1                 We show that samples from 10 ANLL and ALL patients patients tested for sensitivity to

2 A of leukemia cells from 4 other patients (2 ANLL and 2 ALL).

3                           We investigated 22 ANLL samples and found a high frequency of Nras and Kras

4 T-cell ALL but present in pre-B-cell ALL and ANLL.

5  results, approximately eight to nine excess ANLLs might be expected to occur among 100 NHL patients

6 ian/Pacific Islanders had increased risk for ANLL (OR = 2.00, 95% CI: 1.19, 3.36).

7  and 2 with acute nonlymphoblastic leukemia (ANLL).

8 patients with acute nonlymphocytic leukemia (ANLL) who required therapeutic leukocytopheresis for hyp

9 nts developed acute nonlymphocytic leukemia (ANLL), which represents a relative risk (RR) of 117 (95%

10 ome (MDS) and acute nonlymphocytic leukemia (ANLL).

11 ukemia (ALL) and acute nonlymphoid leukemia (ANLL).

12 al (24 with acute nonlymphoblastic leukemia [ANLL] and 25 with acute lymphoblastic leukemia [ALL]).

13 utrophils and chronic myeloid leukemia, most ANLL samples also expressed the globo-series GSLs, globo

14 was strongly associated with a myeloblastic (ANLL M0-M2) and monoblastic phenotype (M5).

15 ted from patients with acute nonlymphocytic (ANLL) or acute lymphocytic (ALL) leukemias.

16 s in a genetically engineered mouse model of ANLL.

17 ns were observed for birth weight and ALL or ANLL.

18                               Globo-positive ANLL samples bound both shiga toxin and parvovirus B19 o

19 ve risks of all second cancers and secondary ANLL were 37% and 17%, respectively.

20 cell lines and patient samples indicate that ANLL cells are more sensitive than ALL cells to all thre

21 port a working hypothesis that predicts that ANLL cases have one mutation which inhibits differentiat

22 four partial responses [PR] in patients with ANLL and one CR and two PRs in patients with ALL), and a