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F H Gilles

Publications and source records attributed to F H Gilles.

At least 37 records · Page 2Linked to original sources
PubMed1995

The applicability of Collins' Law to childhood brain tumors and its usefulness as a predictor of survival.

In 1955, Collins made the observation that tumor recurrence in children with Wilms' tumor was correlated with the child's age plus 9 months. This concept of a period of risk for recurrence was later applied to a variety of tumors in children and became known as Collins' Law (CL). The law has been a successful predictor of survival for some children with neural tumors within the central nervous system and a poor predictor for others. We tested Collins' concept of a period of risk for recurrence and extended it to survival for 14 childhood neural tumors described in the Childhood Brain Tumor Consortium (CBTC) database. The CBTC data describe clinical, surgical, and histological details (over a 49-year period in 10 institutions) from 3921 patients under the age of 21 years at the time of their first surgical procedure for a brain tumor. CL was considered to be a good predictor of survival if fewer than 10% of patients who die survive beyond the expiration of the period of risk for that child. We found that CL applied to tumors such as anaplastic astrocytoma, glioblastoma, pineoblastoma, medulloblastoma or "primitive neuroectodermal tumor," teratoma, and germinoma, as well as ependymoma, papilloma, and tumors that could not be classified; it had no predictive value in craniopharyngioma, oligodendroglioma, or plain, fibrillary, pilocytic, or protoplasmic astrocytoma. We had sufficient follow-up data to determine adherence to CL when the child's age at diagnosis was less than 8 years; it is likely that CL applies to older children with these tumors, but we did not have the data to show this unequivocally.

Adolescent↗
PubMed1995

Age-related changes in diagnoses, histological features, and survival in children with brain tumors: 1930-1979. The Childhood Brain Tumor Consortium.

In the Childhood Brain Tumor Consortium database, the proportions of older children (> or = 11 yr) with pilocytic astrocytomas, fibrillary astrocytomas, and ependymomas significantly increased (P < 0.05) over the 50 years (1930-1979) of the study. The increased proportions of pilocytic astrocytomas occurred whether the tumors were located in the supratentorial or infratentorial compartments. The increases in fibrillary astrocytomas and ependymomas were found only within the supratentorial tumor location. Some histological features found in pilocytic astrocytomas (e.g., Rosenthal fibers, granular bodies, and very low cell density) were more likely to be found in older children. Other histological features were also more likely to be found in older children (e.g., parenchymal calcification, intertwined fascicles, intermediate and large-size nuclei, pleomorphic, elongated, or irregular nuclei, prominent nucleoli, multinucleated cells, thick hyaline blood vessels, hemosiderin, and parenchymal and perivascular lymphocytes). The probability of 5-year survival for young children with supratentorial ependymomas remained at approximately 0.4 in contrast to that for young children with infratentorial ependymomas, for whom it improved, but without significant linear trend. The probability of 5-year survival for both younger and older children with primitive neuroectodermal tumors (medulloblastomas) improved, but without significant linear trend. The changes in the proportions of childhood brain tumors and histological features occurred without similar changes in the proportions of older and younger children in the cities involved between 1930 and 1979. These changes were so distinctive as to raise the possibility of significant shifts in environmental exposures in younger and older children over the 50 years of this study.

Adolescent↗
PubMed1994

The role of family history in risk of childhood brain tumors.

