Infant acute lymphoblastic leukemia with t(11;16)(q23;p13.3) and lineage switch into acute monoblastic leukemia

Stasik, Christopher J.; Ganguly, Siddhartha; Cunningham, Mark T.; Hagemeister, Stacey; Persons, Diane L.

doi:10.1016/j.cancergencyto.2006.02.013

Cited by 33 publications

(36 citation statements)

References 7 publications

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“…The mostly single case pediatric reports in the literature also support this notion, describing switches from Bcp to myelo-monocytic lineages [5,6,9,25,26,[31][32][33][34][35][36][37]. Conversions from AML (or bilineal) to ALL are even more rare [38][39][40][41][42][43], also involve mostly Bcp and myelo-monocytic lineages, as was the case with the 2 patients from our own series that switched from myeloid to Pro-B.…”

Section: Discussionsupporting

confidence: 68%

Lineage switch in childhood acute leukemia: An unusual event with poor outcome

Rossi¹,

Bernasconi²,

Alonso³

et al. 2012

American J Hematol

134

117

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Although rarely, switches between lymphoid and myeloid lineages may occur during treatment of acute leukemias (AL). Correct diagnosis relies upon confirmation by immunophenotyping of the lineage conversion and certification that the same cytogenetic/molecular alterations remain despite the phenotypic changes. From a total of 1,482 AL pediatric patients, we report nine cases of lineage conversion (0.6%), seven from lymphoid (four Pro-B, two Pre-B, one Common) to myelo-monocytic, and two from myeloid (bilineal, with myeloid predominance) to Pro-B. Eight patients were infants. Switches were suggested by morphology and confirmed with a median of 15 days (range: 8 days-6 months) from initiation of therapy. Of note, in five cases switches occurred before day 15. Stability of the clonal abnormalities was assessed by cytogenetic, RT-PCR/Ig-TCR rearrangement studies in all patients. Abnormalities in 11q23/MLL gene were detected in seven cases. Treatment schedules were ALL (two pts), Interfant-99 (five pts) and AML (two pts) protocols. Despite changing chemotherapy according to the new lineage, all patients died. Our findings support the association of lineage switches with MLL gene alterations and the involvement of a common lymphoid B-myeloid precursor. New therapies should be designed to address these rare cases. Possible mechanisms implicated are discussed. Am. J. Hematol. 87:890-897, 2012. V

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Section: Discussionsupporting

confidence: 68%

Lineage switch in childhood acute leukemia: An unusual event with poor outcome

Rossi¹,

Bernasconi²,

Alonso³

et al. 2012

American J Hematol

134

117

View full text Add to dashboard Cite

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“…A lineage switch has been previously described in seven cases of infant leukemia (Table 1) [3][4][5][6][7][8][9]. Five cases showed a lineage switch from B-precursor ALL (pro-B or pre-B) to AMoL, while the other two cases showed a switch from AMoL to B-precursor ALL.…”

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confidence: 95%

“…However, infant leukemia still has a poor prognosis, which is associated with leukemic cell abnormalities involving the MLL (also known as ALL1 or HRX) gene [2]. Lineage switches of the leukemic cell clones are rarely observed, especially in infant leukemia [3][4][5][6][7][8][9]. This phenomenon may cause poor prognosis for infant leukemia.…”

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confidence: 99%

Early lineage switch in an infant acute lymphoblastic leukemia

et al. 2009

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Childhood acute leukemia is usually associated with a good prognosis due to intensive chemotherapy [1]. However, infant leukemia still has a poor prognosis, which is associated with leukemic cell abnormalities involving the MLL (also known as ALL1 or HRX) gene [2]. Lineage switches of the leukemic cell clones are rarely observed, especially in infant leukemia [3][4][5][6][7][8][9]. This phenomenon may cause poor prognosis for infant leukemia. This report presents a case of infant acute lymphoblastic leukemia (ALL) that demonstrated an early lineage switch to acute monocytic leukemia (AMoL).The patient was a male infant born after a 37-week gestation and weighed 2.96 kg. He was delivered via a cesarean section because of fetal bradycardia. The family history was negative for cancer. He began vomiting frequently at 21 days of age and visited a family physician at 23 days of age. The gain in body weight was poor, and he presented with jaundice and marked hepatosplenomegaly. A laboratory examination showed a hemoglobin level of 5.2 g/dl, platelet count of 16,000/ll, white blood cell (WBC) count of 400,000/ll, aspartate amino transferase of 2,960 IU/l, alanine transferase of 745 IU/l and lactate dehydrogenase of 2,971 IU/l. He was diagnosed with acute leukemia, and admitted to the Toyama University Hospital. A physical examination at admission showed a body weight of 3,122 g (7 g gain per day from birth), a temperature of 37.3°C and a pulse of 150/min. His skin color was pale and icteric, and a bluish nodule was found on the right cubital fossa. Hepatosplenomegaly was detected, but no lymph node swelling was observed. The WBC count was 391,500/ll with 0.5% lymphocytes, 3.5% monocytes and 96% blastic cells (Fig. 1a). The blastic cells were negative for myeloperoxidase staining, and the immunophenotypic analysis disclosed that the cells were negative for CD10 and positive for CD19, CD22, CD34 and CD38. He was thus diagnosed with ALL of the pro-B phenotype. A cytogenetic analysis disclosed the karyotype of 46, XY, t(4;11)(q21;q23). Southern blotting revealed a rearrangement of the MLL gene, and a fluorescence in situ hybridization (FISH) analysis revealed split signals of the MLL gene. The patient underwent an exchange transfusion, resulting in the reduction of the WBC to 85,000/ll. The patient was treated with prednisolone for 7 days and the WBC count fell to 5,100/ll with 2.5% blastic cells. However, on day 8, the WBC count increased to 11,400/ll with 12.5% neutrophils, 6.5% lymphocytes, 70.5% monocytes, and 9% blastic cells (Fig. 1b), and atypical monocytes increased. An immunophenotype analysis disclosed that the cells were positive for CD20, CD13, CD14, CD15, CD33, CD41, CD61 and CD38. The patient was then diagnosed with AMoL. The peripheral blood smear at diagnosis was therefore reevaluated, and a small component of the monocytes showed an atypical morphology (Fig. 1c). The central nervous system was also involved.

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“…Cases of conversions from AML to ALL and vice versa are extremely rare [1][2][3][4][5][6][7][8][9][10][11][12][13]. Several hypotheses have been suggested to explain lineage conversion in leukemias, but the precise mechanism remains unclear.…”

Section: Discussionmentioning

confidence: 99%