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Biomedical subjects

P H Fitzgerald

Publications and source records attributed to P H Fitzgerald.

At least 91 records · Page 5Linked to original sources
PubMed1977

Major karyotypic abnormality in a child born to a woman with untreated malignant melanoma.

The karyotype of a 7-month-old child had 46 chromosomes, including five abnormal chromosomes in cultured lymphocytes. G-banding indicated the presence of reciprocal translocation products between chromosomes 1 and 7 and between chromosomes 4 and 15. A probable third translocation involved the same chromosome 4p arm and 12q. All metaphases showed these changes. C-band markers and the presence of reciprocal exchange products indicated that the chromosome changes occurred in the zygote or a post-zygotic cell of the child. The mother developed malignant melanoma while carrying the child but did not receive therapy before its birth. The suggestion is made that an undetected common agent was involved in the aetiology of the mother's tumour and the clastogenic change to the child's chromosomes.

Adult↗
PubMed1976

Evidence that chromosome band 22q12 is concerned with cell proliferation in chronic myeloid leukaemia.

A man and two of his three children carried an abnormally short chromosome 22 resembling the Philadelphia chromosome (Ph1). Giemsa banding showed that the abnormal chromosome resulted from a translocation t(11;22) (q25;q13). The breakpoint on chromosome 22 was at the q12/q13 band interface compared with the breakpoint of Ph1 at the q11/q12 band interface. The absence of leukaemia or haematological disorder in members of this family suggests that the critical genetic site on chromosome 22 concerned with abnormal myeloid cell proliferation in human leukaemia is contained in the 22q12 band.

Adult↗
PubMed1976

Karyotope and survival in human acute leukemia.

Of 111 patients presenting with acute forms of leukemia, 44% had a chromosomally abnormal cell line in the bone marrow at diagnosis. In each of the acute leukemia forms (myeloid, lymphatic, stem-cell), patients with karyotypic abnormalities showed mean and median survival times like those with normal chromosomes. Both groups showed a wide range of survival times. The mean and median survival times of patients with mixed populations of chromosomally normal and abnormal cells did not differ from those of patients with exclusively abnormal cells in the bone marrow. The karyotypic abnormalities associated with acute leukemia, as well as having no etiologic significance, probably do not determine the subsequent course of the leukemia.

Adult↗
PubMed1975

A mechanism of x chromosome aneuploidy in lymphocytes of aging women.

One and sometimes both X chromosomes in cultured lyphocytes of women donors showed division of the centromere when the centromeres of other chromosomes were entire. This premature centromere division (PCD) was associated with evidence of non-disjunction of the X chromosome. On average, 2% of metaphases from 32 women donors showed PCD, but the incidence was 4 times greater in women over 59 years of age than in women under 40 years. Increased X chromosome aneuploidy was associated with the higher frequency of PCD in cultured lymphocytes from older women. PCD of the X chromosome is considered to be the mechanism of non-disjunction causing the previously described aneuploidy in cultured lymphocytes of aging women.

Adult↗
PubMed1975

Isochromosome for the short arm of X: a human mosaic 45,x/46,XXpi.

An 18 year female patient with short stature, amenorrhoea and poorly developed secondary sexual characteristics, has subnormal oestrogen excretion and increased levels of plasma gonadotrophin. Laparoscopy revealed streak ovaries. A reduced number of buccal mucosal cells showed positive sex chromatin. Chromosome studies of blood lymphocytes indicated mosaicism: the major cell line was characterized by an isochromosome for the X short arm, 46,XXpi; the minor cell line had a single X chromosome, 45,X.

Adolescent↗
PubMed1975

Premature centromere division: a mechanism of non-disjunction causing X chromosome aneuploidy in somatic cells of man.

Apparent acentric fragments which replaced a C-group chromosome in cultured blood lymphocytes from a woman patient were shown by autoradiography, G-banding and C-banding to be complete X chromosomes in which the centromere had divided prematurely in relation to the centromeres of other chromosomes in the same metaphase. Metaphases with multiple 'fragments' suggested that non-disjunction of the 'fragments' had occurred. This anomaly of the X chromosome was associated with increased aneuploidy of a C-group chromosome, presumed to be X. Premature centromere division of the X chromosome (PCD, X) appeared to be a mechanism of non-disjunction which caused significant monosomy and trisomy of the X chromosome in blood cells and skin fibroblasts. The frequency of cells with multiple fragments and the extent of the aneuploidy in 48 hr. blood cultures indicated that this mechanism of non-disjunction operated during mitosis both in vivo and in vitro. Premature centromere division occurred at a lower frequency in normal women donors, and was age-related, being four times more frequent in women 60 years and older than in women under 40. Associated with the higher frequency of PCD, the older women also showed evidence of increased X chromosome aneuploidy. Premature centromere division of the X chromosome is considered to be the mechanism of non-disjunction, causing the well-documented increased number of 45, -C metaphases in ageing women. Premature centromere division was rare in men, but an age effect was again suggested.

Adult↗