TATUM BABY DAUGHTER OF DEREK FISHER UTAH JAZZ PT GUARD Retinoblastoma is sometimes due to paternal age >= 45 YEAR WAS 3.0(95 % ci: 0.2-41.7)

Tatum, the little daughter of Utah Jazz point guard Derek Fisher has been diagnosed with a type of cancer called retinoblastoma

It is being reported that the little 10-month-old daughter of Utah Jazz point guard Derek Fisher is in hospital with a very serious medical condition.

Tatum Fisher has recently been diagnosed with a type of cancer known as retinoblastoma, which is a cancer of the eye. Treatment options include, removal of the eye, or a combination of chemotherapy and surgery.

The little girl's condition was first identified by her mother who noticed a weird reflection of light coming from her eye. A few doctor visits and a pediatrician visit later the family learned of the troubling diagnosis.

Doctors at New York Presbyterian Hospital performed a procedure on the baby girl in which they injected chemotherapy drugs directly into the tumor hoping to shrink it. If three such surgeries do not shrink the tumor to the point where it can be removed, then the little girl will lose her eye altogether.

“My wife and I definitely plan to try and help as many people as we can,” Fisher said. “I don’t know how we’ll be able to at this point. If there’s a treatment out there, they should be able to get it. Some people can’t afford to get it. Some people don’t have the resources.

"They've done nine cases," Fisher said. "(In) one case the child's arterial structure wasn't strong enough, but the other eight kids that had the treatment, all of their tumors have reduced in size."

Twin brother of Tatum, little Drew Fisher was also examined for signs of the condition however he is perfectly healthy.










1: Int J Epidemiol. 2001 Dec;30(6):1428-37. Links
Comment in:
Int J Epidemiol. 2001 Dec;30(6):1438-9.
Case-control study of parental age, parity and socioeconomic level in relation to childhood cancers.Dockerty JD, Draper G, Vincent T, Rowan SD, Bunch KJ.
Childhood Cancer Research Group, Department of Paediatrics, University of Oxford, 57 Woodstock Road, Oxford OX2 6HJ, UK.

BACKGROUND: Parental ages, parity, and social class have been found in some studies to be associated with particular childhood cancers. Further investigation is warranted because of conflicting findings, biases, and the need to test specific hypotheses. METHODS: A case-control study was conducted (England and Wales, ages 0-14 years). Cases were ascertained from the National Registry of Childhood Tumours, and were born and diagnosed during 1968-1986. Birth record controls were matched 1:1 to cases on date of birth, sex and area. Information on variables of interest for both groups came from birth records. In all, 10 162 pairs could contribute to matched analyses. RESULTS: The odds ratio (OR) for retinoblastoma resulting from assumed new germ cell mutations among children of fathers aged > or =45 years was 3.0 (95% CI : 0.2-41.7). The risk of childhood acute lymphoblastic leukaemia (ALL) was significantly higher among children of older mothers and fathers, and significant trends with increasing mothers' (P < 0.001) and fathers' (P = 0.002) ages were found. There was a strong and significant protective effect of increasing parity on risk of childhood ALL. The adjusted OR for parity of > or =5 (versus 0) was 0.5 (95% CI : 0.3-0.8). Children in more deprived communities had a lower risk of ALL; but this was not significant after confounders were allowed for. There was no significant effect of social class based on parental occupation on ALL risk, but the numbers were small in those analyses. CONCLUSIONS: The associations between ALL and parental ages did not disappear when children with Down syndrome were excluded, suggesting an additional explanation beyond known links. The strong ALL association with parity may be because of an unknown


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1: Ophthalmic Epidemiol. 2000 Dec;7(4):285-91. Links
Parental age in Indian patients with sporadic hereditary retinoblastoma.Sivakumaran TA, Ghose S, Kumar H, A S, Kucheria K.
Division of Genetics, Department of Anatomy, Dr. Rajendra Prasad Centre for Ophthalmic Science, All India Institute of Medical Sciences, New Delhi, India.

There is a consistent correlation between sporadic hereditary retinoblastoma and parental age. It has been proven beyond doubt that the birth rank is correlated with parental age. In the present study, a test for the effect of birth rank was performed in order to assess the risk of developing retinoblastoma with increased parental age. The study of the effect of birth rank showed a significant association between sporadic retinoblastoma (bilateral and unilateral) and late para, indicating that fresh germline mutations must have taken place in some of the sporadic cases. An investigation of the effect of birth rank on familial cases, obtained from published papers and our own series, showed that familial retinoblastoma is significantly associated with early para, suggesting early parental age. Further analysis of the mean paternal and maternal ages of sporadic cases (bilateral and unilateral) showed that the mean paternal age of sporadic bilateral (sporadic hereditary) cases was higher than that of sporadic unilateral cases (p<0.05). No such correlation was seen with mean maternal age. Thus, the present study shows that a high paternal age may be associated with sporadic bilateral (sporadic hereditary) retinoblastoma.

