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Abramson Cancer CenterNCI CANCERLIT® Search: Diagnosis-Histopathology-Pathogenesis of Brain Tumor - August 2002
National Cancer Institute®
Last Modified: August 1, 2002
- Gamma knife radiosurgery for neuroepithelial tumors: radiological and histological changes.
- Choroid plexus carcinoma.
- Genetic signature of oligoastrocytomas correlates with tumor location and denotes distinct molecular subsets.
- Tumours around the foramen of Monro: clinical and neuroimaging features and their differential diagnosis.
- Expression and distribution of id helix-loop-helix proteins in human astrocytic tumors.
- Gangliogliomas: an intriguing tumor entity associated with focal epilepsies.
- Intracranial germ cell tumors: a retrospective study of 44 children.
- Relation of childhood brain tumors to exposure of parents and children to tobacco smoke: the SEARCH international case-control study.
- Hypermethylation of HIC-1 and 17p allelic loss in medulloblastoma.
- A novel low-penetrance locus for familial glioma at 15q23-q26.3.
- Calbindin-d(28k): a marker of recurrence for medulloblastomas.
- Comparative genomic hybridization in glioma: a meta-analysis of 509 cases.
- Increased mortality from brain tumors: a combined outcome of diagnostic technology and change of attitude toward the elderly.
- Re: "Increased mortality from brain tumors: a combined outcome of diagnostic technology and change of attitude toward the elderly".
- Childhood brain tumor occurrence in relation to residential power line configurations, electric heating sources, and electric appliance use.
- Invited commentary: evolution of epidemiologic evidence on magnetic fields and childhood cancers.
- Identification of gliomas by morphological and immunocytochemical analysis in cell cultures.
- Medulloblastomas and primitive neuroectodermal tumors rarely contain polyomavirus DNA sequences.
- Prognostic significance of an apoptotic index and apoptosis/proliferation ratio for patients with high-grade astrocytomas.
- Mutations in SUFU predispose to medulloblastoma.
- Fetal pericallosal lipoma: US and MR findings.
- Comprehensive analysis of genomic alterations in gliosarcoma and its two tissue components.
- Primary brain lymphoma: a report of eight cases from a medical center in southern Taiwan.
- The completeness of brain tumour registration in Devon and Cornwall.
- Molecular evidence of apoptotic death in malignant brain tumors including glioblastoma multiforme: upregulation of calpain and
- Correlation between CT scan and automated perimetry in supratentorial tumors.
- Guest editorial: the conception of FDG-PET imaging.
- Palmar erythema: cutaneous marker of neoplasms.
- Measurement and analysis of the chemotherapy-induced genetic instability in pediatric cancer patients.
- Colloid cysts of the third ventricle: some comments.
- Atypical teratoid/rhabdoid tumor of the central nervous system: report on workshop.
- Macrophage/microglial cell subpopulations in glioblastoma multiforme relapses are differentially altered by radiochemotherapy.
- Optimizing brain tumor resection. Low-field interventional MR imaging.
- Optimizing brain tumor resection. Midfield interventional MR imaging.
- Optimizing brain tumor resection. High-field interventional MR imaging.
- Neuronavigation in interventional MR imaging. Frameless stereotaxy.
- Neuronavigation in interventional MR imaging. Prospective stereotaxy.
- Minimally invasive procedures. Interventional MR image-guided neurobiopsy.
- Thermal therapies in interventional MR imaging. Laser.
- Predicting major depression in brain tumor patients.
- [Tumor pathology]
- Relationship between thallium-201 kinetics and proliferative activity assessed by monoclonal antibody MIB-1 in brain tumours.
- Metabolic imaging of low-grade gliomas with three-dimensional magnetic resonance spectroscopy.
- Intracranial lipomas in neonate.
- [Genetic and epidemiologic aspects of brain tumors in children and adolescents]
- Molecular markers of prognosis in astrocytic tumors.
- High-resolution genome-wide allelotype analysis identifies loss of chromosome 14q as a recurrent genetic alteration in astrocytic tumours.
- Primary sarcomas of the brain and spinal cord: a study of 18 cases.
