Table 1

Risk factors, mechanisms, and strategies to optimize collection in predicted poor mobilizer patients

Risk factorPostulated mechanismMobilization strategy
Low steady-state platelet counts and PB CD34+ levelReflects overall HSC reserveRegimen promoting HSC proliferation, eg, SCF, cyclophosphamide
Low steady-state TNF-α levelMay reflect niche dysfunction, including the macrophage response to G-CSFRegimen bypassing the macrophage-dependent pathways, eg, plerixafor-containing regimen
Increasing ageReduced HSC reserve because of the following:
  • Age-related HSC senescence

  • Age-related loss or dysfunction of HSC niche

  • Age-related bone loss or altered bone metabolism

Regimen promoting HSC proliferation, eg, SCF, cyclophosphamide
Add risk-adapted plerixafor to augment niche response to G-CSF
Bisphosphonate treatment continued throughout collection PTH of interest in experimental models
Underlying diseaseParaneoplastic niche dysfunction Loss of niche to mass effect of tumorAim to clear BM of disease before collection
Prior extensive radiotherapy (RT) to red marrowDirect HSC toxicity
Toxicity to HSC niche
Rainy day collection before extensive RT when possible
Risk-adapted plerixafor
Regimen promoting HSC proliferation, eg, SCF, cyclophosphamide
Prior chemotherapy
    MelphalanDirect HSC toxicityAvoid melphalan until autologous cells collected
    FludarabineDirect HSC toxicity, niche damageCollect HSCs early, after < 4 cycles of fludarabine
    Intensive chemotherapy (eg, hyper-CVAD)Dose-dense cycles may cause niche damage, and HSCs forced into cell cycle may not engraft as wellUse SCF or preemptive risk-adapted plerixafor for fludarabine-exposed and heavily pretreated patients
Prior lenalidomidePossible effects on HSC motility
Possible dysregulated HSC niche because of antiangiogenic effects
Collect HSC early, after < 4 cycles of treatment
Temporarily withhold lenalidomide during collection.