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1: Am J Ophthalmol. 1990 Dec 15;110(6):605-9. Links
Parental age in sporadic hereditary retinoblastoma.DerKinderen DJ, Koten JW, Tan KE, Beemer FA, Van Romunde LK, Den Otter W.
Department of Pathology, Academisch Ziekenhuis Utrecht, The Netherlands.Of 104 children with sporadic hereditary retinoblastoma born between 1945 and 1970, we studied the age of their parents at the birth and compared this age with the mean age of parents at the birth of their children during the same period in The Netherlands. The mean age of fathers at the birth of their children with sporadic hereditary retinoblastoma (33.7 years) was significantly higher than the mean age of fathers at the birth of their children in the general population (32.5 years) (P less than .05, one sided). Similarly, the mean age of mothers at the birth of their children with sporadic hereditary retinoblastoma (31.2 years) was significantly higher than the mean age of mothers at the birth of their children in the general population (29.5 years) (P less than .05, one sided). We further analyzed this parental age factor by measuring the relative risk of age groups and comparing the incidence of sporadic hereditary retinoblastoma in the various parental age groups with the incidence of sporadic hereditary retinoblastoma in the total population. Mothers 35 years of age or older had a relative risk of 1.7 to have a child with sporadic hereditary retinoblastoma compared with mothers in the population in general (P = .006, one sided). Similarly, fathers 50 years of age or older had a relative risk of 5.0 to have a child with sporadic hereditary retinoblastoma compared with fathers in the population in general (P = .04, one sided). No parental age effect was found in children with nonhereditary retinoblastoma. We conclude that a high paternal and a high maternal age are significant risk factors for sporadic hereditary retinoblastoma.


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INCIDENCE OF WILM'S TUMOR INCREASED WITH PATERNAL AGING


Br J Cancer. 1993 Apr;67(4):813-8. Links
Wilms' tumour and parental age: a report from the National Wilms' Tumour Study.Olson JM, Breslow NE, Beckwith JB.
Department of Biostatistics, University of Washington, Seattle 98195.

Age distributions of parents at birth of patients registered in the National Wilms' Tumour Study were compared to those of the general population. An increasing incidence of sporadic Wilms' tumour with increasing paternal age was found, with a relative risk of 2.1 of tumour in children of fathers over 55 compared to children of fathers younger than 20. A similar effect for maternal age was found, with a relative risk of 1.4 in children of mothers over 40 compared to children of mothers younger than 20. The maternal age effect was much weaker among patients registered later in the study; in the later, more completely ascertained cohort, paternal age appears to be the major contributor to the parental age effect. Little difference in paternal age distribution was found between patients with bilateral and unilateral tumour and between male and female patients. In contrast, patients with reported associated congenital anomalies, patients with evidence of nephrogenic rests, and patients with early or late age-of-onset of tumour had parents who were, on average, substantially older than the remainder. These findings lend support to the idea that many Wilms' tumours result from new germline mutations. Further, the histologic composition of such tumours may be sufficiently distinct as to provide a valuable diagnostic indicator of the etiology of these tumours.

PMID: 8385980 [PubMed - indexed for MEDLINE]





Epidemiol. 1999 Apr;13(2):138-43. Links
Comment in:
Paediatr Perinat Epidemiol. 2000 Jul;14(3):283-5.
The influence of parental age on the risk of Wilms' tumour.Sharpe CR, Franco EL, de Camargo B, Lopes LF, Barreto J, Johnsson R, Mauad M.
Department of Epidemiology & Biostatistics, McGill University, Montreal, Canada.

The Brazilian Wilms' Tumour Study Group carried out a hospital-based multicentre case-control study of potential risk factors for the disease between April 1987 and January 1989. The parents of 109 cases of Wilms' tumour (WT) were interviewed when they were admitted to hospital for diagnosis and treatment. Also interviewed were the parents of two controls per case, matched for age, sex and interviewer, who were admitted to the same or nearby hospitals for treatment of non-neoplastic conditions. Odds ratios adjusted for family income and parental education were calculated by conditional logistic regression. Among cases diagnosed before 25 months of age there was a marked gradient of increasing risk of WT with increasing maternal age at the time of the child's birth. There was no increased risk for cases diagnosed after 25 months of age. The effects of paternal age were less marked. Possible explanations for these are discussed.