, et al. Ruxolitinib for steroid-refractory acute graft-versus-host disease (REACH2). N Engl J Med. 2021;385(3):228-237.
4. Marty FM, et al. Letermovir prophylaxis for cytomegalovirus in hematopoietic-cell transplantation. N Engl J Med. 2017;377(25):2433-2444.
5. Luznik L, et al. HLA-haploidentical bone marrow transplantation for hematologic malignancies using nonmyeloablative conditioning and high-dose, posttransplantation cyclophosphamide. Biol Blood Marrow Transplant. 2008;14(6):641-650.

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