Table of Contents
1
UI - 11837537
AU - Uematsu Y; Fujita K; Tanaka Y; Shimizu M; Oobayashi S; Itakura T; Kubo K
TI -
Gamma knife radiosurgery for neuroepithelial tumors: radiological and
histological changes.
SO - Neuropathology 2001 Dec;21(4):298-306
AD - Department of Neurological Surgery, Wakayama Medical University,
Wakayama City, Japan. yujiue@wakayama-med.ac.jp
Gamma knife radiosurgery (RS) has been introduced as a modern therapy
for brain tumors. However, the effects of RS for neuroepithelial tumors
are still obscure. The present study investigates the radiological and
histological changes after RS to elucidate the biological effect. There
were seven cases (two males and five females), ranging from 4 to 71
years with a mean age of 33 years. Two cases were located in the
brainstem, another two in the cerebellum, and one each in the thalamus,
the hypothalamus, and the frontal lobe. Histologically, two cases had
gangliogliomas, four astrocytomas (1 pilocytic, 1 fibrillary, 2
anaplastic), and one glioblastoma. RS was performed after surgery with a
central dose of 30-36 Gy. All cases were evaluated radiologically on MRI
before and after RS. Four cases (3 astrocytomas and 1 glioblastoma)
which neurologically deteriorated after RS were reoperated. These cases
were examined using HE and immunohistochemical studies with antibodies
of CD34, alpha-smooth muscle actin (SMA), p53, p21 and MIB-1 on the
sections before and after RS. MRI demonstrated perifocal edema and
intratumoral hypointensity on T2 weighted imaging (T2WI), suggesting
radionecrosis in most of the cases within 6 months after RS. In the
central part of the RS, destructive changes were observed in the tumor
cells and endothelial cells: decrease in the tumor cell population,
coagulation necrosis, and fibrinoid degeneration of vascular walls were
revealed. In the peripheral part, however, some tumors contained viable
tumor cells intermingled with blood vessels showing endothelial and
pericytic proliferations. The increase of MIB-1 staining index was found
in only one case. The p21 immunoreactivity was increased in endothelial
cells, although the p53 immunoreactivity was unchanged. These results
suggested that radionecrosis occurred earlier and more frequently in
neuroepithelial tumors after RS than after conventional radiation.
2
UI - 12116091
AU - Moss L; Saran F; English MW
TI -
Choroid plexus carcinoma.
SO - Med Pediatr Oncol 2002 Jul;39(1):75
3
UI - 12107116
AU - Mueller W; Hartmann C; Hoffmann A; Lanksch W; Kiwit J; Tonn J; Veelken
TI -
J; Schramm J; Weller M; Wiestler OD; Louis DN; von Deimling A
Genetic signature of oligoastrocytomas correlates with tumor location
and denotes distinct molecular subsets.
SO - Am J Pathol 2002 Jul;161(1):313-9
AD - Department of Neuropathology, Charite, Humboldt University, Berlin,
Germany.
Oligoastrocytomas are heterogeneous tumors that have molecular features
that overlap with either oligodendrogliomas or astrocytomas. Differences
in the frequency of chromosomal losses of 1p and 19q in
oligodendrogliomas are related to tumor location, with a low rate of
allelic loss in tumors of the temporal and a high rate in tumors of the
frontal, parietal, and occipital lobes. To test the possibility of
regional molecular heterogeneity in oligoastrocytoma, we examined a
series of 203 gliomas including 68 oligoastrocytomas and two control
groups of 73 oligodendrogliomas and 62 astrocytomas for allelic losses
of chromosomal arms 1p and 19q, and TP53 mutations, and compared these
data with tumor localization. Common molecular alterations were found in
oligodendrogliomas and oligoastrocytomas arising in extratemporal sites.
In respect to the molecular parameters analyzed, temporal
oligoastrocytomas were either indistinguishable from astrocytoma or
similar to temporal oligodendrogliomas. Oligodendroglial neoplasms can
thus be separated into three molecular subsets, two of which include
lesions with the morphological features of oligodendrogliomas and
oligoastrocytomas and one resembling temporal oligoastrocytoma.