BACKGROUND: Although brain tumors are the second most frequent malignancy in children, relatively little is known about the role of family history in risk of these tumors. METHODS: Children under the age of 18 years (n = 361) in whom primary brain tumors were diagnosed were identified from eight United States population-based Surveillance, Epidemiology, and End Results registries and compared to matched controls (n = 1083) identified by random-digit dialing. Information regarding family history of birth defects or tumors was obtained, along with data on other potential risk factors, from interviews with the mothers and fathers of the index children. RESULTS: No significant differences were found in family history of epilepsy. However, moderate elevations in risk were observed for a history of birth defects in maternal relatives, particularly for female propositi. Significantly more mothers (odds ratio [OR] = 1.63, 95% confidence limits [CL] = 1.03, 2.57) and maternal female relatives (OR = 2.15, 95% CL = 1.14, 4.06) of cases than of controls were reported to have had birth defects. History of birth defects in maternal relatives was particularly associated with childhood brain tumors of "other" (not astrocytoma or medulloblastoma) histologic type (OR = 2.37, 95% CL = 1.25, 4.53) and infratentorial tumors (OR = 1.76, 95% CL = 1.06, 2.93). Slight excesses of tumors were observed in paternal relatives of children with astrocytomas (OR = 1.43, 95% CL 0.93, 2.20) or with infratentorial tumors (OR = 1.46, 95% CL 0.97, 2.20). Risk of childhood brain tumors did not increase with the number of relatives affected with brain tumors, breast cancer, leukemia or lymphoma, soft tissue sarcomas, or all of these tumor types combined (the Li-Fraumeni syndrome). CONCLUSIONS: These findings suggest a modest increase in risk of childhood brain tumors associated with maternal family history of birth defects. Family history of tumors does not appear to contribute appreciably to an increased risk of brain tumors in children.

Adolescent↗
PubMed1994

Subacute sclerosing panencephalitis in an infant: diagnostic role of viral genome analysis.

Subacute sclerosing panencephalitis (SSPE) is related to "defective" measles virus or vaccination, though an association with parainfluenza viruses has been reported. SSPE is characterized by a slow, erratic course and elevated cerebrospinal fluid measles titers. An immunocompetent, vaccinated infant, with onset of symptoms in parainfluenza virus season and a catastrophic course is described. Cerebrospinal fluid titers were negative, but postmortem brain had typical SSPE lesions. Patient brain-derived RNA, subjected to reverse transcription followed by polymerase chain reaction yielded polymerase chain reaction products with measles virus but not parainfluenza virus genes. The sequenced fragment revealed multiple mutations, typical for SSPE. SSPE can thus present in infants, with short latency and no cerebrospinal fluid antibodies. Viral genomic analysis may be diagnostic, permitting early therapy.

Antigens, Viral↗
PubMed1994

Histologic feature reliability in childhood neural tumors. Childhood Brain Tumor Consortium.

We studied intraobserver reproducibility in recognizing the presence or absence of 57 histologic feature or patterns in a random subset of tumors (822) from the Childhood Brain Tumor Consortium database. The study protocol maximized consistency of the observer. We found that only six histologic features had high (> or = 0.75) reliability estimates while a large number had intermediate estimates of 0.50-0.74. Supratentorial or infratentorial tumor location sometimes altered reliability. Reliability estimates were unacceptable for certain histologic features often used as diagnostic criteria, descriptors of tumor characteristics, or markers of anaplasia. We hypothesize that low reliability reflects, in part, the need for more specific operational definitions, particularly those with subjective boundaries (e.g. granular bodies) may also contribute to low reliability. We also show that the kappa statistic, a commonly used measure of reliability, is inappropriate for very common or uncommon histologic features (e.g. features at the extremes of prevalence in the study cases) and we offer a simple empiric method for determining when an alternative measure, the Jaccard statistic, is appropriate.

Brain Neoplasms↗
PubMed1993

Parental smoking and risk of childhood brain tumors.

