Table 3.

Possible causes of discrepancies in the antitumorigenic effects of MSC populations

Contributing parameters to outcome disparity of MSC-based cancer cytotherapy	Variability range of differentially expressed parameters	Proposed optimal experimental parameter
MSC isolation source	BM (human fetal or adult, mouse) AT (human), UC (human, rat)	Human UC
MSC in vitro/ex vivo expansion	MSC passage, MSC confluence, high serum or growth factor supplemented media, possible contamination with tumor cells	Determine maximum passage No. for MSC/check senescence status, minimize serum of animal origin
In vivo tumor model	Over 60 cell lines representing 15 tumor types (including sarcoma, hepatoma, adenocarcinoma, melanoma, glioblastoma, lymphoma)	At least two different tumor cell lines per cancer
	SCID, athymic nu/nu mice	Athymic nu/nu mice (or nude variants)
MSC species origin	Syngeneic, xenogeneic	Human xenograft
MSC : Cancer cell ratio	BM-MSC: 2:1–1:1–1:12 AT-MSC: 1:1–1:10 UC-MSC: 6:1–1:1–1:6 (ratios more frequently associated with tumor suppression)	Dependent on MSC type and in vivo or in vitro experiment. 1:1 and 1:2 should be used as starting ratios
Cell administration route	Orthotopic/intratumoral, subcutaneous (s.c.), intraperitoneal (i.p), intravenous (i.v.)	Ideally, i.v. if homing also needs to be demonstrated. Otherwise, orthotopic, good for mimicking human carcinogenesis
Timing (latency) of MSC administration	Simultaneously with tumor cells, successive (variable time lag)	Successive (lag depends on type of tumor model; usually 7 days)
Repetition of administration	Single (“one-off”) administration or repeated dosing	Repeated (once or twice); doses > 1 week apart