Molecular subclassification thus unifies previous findings about
prognosis, behavior, response to therapy, genotype, and location in
oligodendroglial tumors.
4
UI - 11922700
AU - Nishio S; Morioka T; Suzuki S; Fukui M
TI -
Tumours around the foramen of Monro: clinical and neuroimaging features
and their differential diagnosis.
SO - J Clin Neurosci 2002 Mar;9(2):137-41
AD - Department of Neurosurgery, Kyushu University Hospital, Fukuoka, Japan.
shunji@ns.med.kyushu-u.ac.jp
The clinical and neuroimaging features of 20 patients with lateral
ventricular tumours located around the foramen of Monro were reviewed
retrospectively with special emphasis on the differential diagnoses.
Histologic types were: eight neurocytomas, four subependymal giant cell
astrocytomas (SGCAs), three subependymomas, two fibrillary astrocytomas,
and one each of pilocytic astrocytoma, malignant astrocytoma and
malignant teratoma. The mean age of the patients with neurocytoma was
29.6 years, with SGCA 13.3 years and with subependymoma 55.3 years. All
tumours appeared nodular in shape, and on computed tomography (CT)
neurocytomas were either isodense or highdense with the brain, while all
subependymomas and SGCAs were lowdense. Calcification was observed in
two SGCAs, and one neurocytoma. Five neurocytomas and all four SGCAs
showed mild to moderate contrast enhancement, while all three
subependymomas showed either no, or scarce, enhancement. Magnetic
resonance imaging (MRI) studies were available in 10 patients, with the
signal characteristics of four neurocytomas and three SGCAs being
nonspecific, while two subependymomas were both hypointense on
T1-weighted images and hyperintense on T2-weighted images. Thus
important features for differential diagnosis included age of the
patient and density on precontrast CT. In this series, either an
extensive excision of the tumour or a partial removal, thus relieving
the obstruction of the foramina of Monro, usually provided long term
survival, with 18 patients surviving a mean of 10.8 years. Copyright
2002, Elsevier Science Ltd. All rights reserved.
5
UI - 12007145
AU - Vandeputte DA; Troost D; Leenstra S; Ijlst-Keizers H; Ramkema M; Bosch
TI -
DA; Baas F; Das NK; Aronica E
Expression and distribution of id helix-loop-helix proteins in human
astrocytic tumors.
SO - Glia 2002 Jun;38(4):329-38
AD - Department of (Neuro)Pathology, Academic Medical Center, University of
Amsterdam, Amsterdam, The Netherlands.
The Id family of helix-loop-helix proteins is involved in a variety of
processes, such as development, proliferation, and angiogenesis. In this
study, we investigated the expression pattern of Id1, Id2, and Id3 in
surgical specimens of human glial tumors. Western blot analysis
demonstrated that all three Id proteins were expressed in astrocytic
tumors. Expression levels in high-grade tumors were higher than in
low-grade tumors. Immunohistochemical analysis confirmed that many of
the tumor astrocytes exhibited strong Id1-3 IR. In contrast, in adult
human normal brain, Id expression was low both in resting astrocytes and
in endothelial cells. In tumor cells, Id proteins displayed cytoplasmic
as well as nuclear localization. Id1-3 IR scores in tumor cells were
positively correlated with proliferation indices. Moreover, Id1-3 IR was
detected in endothelial cells of the astrocytic tumor blood vessels. The
vascular Id1-3 expression correlated positively with tumor vascularity
and grade. These results support the role of the Id gene family in the
enhanced proliferative potential of tumor astrocytes. The evidence also
supports the involvement of the Id gene family in tumor angiogenesis, a
process that critically influences the malignant behavior of glial
tumors. Copyright 2002 Wiley-Liss, Inc.
6
UI - 12125736
AU - Blumcke I; Wiestler OD
TI -
Gangliogliomas: an intriguing tumor entity associated with focal
epilepsies.
SO - J Neuropathol Exp Neurol 2002 Jul;61(7):575-84
AD - Department of Neuropathology, University of Erlangen, Germany.