Data from a large, population-based, case-control study were analyzed to assess the role of parental smoking in childhood brain tumors. Parents of 361 cases, newly diagnosed between January 1, 1977 and December 31, 1981 and ascertained from eight Surveillance, Epidemiology, and End Results (SEER) program registries, and 1,083 controls had been interviewed. No significant differences in risks were found to be associated with maternal or paternal smoking at any time (odds ratio (OR) = 0.92 for mothers and 1.06 for fathers), during the year of birth of the child (which included both the prenatal and postnatal periods) (ORs = 0.84 for < 1 pack/day and 1.0 for > or = 1 pack/day for mothers, and 0.68 for < 1 pack/day and 1.07 for > or = 1 pack/day for fathers), or 2 years before the child was born, i.e., the pre-conception period (ORs = 0.75 for < 1 pack/day and 1.01 for > or = 1 pack/day for mothers, and 0.90 for < 1 pack/day and 1.15 for > or = 1 pack/day for fathers). Mothers were also specifically asked if they smoked during the pregnancy, and no association was found compared with never smokers (OR = 1.08, 95% confidence interval (CI) 0.80-1.45) or for ever-smokers who continued to smoke during pregnancy compared with those who stopped smoking during pregnancy (OR = 1.15, 95% CI 0.75-1.78). Finally, no significant increase in risk of brain tumors was found for the child's passive exposure to parental smoking during the period from birth to diagnosis of the brain tumor in the case. The lack of an effect of parental smoking was observed for both the major histologic types and locations of brain tumors. These findings and those from earlier studies provide no support for the hypothesis that parental cigarette smoking influences the risk of brain tumors in children.

Adult↗
PubMed1992

Childhood brain tumors that occupy more than one compartment at presentation. Multiple compartment tumors.

Children whose brain tumor involves two or more compartments at presentation differ clinically and pathologically from children whose brain tumor is confined to one compartment. In this study of 3,291 children with a brain tumor, at least 10% had a tumor that occupied two or three compartments at first hospitalization. Infratentorial tumors occupying multiple compartments were 1.7 times more likely to involve the cervicomedullary junction than the mesodiencephalic junction. Younger children (1-3 years) were more likely to have had multiple compartment tumors than older children. Children whose tumor was limited to the infratentorial compartment had a longer survival than children whose tumor also occupied other compartments. Ependymoma, anaplastic ependymoma, and astrocytoma (nos) were over represented among infratentorial multiple compartment tumors. Pilocytic astrocytoma, primitive neuroectodermal tumor (medulloblastoma), and desmoplastic medulloblastoma were less likely to have occupied multiple compartments at the time of the first surgical exploration. The distributions of histologic features in tumors at the cervicomedullary junction differed from those in tumors limited to the posterior fossa or to the spinal canal. Seizures were more likely if the tumor was confined to the supratentorial compartment, whereas nausea or vomiting and headache were more likely if the tumor was confined to the infratentorial compartment. Children whose tumor was confined to the spinal canal were significantly more likely to have bladder symptoms and back and/or abdominal pain than those whose tumor also involved compartments above the foramen magnum. We conclude that brain tumors apparently confined to one compartment at presentation are biologically and structurally different from tumors evident in two or more compartments.

Adolescent↗
PubMed1992

Epidemiology of seizures in children with brain tumors. The Childhood Brain Tumor Consortium.

We examined potential clinical and pathologic correlates of seizures among the 3,291 children in the Childhood Brain Tumor Consortium database. Fourteen percent had seizures prior to their hospitalization for a brain tumor. Among children who had a supratentorial tumor, seizures occurred in 22% of those less than 14 years of age. The prevalence of seizures increased to 68% of older teenagers. Among children with an infratentorial tumor, the prevalence of seizures was relatively constant at 6% over all age groups. The onset of seizures began more than one year prior to surgical tumor removal in over half of the children aged five or more with supratentorial tumors, significantly longer than for those of the same age with infratentorial tumors. Almost all children (98.9%) with an infratentorial tumor and seizures had at least one other symptom and more than three-fourths of them had at least three. Eighty-nine percent of children with a supratentorial tumor and seizures had at least one other symptom and more than one-half had at least three symptoms. Regardless of whether the tumor was above or below the tentorium, confusion or stupor and coma were more common in children with seizures than in children without seizures. Among children with supratentorial tumors, symptoms of a declining academic performance or an abnormality of personality, speech, walking, or sensation were significantly more frequent in children with seizures, while visual symptoms (other than visual loss or diplopia) and nausea or vomiting were less frequent. Among children with supratentorial tumors, those who had seizures were more likely to have paralysis of an arm, hand, or face, confusion or stupor, or coma and less likely to exhibit irritability, papilledema, optic atrophy, decreased visual acuity, pupillary abnormalities, or abducens paresis. Among children with infratentorial tumors, those with seizures were significantly less likely to have truncal ataxia, but more likely to experience confusion, stupor, or coma. In the supratentorial compartment, astrocytoma (nos), protoplasmic astrocytoma, anaplastic astrocytoma, and ependymoma were more frequently associated with seizures than was craniopharyngioma. No infratentorial tumor type was more or less likely to be associated with seizures. All common tumor types that were represented in both the supratentorial and the infratentorial compartment except astrocytoma (nos) were associated with significantly greater rates of seizures when located in the supratentorial compartment. The tumor location with the highest incidence of seizures was, as expected, the superficial cerebrum. More than 40% of the children with such tumors had seizures.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1992

