Trisomy 11 in Nonlymphocytic Neoplasia

Clinical characteristics of patients with de novo acute myeloid leukaemia and isolated trisomy 11: a Cancer and Leukemia Group B study

“…In our study none of the four patients with exclusively abnormal metaphases (cases 1, 6, 7 and 10) achieved a CR compared to six of nine (67%) patients with a karyotypically normal clone. However, the CR rate in a subgroup of six previously reported þ11 patients with de novo AML who had only abnormal cells was almost the same as in a subgroup of 21 patients with a normal clone present in addition to a clone with þ11 (67% v 71%) (Li et al, 1983;Ohyashiki et al, 1988;Weh et al, 1988;Nakamura et al, 1989;Bilhou-Nabera et al, 1994;Cuneo et al, 1994;Slovak et al, 1995;Caligiuri et al, 1996;Satake et al, 1997). Thus at present it is unclear if the presence of a cytogenetically normal clone influences prognosis of patients with þ11.…”

“…Similarly, a cytogenetically normal cell line has been detected in most published þ11 cases with de novo AML (Yunis et al, 1981;Fitzgerald et al, 1983;Li et al, 1983;Gustavsson et al, 1984;Testa et al, 1985;Berger et al, 1987;Ohyashiki et al, 1988;Weh et al, 1988;Nakamura et al, 1989;Keinänen et al, 1989;Kadam et al, 1991;Furuya et al, 1992;Marosi et al, 1992;UKCCG, 1992;Fagioli et al, 1993;Suciu et al, 1993;Bilhou-Nabera et al, 1994;Cuneo et al, 1994;Bernard et al, 1995;Slovak et al, 1995;Caligiuri et al, 1996;Satake et al, 1997). In two-thirds of patients with normal metaphase cells in our series we observed more abnormal than normal cells, and this was the case in previous studies as well.…”

“…The reason why other groups did not recognize the correlation between þ11 and de novo AML of M2 and M1 subtypes may be that they reviewed not only þ11 cases with de novo AML but also patients with secondary AML and MDS (Bilhou-Nabera et al, 1994;Slovak et al, 1995). When we restricted our review of the literature to AML patients with no history of antecedent neoplasia, 80% of them (37/46 FAB classified patients) had M1 or M2 morphology (Yunis et al, 1981;Fitzgerald et al, 1983;Li et al, 1983;Testa et al, 1985;Berger et al, 1987;Ohyashiki et al, 1988;Weh et al, 1988;Keinänen et al, 1989;Nakamura et al, 1989;Tien et al, 1990;Kadam et al, 1991;Cuneo et al, 1992Cuneo et al, , 1994Hurwitz et al, 1992;Marosi et al, 1992;UKCCG, 1992;Fagioli et al, 1993;Suciu et al, 1993;Bilhou-Nabera et al, 1994;Bernard et al, 1995;Slovak et al, 1995;Caligiuri et al, 1996;Satake et al, 1997).…”

“…Isolated trisomy 11 has been reported in 15 patients diagnosed with MDS (Gangji et al, 1985;Morgan et al, 1988;Ohyashiki et al, 1988Ohyashiki et al, , 1989Takasaki et al, 1988;Weh et al, 1988;Suciu et al, 1990;Bergamaschi et al, 1991;Rubin et al, 1991;UKCCG, 1992;Yamamoto et al, 1997) and in 17 patients with secondary AML, including 12 with evidence of a preleukaemic or myelodysplastic phase (Hagemeijer et al, 1981;GFCH, 1984;Dang et al, 1985;Avanzi et al, 1989;Bartram et al, 1989;Ingram et al, 1989;Johansson et al, 1991;UKCCG, 1992;Bilhou-Nabera et al, 1994;Najfeld et al, ᭧ 1998 Blackwell Science Ltd, British Journal of Haematology 101: 513-520 1994; Bernard et al, 1995;Slovak et al, 1995;Trakhtenbrot et al, 1995;Caligiuri et al, 1996). Avanzi et al (1989) suggested that trisomy 11 represented an abnormality specifically associated with MDS and AML secondary to MDS.…”

“…This is true for isolated trisomy 11 (þ11) despite the fact that þ11 is the third most common sole trisomy in de novo AML, following trisomies of chromosomes 8 and 13 [Cancer and Leukemia Group B (CALGB) cytogenetic data base, C. D. Bloomfield, personal communication, April 1996]. Many cases with þ11 have been reported as part of large series of AML patients with divergent cytogenetic abnormalities and often limited clinical data (Yunis et al, 1981;Fitzgerald et al, 1983;Li et al, 1983;Gustavsson et al, 1984;Testa et al, 1985;Berger et al, 1987;Keinänen et al, 1989;Kadam et al, 1991;Cuneo et al, 1992;Hurwitz et al, 1992;Marosi et al, 1992;UKCCG, 1992) or as case reports (Ohyashiki et al, 1988;Nakamura et al, 1989;Cuneo et al, 1994). The three largest series of de novo AML patients with þ11 detected at diagnosis we know of, were composed of 10 (Caligiuri et al, 1996), seven (Bilhou-Nabera et al, 1994) and six (Slovak et al, 1995) patients.…”