Gangliogliomas represent the most frequent tumor entity in young
patients suffering from chronic focal epilepsies. In a series of 326
gangliogliomas collected from the University of Bonn Epilepsy Surgery
Program and other departments of neuropathology in Germany, Austria, and
Switzerland, epidemiological findings and histopathological hallmarks of
gangliogliomas are systematically reviewed. The majority of these tumors
occur within the temporal lobe and reveal a biphasic histological
architecture characterized by a combination of dysplastic neurons and
neoplastic glial cell elements. However, gangliogliomas exhibit a
considerable variability in their histopathological appearance.
Immunohistochemical studies are an important tool to discriminate these
neoplasms from other tumor entities. Almost 80% of gangliogliomas reveal
immunoreactivity for CD34, a stem cell epitope not expressed in normal
brain. Immunohistochemical reactions for MAP2 or NeuN can be employed to
characterize the dysplastic nature of neurons in those areas difficult
to discriminate from pre-existing brain parenchyma. Less than 50% of the
cases display binucleated neurons. With the frequent finding of
"satellite" tumor clusters in adjacent brain regions, gangliogliomas are
microscopically less circumscribed than previously assumed. The
distinction from diffusely infiltrating gliomas is of considerable
importance since tumor recurrence or malignant progression are rare
events in gangliogliomas. Only little is known about the molecular
pathogenesis of these glioneuronal tumors. Our findings support a
dysontogenic origin from a glioneuronal precursor lesion with
neoplastic, clonal proliferation of the glial cell population. Candidate
genes appear to associate with neurodevelopmental signaling cascades
rather than cell cycle control or DNA repair mechanisms. The reelin
signaling and tuberin/insulin growth receptor pathways have recently
been implicated in ganglioglioma development. Powerful new molecular
genetic and biological tools can now be employed to unravel the
pathogenesis of these intriguing lesions.
7
UI - 12057797
AU - Jaing TH; Wang HS; Hung IJ; Tseng CK; Yang CP; Hung PC; Lui TN
TI -
Intracranial germ cell tumors: a retrospective study of 44 children.
SO - Pediatr Neurol 2002 May;26(5):369-73
AD - Division of Hematology, Chang Gung Children's Hospital, Taoyuan, Taiwan.
This 16-year retrospective study review sought to determine the factors
influencing prognosis and treatment results of all patients with primary
intracranial germ cell tumors treated at our hospital who were younger
than 17 years of age at the time of diagnosis. A total of 44 patients
were treated during the study period, including 32 males and 12 females
with a male:female ratio of 2.67:1. The median age at diagnosis was 12
years and 5 months of age (range = 2-16 years). The 44 intracranial germ
cell tumors consisted of 27 pure germinomas (61.4%) and 17
nongerminomatous germ cell tumors, including 10 mixed germ cell tumors
(22.7%), three yolk sac tumors (7.8%), two immature teratomas (4.5%),
and two choriocarcinomas (4.5%). Univariate analysis of prognostic
factors using Kaplan-Meier survival estimates revealed that only
histologic tumor type was correlated with outcome (P < 0.005). The
projected 5-year overall survival and event-free survival rate of
patients with germinomas vs those with intracranial germ cell tumors
were 92.6%, 92.6% vs 47.3%, and 42.1%, respectively. Our analysis
suggests that radiation involving the spinal axis has limited usefulness
in patients with intracranial germ cell tumor, although better results
have been obtained for germinomas using radiotherapy in this study.
8
UI - 12115571
AU - Filippini G; Maisonneuve P; McCredie M; Peris-Bonet R; Modan B;
TI -
Preston-Martin S; Mueller BA; Holly EA; Cordier S; Choi NW; Little J;
Arslan A; Boyle P
Relation of childhood brain tumors to exposure of parents and children
to tobacco smoke: the SEARCH international case-control study.
Surveillance of Environmental Aspects Related to Cancer in Humans.