Temporal trends among childhood brain tumor biopsies. The Childhood Brain Tumor Consortium.

We sought temporal trends in the demographic, clinical, histologic feature, diagnostic class, and quality of life data over the interval 1930-1979 in the Childhood Brain Tumor Consortium database. The proportion of children younger than eight years old declined from 72% to 55% and the proportion of those older than ten more than doubled from 12% to 27%. The relative frequency of tumors in the supratentorial compartment increased significantly, while infratentorial tumors decreased. We found significant declines in supratentorial ependymomas and pilocytic astrocytomas. Similarly, some infratentorial tumors, especially ependymomas, decreased and brain stem tumors increased. Infratentorial medulloblastoma (primitive neuroectodermal tumor) increased significantly. Some individual histologic features which are markers of anaplasia increased in frequency in both supratentorial and infratentorial tumors. There was a significant increase in biopsies that contained nonneoplastic neural tissue in addition to tumor for both compartments and among supratentorial tumors there was a marked increase in the proportion of cases containing an indistinct neural tissue boundary. The probability of postoperative death declined, but the probability of survival five or ten years after surgery did not improve significantly for children who had tumors in either compartment. Among children who survived five years after the initial craniotomy, the proportion who had significant long term deficits increased. Most of this increase occurred in the last decade (1970-79). In this decade, the proportion of children for whom no deficits were reported five years following operation was 4% if they had a supratentorial tumor and 27% if they had an infratentorial tumor. The proportions of children alive five years following first surgery who had arachnoidal metastases increased significantly for infratentorial tumors.

Adolescent↗
PubMed1992

Cytogenetic analysis of 39 pediatric central nervous system tumors.

Consistent cytogenetic abnormalities have been described in many pediatric solid tumors, including Ewing's sarcoma, Wilms' tumor, and neuroblastoma. Similar analysis of pediatric central nervous system (CNS) tumors has been hampered by technical problems. We report chromosome results from 39 pediatric CNS tumors. Abnormalities of chromosome 17 were noted in 3 of 11 primitive neuroectodermal tumors (including i(17q) in 2 tumors), confirming data observed by other investigators. Cells from 2 of 11 primitive neuroectodermal tumors (PNET) exhibited loss or structural abnormalities involving chromosome 11. Loss or distal deletion of chromosome 7q was noted in cells from two PNETs. Because other investigators have shown loss of heterozygosity on 17p in about one-third of PNET, we propose that chromosome regions 7q and 11 are areas worthy of further study in pediatric PNET. Numerical abnormalities were noted in 6 of 21 astrocytomas. Hyperdiploidy was demonstrated in 1 of 4 pilocytic astrocytomas and pseudopolyploidy was demonstrated in 4 of 13 anaplastic astrocytomas. Structural chromosome abnormalities (translocations, deletions) were noted in 4 of 13 anaplastic astrocytomas. Complex structural anomalies were observed in one craniopharyngioma. A rhabdoid tumor of the brain exhibited multiple complex structural rearrangements but did not exhibit the monosomy 22 observed in some rhabdoid tumors. Hypodiploidy and loss of chromosome 22 were noted in a clinically aggressive meningioma, corroborating observations by other investigators.

