Kwame Yeboa

CUNY Graduate Center, New York City, New York, United States

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Publications (4)14.2 Total impact

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    ABSTRACT: Three cases of distal duplication 14q are presented. The first two cases are cousins in a kindred segregating a balanced translocation t(14;18)(q31;q23). The third case resulted from a maternal translocation t(14;18)(q24;p11). By review of these cases and those previously reported, a distal duplication 14q syndrome is further delineated. Common features include postnatal growth retardation, mental retardation, hypotonia, microcephaly, slanted palpebral fissures, ocular hypertelorism, sparse eyelashes and eyebrows, nasal dysmorphism, tented lip, micrognathia, posteriorly rotated ears, and minor skeletal anomalies.
    Human Genetics 02/1984; 68(2):159-64. DOI:10.1007/BF00279307 · 4.82 Impact Factor
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    ABSTRACT: A fetus was identified by prenatal cytogenetic diagnosis as having a karyotype 46,XY,r(13) (p11q13). Termination of the pregnancy yielded a severely malformed fetus. Fetal abnormalities included anencephaly, imperforate anus and urethral meatus, severe talipes, syndactyly, cardiac defects and other anomalies. Confirmatory studies on cultured placental villi cells indicated a second cell line, 46,XY, −13,+ 13qter→cen::13ql3→qter. This cell line was not detectable in cells derived from the fetus despite extensive studies. It seems likely that the two cell lines arose simultaneously with selection favouring the 46,XY,r(13) line. How the chromosome rearrangements may have arisen is discussed. We are unaware of other cases where a cell line identifiable by a chromosome abnormality appeared to be confined to placental tissue. However, studies on placental tissue may be helpful in understanding the origin of other unbalanced de novo rearrangements.
    Prenatal Diagnosis 10/1983; 3(4):297-302. DOI:10.1002/pd.1970030406 · 3.27 Impact Factor
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    ABSTRACT: A six-year-old girl with Fanconi anemia (FA) developed acute myeloid leukemia (AML) as the first hematologic manifestation of the syndrome. She remains in remission 18 mo after diagnosis although her management is complicated by unusual sensitivity to chemotherapeutic agents. Marrow cells studied prior to initiation of leukemia therapy showed increased chromosome breakage and an abnormal clone in which a number 7 and a number 8 chromosome were replaced by two marker chromosomes. During the present remission her cultured lymphocytes, bone marrow cells, and fibroblasts showed increased "spontaneous" chromosome breakage as well as enhanced sensitivity to the clastogenic effect of the difunctional alkylating agent diepoxybutane (DEB), features characteristic of FA. Eight months into remission 50% of her marrow cells comprised an abnormal clone, which was monosomic for the number 7 chromosome but had both copies of number 8; in addition a variable number of unique marker chromosomes were present in clonal as well as nonclonal cells. This same marrow sample, upon culture, showed an abnormal growth pattern of CFU-GM, absence of detectable CFU-GEMM and BFUe, non-responsiveness of CFU-GM to inhibition by acidic isoferritins, increased bone marrow acidic isoferritin inhibitory activity, and absence of detectable bone marrow cell-derived GM-CSF. The implications of these findings to leukemogenesis in FA are discussed.
    American Journal of Hematology 05/1982; 12(3):289-300. DOI:10.1002/ajh.2830120312 · 3.80 Impact Factor
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    ABSTRACT: Chromosome instability and an increased sensitivity to DNA cross-linking alkylating agents appears to be present in patients with Fanconi anemia (FA). A 5½ year old white female with short stature and microcephaly developed acute myelomonocytic leukemia (AMML). Chromosome analysis of the bone marrow showed a karyotypically abnormal clone with rearrangements consistent with AMML, as well as an increased rate of spontaneous chromosome breakage. The diagnosis of FA was confirmed by finding 8.07 (normal 0-0.10) chromosome breaks per cell in lymphocytes cultured with the difunctional alkylating agent diepoxybutane. A complete bone marrow remission was induced with 1 course of cytosine arabinoside 100mg/M2/day IV X 7 by continuous infusion and adriamycin 30mg/M2/day IV X 3. Severe pancytopenia presumably secondary to heightened chromosomal instability of the normal regenerating bone marrow elements necessitated significant drug reduction of all subsequent anti-leukemia treatment. Despite minimal chemotherapy the patient remains in a complete remission. This patient's course illustrates three points: first, the clinical spectrum of FA is quite varied; second, AMML may be the first hematologic event in FA without prior therapy with either androgens or corticosteroids; third, treatment requires significant chemotherapy dosage modification.
    Pediatric Research 04/1981; 15(4):590-590. DOI:10.1203/00006450-198104001-00913 · 2.31 Impact Factor