SO - Int J Cancer 2002 Jul 10;100(2):206-13
AD - Neuroepidemiology Research Unit, Istituto Nazionale Neurologico C Besta,
Milan, Italy. gfilippini@istituto-besta.it
The etiology of childhood brain tumors (CBTs) remains unknown. Tobacco
smoke contains several known carcinogens and can induce DNA adducts in
human placenta and hemoglobin adducts in fetuses. We present the results
of an international case-control study to evaluate the association
between CBTs and exposure of parents and children to cigarette smoke.
The study was undertaken as part of the SEARCH program of the IARC. Nine
centers in 7 countries were involved. The studies mainly covered the
1980s and early 1990s. Cases (1,218, ages 0-19 years) were children
newly diagnosed with a primary brain tumor; there were 2,223
population-based controls. Most mothers who agreed to participate were
interviewed in person at home. Odds ratios (ORs) were calculated by
unconditional logistic regression, adjusted for age, sex and center, for
all types of CBT combined, 4 CBT histotypes, 5 age groups and each
center. There was no association between the risk of brain tumors in the
child and parental smoking prior to pregnancy, maternal smoking or
regular exposure to others' cigarette smoke during pregnancy at home or
at work, or passive smoking by the child during the first year of life.
These results did not change considering the child's age at diagnosis,
the histologic type of tumor or center. Copyright 2002 Wiley-Liss, Inc.
9
UI - 12097291
AU - Rood BR; Zhang H; Weitman DM; Cogen PH
TI -
Hypermethylation of HIC-1 and 17p allelic loss in medulloblastoma.
SO - Cancer Res 2002 Jul 1;62(13):3794-7
AD - Department of Pediatric Hematology/Oncology, Children's Research
Institute, Children's National Medical Center, Washington, DC. 20010,
USA.
Medulloblastoma is the most common malignant brain tumor in
children.Chromosome arm 17p13.3 is reduced to homozygosity in 35-50% of
medulloblastomas,making it the most frequent genetic alteration in these
tumors. HIC-1 (hypermethylated in cancer) is a putative tumor suppressor
gene located in the area of common deletion. HIC-1 resides in a CpG
island and is hypermethylated in many different tumor types. Therefore,
we studied a series of tumor specimens for hypermethylation and deletion
of the region containing the HIC-1 gene to determine whether these two
mechanisms of gene inactivation play a complimentary role in
medulloblastoma. Southern blotting was performed using the
methylation-sensitive restriction endonuclease NotI. Methylation of NotI
restriction sites located in HIC-1 was demonstrated in 26 (72%) of 36
tumors and 11 (92%) of 12 specimens of normal brain. Of these 26 tumors,
23 differed significantly from normal brain. A greater proportion of the
cells from the tumors showed methylated alleles of the HIC-1 gene. A
group of 15 (42%) of 36 tumors exhibited loss of heterozygosity (LOH)
for DNA sequences located on chromosome arm 17p. There was no
significant correlation between LOH and methylation status (P = 0.19).
Methylation in tumors beyond that seen in normal brain predicted poor
overall survival independent of clinical risk category (P = 0.014). The
results of our study show that methylation of the CpG island that
contains the HIC-1 gene is common in medulloblastoma and, together with
LOH of 17p, may be a critical event in the formation and aggressiveness
of this tumor.
10
UI - 12097292
AU - Paunu N; Lahermo P; Onkamo P; Ollikainen V; Rantala I; Helen P; Simola
TI -
KO; Kere J; Haapasalo H
A novel low-penetrance locus for familial glioma at 15q23-q26.3.
SO - Cancer Res 2002 Jul 1;62(13):3798-802
AD - Department of Pathology, Tampere University Hospital, FIN-33521 Tampere,
Finland. niina.paunu@uta.fi
Epidemiological studies and case reports suggest that familial
clustering of gliomas may occur in families that do not fit any known
tumor syndromes. In the present study, 15 familial glioma pedigrees from
a limited geographical area were hypothesized to carry the same
low-penetrance susceptibility allele. We used a two-stage strategy for
disease gene mapping. A genome scan in four glioma families revealed
four interesting loci at chromosome arms 1q, 6q, 8p, and 15q. Additional
markers in these regions provided evidence of significant linkage to
15q23-q26.3 with a maximum nonparametric linkage score of 3.35 with
marker D15S130. Investigation of all 15 glioma families by association
analysis (haplotype pattern mining) and through use of the
transmission/disequilibrium test gave further evidence of significant
association/transmission distortion at the same 15q locus (P = 0.02 and
P = 0.03, respectively). No evidence of involvement of known tumor
syndromes was obtained from the data provided by the linkage analysis or
hospital records. Thus, the first genome-wide linkage analysis of
familial glioma suggests a novel susceptibility locus at 15q23-q26.3.