Astrocytoma↗
PubMed1991

Delayed central nervous system myelination in the sudden infant death syndrome.

This study was designed to assess whether development of the central nervous system (CNS) is delayed in victims of the sudden infant death syndrome (SIDS). We selected the parameter of myelination because it is a continuously changing and readily accessible marker of CNS development in the SIDS age-range. We assessed myelination blindly in 61 SIDS and 89 autopsy controls. In 62 sites the degree of myelination was visually graded in myelin-stained histological sections on an ordinal scale of 0-4 using the inferior cerebellar peduncle as an internal standard of degree 3. Cases were stratified by postconceptional age at death and SIDS and controls were compared with respect to myelin degree at each site. Significantly delayed myelination (p less than 0.05) occurred in the SIDS group in 25 of the 62 sites examined. Hypomyelination affected fiber systems in which myelination is initiated before or after birth and which myelinate with different tempos and preferentially affect pyramidal and cerebellar (somatomotor) and prefrontal-temporal-limbic (visceromotor) systems. Hypomyelination was not associated with individual clinicopathologic variables in the SIDS group. Somatic growth and brain weight were significantly greater in SIDS than controls. Therefore, we suggest that SIDS is associated with a developmental CNS disorder. Although delayed CNS myelination most likely shares a common antecedent with sudden death and is not its cause, the role of somato- and viscero-motor systems in central cardiorespiratory control and arousal warrants further analysis in SIDS.

Birth Weight↗
PubMed1991

Co-expression of four intermediate filament subclasses in childhood glial neoplasms.

Immunohistochemical analysis of intermediate filament (IF) proteins was performed on frozen sections of 16 childhood glial tumors using a library of 10 antigen-specific IF protein directed monoclonal antibodies (MoABs) and a four-step biotin-streptavidin-alkaline phosphatase conjugated antigen detection immunocytochemical technique. Human glial fibrillary acidic protein (GFAP) and vimentin were expressed in all brain tumors. High molecular weight (200 kDa) neurofilament (NF-H) protein was expressed in 15 out of 16 tumors; medium molecular weight (160 kDa) neurofilament (NF-M) in seven out of 16 tumors; and low molecular weight (68 kDa) neurofilament (NF-L) in five out of 16. Positive acidic keratin reactivity was found in five out of 16 tumors using MoAB AE1. Expression of a keratin pair was detected with MoAB AE2 in five out of 16 tumors. A second keratin pair in 14 out of 16 glial tumors was demonstrated with MoAB AE3. Immunostaining with AE5 defined the expression of another basic keratin (64 kDa) in nine out of 16 glial tumors. Finally, in 14 out of 16 astrocytomas an individual 51 kDa acidic keratin (detected with MoAB AE8) was expressed. Glial tumor cells contain cell lineage specific and nonspecific IF proteins in the following IF pattern: AE3+, AE8+, GFAP+, vimentin+, and NF-H+. The heterogenous composition of these cytoskeletal IF proteins in childhood glial tumors may reflect a direct stage dependent correlation with their neoplastic transformation.

Adolescent↗
PubMed1990

Childhood brain tumor: presentation at younger age is associated with a family tumor history.

In a registry-based sample of 361 children with a brain tumor, those whose grandparents and great-grandparents had a history of any kind of tumor were younger at the time of presentation than were those who lacked this family history (p = 0.1). In post hoc analyses, the age difference was most apparent among children with cerebral tumors, and when family history was limited to brain tumors and to great-grandparents. These findings are in keeping with the hypothesis that a familial tumor diathesis contributes to an early age at onset of a brain tumor in some children.

Age Factors↗
PubMed1989

Spinal cord central echo complex: histoanatomic correlation.

