Microfluidic image cytometry (MIC) has been developed to study phenotypes of various hPSC lines by screening several chemically defined serum/feeder-free conditions. A chemically defined hPSC culture was established using 20 ng mL −1 of bFGF on 20 μg mL −1 of Matrigel to grow hPSCs over a week in an undifferentiated state. Following hPSC culture, we conducted quantitative MIC to perform a single cell profiling of simultaneously detected protein expression (OCT4 and SSEA1). † Electronic supplementary information (ESI) available: Fabrication of microfluidic hPSC array, generation of hiPSC (i.e., hiPSA1 and hiPSB2), microscopy settings and image processing are available. See

Leukemias and lymphomas arise by genetic and epigenetic alterations of previously healthy lymphocytes. B-cell lymphoma is the most frequent lymphocyte malignancy, with certain tumor subtypes characterized by recurring genetic alterations that include reciprocal chromosome translocations between IG loci and CCND1, BCL2, MYC, and BCL6.1 These rearrangements place tumor-promoting genes under the control of IG rather than endogenous regulatory elements, leading to their dysregulated expression. Epigenetic changes, including DNA hypermethylation, aberrant histone modifications, and altered microRNA expression are also linked to B-cell transformation.2-4 In particular, DNA hypermethylation promotes chromatin compaction and gene silencing, with consistent repression of specific tumor suppressor genes associated with multiple types of cancer, including subtypes of B-cell leukemia and lymphoma. 5Aberrant expression of the TCL1 oncogene, first identified from rearrangements with TCR loci in T-cell prolymphocytic leukemia, also occurs frequently in mature B-cell leukemias and lymphomas, although not by gene rearrangement [reviewed in 6 ]. A causative role for ectopic TCL1 expression in lymphocyte transformation is supported by three different TCL1 transgenic (TCL1-tg) mouse models that develop mature B-and T-cell malignancies.6,7 TCL1-tg mice and patients with dysregulated TCL1 expression exhibit polyclonal lymphocyte hyperplasia and a long delay to tumor formation,