11
UI - 12124842
AU - Pelc K; Vincent S; Ruchoux MM; Kiss R; Pochet R; Sariban E; Decaestecker
TI -
C; Heizmann CW
Calbindin-d(28k): a marker of recurrence for medulloblastomas.
SO - Cancer 2002 Jul 15;95(2):410-9
AD - Department of Pediatrics, Hopital des Enfants, Brussels, Belgium.
BACKGROUND: The expression of the Ca(2+)-binding protein
calbindin-D(28k) was analyzed in medulloblastomas in relation to
clinical features and other biologic markers related to cell
proliferation, differentiation, p53, and cerebellar developmental
regulated gene expression. METHODS: Immunohistochemistry was carried out
on histologic slides from a first retrospective series of 29
nonmetastatic and 10 metastatic medulloblastoma formalin-fixed,
paraffin-embedded tissues, using specific antibodies against
calbindin-D(28k), calretinin, alpha-parvalbumin and beta-parvalbumin,
and S100 proteins. Informed consent was obtained from the subjects
and/or guardians. Other biologic markers for differentiation, cell
proliferation, the expression of the p53 tumor suppressor gene protein,
and cerebellar developmental regulated genes were similarly
investigated. A second series of 16 medulloblastomas from young patients
(younger than 15 years) was added in order to validate the results
obtained in the first series. RESULTS: Of all the markers investigated,
only calbindin-D(28k) was significantly associated with prognosis.
Survival and remission (i.e. recurrence free) time analysis performed on
all the cases (n = 55) confirmed a high risk of death (P = 0.004) and
recurrence (P = 0.003) associated with calbindin-positivity. As
calbindin-positivity was predominantly observed in tumors from young
patients, the authors confirmed its prognostic value in the subgroup of
patients younger than 15 years (n = 37). Cox regression analysis showed
a significant and independent prognostic value for calbindin expression
and, to a lesser extent, the type of surgery (total or subtotal). Three
risk groups were thus identified, distinguishing among the cases
characterized by a total resection and calbindin-negativity (good
prognosis), by a subtotal resection and calbindin-negativity
(intermediary), and by calbindin-positivity (bad prognosis).
CONCLUSIONS: The current study suggests that calbindin-positive
medulloblastomas represent a subclass of aggressive tumors more
frequently seen in younger patients. Copyright 2002 American Cancer
Society.DOI 10.1002/cncr.10666
12
UI - 12127399
AU - Koschny R; Koschny T; Froster UG; Krupp W; Zuber MA
TI -
Comparative genomic hybridization in glioma: a meta-analysis of 509
cases.
SO - Cancer Genet Cytogenet 2002 Jun;135(2):147-59
AD - Institute of Human Genetics, University of Leipzig,
Philipp-Rosenthal-Strasse 55, 04103 Leipzig, Germany.