Real-time sonography consistently demonstrates an echo complex centrally located in the spinal cord. This echogenic focus is currently attributed to the central canal. The authors sought the source of this central echo with ultrasound (US) and histoanatomic study of both fresh and fixed cadaver spinal cords. Correlative transverse sections of the spinal cord were stained with hematoxylin-eosin and Luxol fast blue for cells and myelin and with Holzer stain for glial fibrils. The central echo complex is produced by the interface between the myelinated ventral white commissure and the central end of the anterior median fissure. Variations in the shape of the central complex seem to reflect varying degrees of flaring of the central end of the anterior median fissure. The inconstant residual central canal and islands of residual ependymal cells are clearly not the source of the central echo complex.

Adolescent↗
PubMed1989

CSF production in acute ventriculitis.

Clinically, there appears to be a significant reduction in cerebrospinal fluid (CSF) formation during acute ventriculitis--an observation that has not been well documented by experimental studies. To examine this phenomenon, an inoculum of Escherichia coli was injected into the lateral ventricles of New Zealand White rabbits. Approximately 18 hours later, the survivors (64%) underwent a 3-hour ventriculocisternal perfusion of carbon-14-dextran (MW 7 X 10(4)) as a reference marker for CSF formation. On the average, CSF formation in this experimental group was reduced by one-half to two-thirds of normal, confirming the clinical observation. Histologically, the stroma of the choroid plexus was the site of an extensive inflammatory infiltrate. Meningitis, ependymitis, and focal encephalitis completed the picture. Vasculitis was not present in the choroid plexus. The epithelium of the choroid plexus underwent patchy cellular swelling or frank necrosis and destruction. It is postulated that the changes in the choroid plexus caused by the inflammatory process were responsible for the diminished CSF formation in this acute setting. Reduced choroidal blood flow and/or enterotoxin may play a role in these alterations.

Acute Disease↗
PubMed1988

Sequence of central nervous system myelination in human infancy. II. Patterns of myelination in autopsied infants.

The timing and synchronization of postnatal myelination in the human central nervous system (CNS) are complex. We found eight time-related patterns of CNS myelination during the first two postnatal years in autopsied infants. The intensity of myelination was graded in 162 infants with diverse diseases on an ordinal scale of degrees 0-4. The Ayer method for maximum likelihood estimates for censored data was utilized to generate curves of the temporal changes in the percent of infants with degrees 0 through 4 of myelin in 62 white matter sites. These sites fall into eight subgroups determined by the presence or absence of microscopic myelin (degree 1) at birth and the median age at which mature myelin (degree 3) is reached. There is variability in the timing of myelination within and across axonal systems, and early onset of myelination is not always followed by early myelin maturation. We reexamined general rules governing the timing of myelination proposed by previous investigators, and found that those rules are neither complete nor inviolate, and that there is a complex interplay among them. This study specifies distinct periods of maturation in which myelinating pathways are potentially vulnerable to insult during the first two postnatal years.

Brain↗
PubMed1987

Sequence of central nervous system myelination in human infancy. I. An autopsy study of myelination.

This study establishes the sequence of myelination in a population of autopsied infants from birth through the second postnatal year. Myelination was assessed in 62 precisely defined central nervous system (CNS) sites of 162 infants with diverse diseases who were autopsied from 1972 to 1984 at Children's Hospital, Boston. The degree of myelination was graded on an ordinal scale of 0-4 using the inferior cerebellar peduncle as an internal standard. This grading system is a modification of that used for fetal myelination in the National Collaborative Perinatal Project (NCPP). The data are summarized by, median degree of myelination for each age group and site; and Ayer estimates for the age at which at least 10, 50, and 90% of infants reach a particular myelin degree in each site. "Marker" sites in the cerebrum are provided for the pathologist to compare myelination between an individual infant brain and the brains from our autopsy population. These data should be useful in identifying diverse peri- and postnatal conditions affecting myelination in human infancy. They also provide guidelines for the assessment of CNS myelination by sophisticated imaging techniques in living infants.

Autopsy↗