Much data about genetic imbalances in tumors have been accumulated by
comparative genomic hybridization (CGH). In order to distinguish between
significantly and coincidentally involved regions in glioma by means of
a meta-analysis, we summarized and analyzed the CGH results of 509 cases
published in 26 reports between 1992 and 2001. The expansion of all
aberrations to the 850-band level impressively visualized distinct
patterns in astrocytoma, oligodendroglioma, and ependymoma as well as
loci of frequent aberrations. For example, in astrocytoma the frequency
of gains culminated at 7p12, 8q24.1, and 12q13-q15 (the loci of EGF-R,
C-MYC and CDK4, respectively) and losses at 9p21 (the locus of p15 and
p16) and 10q23.3 where PTEN resides. Most chromosomes were variably
prone to copy number changes at different scales of aberrations. At the
whole chromosome level the analysis showed +7, -10 in astrocytoma and
+9, +18 in ependymoma, but +20q, -9p in astrocytoma and +1q, -22q in
ependymoma at the p-q arm level. Furthermore, we could confirm the
correlation between the average number of copy alterations per patient
(average number of copy alterations [ANCA] index) and malignancy for
astrocytoma in a refined graduation as well as for oligodendroglioma. As
a new parameter, the average number of affected GTG-bands per patient
(average number of affected GTG bands [ANAG] index) showed an even more
striking correlation with the World Health Organization grade for gains
and losses.
13
UI - 1510081
AU - Modan B; Wagener DK; Feldman JJ; Rosenberg HM; Feinleib M
TI -
Increased mortality from brain tumors: a combined outcome of diagnostic
technology and change of attitude toward the elderly.
SO - Am J Epidemiol 1992 Jun 15;135(12):1349-57
AD - National Center for Health Statistics, Centers for Disease Control,
Hyattsville, MD 20782.
United States national data were used to assess factors responsible for
the increase of brain tumor mortality. Between 1968 and 1988, death
rates increased 50% among those aged 65-74 years, 200% among those aged
75-84 years, and 800% in the oldest old. Rate of increase and maximum
death rate have changed over time. Death rate among the population aged
65-74 years peaked in the mid-1980s, while among those aged 85 years and
older it is projected to continue increasing throughout the 1990s. The
patterns of rate increases were almost identical in the two sexes, as
well as among whites and nonwhites. There was a strong correlation over
time of death rates with head diagnostic procedures (r = 0.96) and with
the pace of computerized axial tomography installation (r = 0.91). The
authors conclude that the reported increase in brain tumor mortality is
not genuine, but represents a combination of three factors: availability
of more sophisticated, noninvasive diagnostic technology; change in the
attitude toward care of the elderly; and introduction of support
programs such as Medicare that facilitate diagnostic procedures in the
elderly.
14
UI - 7998596
AU - Polednak AP
TI -
Re: "Increased mortality from brain tumors: a combined outcome of
diagnostic technology and change of attitude toward the elderly".
SO - Am J Epidemiol 1994 Dec 15;140(12):1138-43
15
UI - 8546112
AU - Gurney JG; Mueller BA; Davis S; Schwartz SM; Stevens RG; Kopecky KJ
TI -
Childhood brain tumor occurrence in relation to residential power line
configurations, electric heating sources, and electric appliance use.
SO - Am J Epidemiol 1996 Jan 15;143(2):120-8
AD - Fred Hutchinson Cancer Research Center, Division of Public Health
Sciences, Seattle, WA, USA.
To assess the relation between childhood brain tumor occurrence and
exposure to potential sources of residential magnetic fields, a
population-based case-control study of incident brain tumors was
conducted in the Seattle, Washington, area at the Fred Hutchinson Cancer
Research Center from 1989 to 1994 among children younger than age 20
years who were diagnosed from 1984 to 1990. The specific aims were to
evaluate whether proximity to high-current residential power lines, as
defined by the Wertheimer-Leeper code, or use of electric appliances or
electric heating sources by the mother while pregnant or by the child
before diagnosis were associated with increased risks of brain tumor
occurrence. The mothers of 133 cases and 270 controls (recruited by
random digit dialing) participated. Risk of brain tumor occurrence did
not increase with increasing exposure, as indicated by the five-level
Wertheimer-Leeper code. When exposure was dichotomized as high versus
low, the odds ratio was 0.9 (95% confidence interval 0.5-1.5) and did
not vary significantly by sex, age, or histology. No elevations in risk
were found for ever versus never use of electric blankets, water beds,
or electric heating sources. Odds ratios were slightly elevated for nine
appliances and were at or below 1.0 for eight others. These data do not
support the hypothesis that exposure to magnetic fields from
high-current power lines, electric heating sources, or electric
appliances is associated with the subsequent occurrence of brain tumors
in children.
16
UI - 8546113
AU - Poole C
TI -
Invited commentary: evolution of epidemiologic evidence on magnetic
fields and childhood cancers.
SO - Am J Epidemiol 1996 Jan 15;143(2):129-32; discussion 133-6
AD - Department of Epidemiology and Biostatistics, Boston University School
of Public Health, MA, USA.
17
UI - 12122877
AU - Fazekas I; Kerekes E; Hegedus B; Nyary I
TI -
Identification of gliomas by morphological and immunocytochemical
analysis in cell cultures.
SO - Ideggyogy Sz 2002 May 20;55(5-6):173-9
AD - National Institute of Neurosurgery, Budapest.
INTRODUCTION: The morphology and immunocytochemical properties of 250
different monolayer cultures derived from various human brain tumor
specimens were investigated on purpose to support and complement the
neuropathological diagnosis. In this study analyses of 124 glioma cases
are presented. METHODS: The tumor samples were mechanically dissociated
and seeded on glass coverslips. After the formation of the monolayer
cultures were fixed and stained by May-Grunwald-Giemsa method for the
morphological examination. Semi-quantitative immunocytochemical labeling
included several different types of mono- and polyclonal primary
antibodies using avidin-biotin visualization system. In nine cases of
the glioblastomas the sufficient proliferation made possible to
establish cell lines from the primary cultures. RESULTS: The glial
origin of the tumors was identified in 124 cases based upon the presence
of glial fibrillary acidic protein. A negative correlation between the
intensity of glial fibrillary acidic protein immunostaining and the
grade of tumor malignancy was found. During long-term cultivation of the
higher grade gliomas the incidence and intensity of glial fibrillary
acidic protein labeled cells was decreasing. Both the vimentin and the
neuron specific enolase labeling were in general stronger than the glial
fibrillary acidic protein and almost all the cells were stained. The
incidence of Ki-67 positive cells increased with the grade of
malignancy. Concerning the tumor classification our immunocytochemical
results correlated with the routine histopathological examination.
CONCLUSIONS: On the basis of these results we conclude that monolayer
cultures obtained from tumor specimens can support and complement the
correct diagnosis of the various human brain tumors.
18
UI - 12084346
AU - Kim JY; Koralnik IJ; LeFave M; Segal RA; Pfister LA; Pomeroy SL
TI -
Medulloblastomas and primitive neuroectodermal tumors rarely contain
polyomavirus DNA sequences.
SO - Neuro-oncol 2002 Jul;4(3):165-70
AD - Division of Neuroscience, Department of Neurology, Children's Hospital,
Harvard Medical School, 300 Longwood Avenue, Boston, MA 02115, USA.
To address the hypothesis that medulloblastoma or supratentorial
primitive neuroectodermal tumor (sPNET) can arise through infection by
polyomaviruses, we examined genomic DNA isolated from 15 primary
medulloblastoma and 5 sPNET biopsy specimens and from 2 medulloblastoma
cell lines for the presence of DNA sequences from the polyomaviruses
simian virus 40 (SV40), JC virus, and BK virus. These polyomaviruses
have oncogenic potential in animals, and their DNA sequences have been
detected in other surveys of various solid tumors, including childhood
brain tumors. The tumor DNA samples were analyzed by Southern blot
hybridization of polymerase chain reaction products that employed probes
designed to detect specific polyomavirus sequences. Neither JC virus nor
BK virus DNA sequences were detected in any of the specimens. None of
the primary medulloblastoma or sPNET specimens contained SV40 sequences.
However, SV40 DNA coding and noncoding sequences were detected in the
D283-Med (medulloblastoma) cell line. Immunocytochemical studies of
D283-Med revealed nuclear expression of SV40 large T antigen. In
contrast to childhood ependymomas and choroid plexus tumors,
medulloblastomas and sPNETs infrequently express evidence of
polyomavirus infection.
19
UI - 12084348
AU - Kuriyama H; Lamborn KR; O'Fallon JR; Iturria N; Sebo T; Schaefer PL;
TI -
Scheithauer BW; Buckner JC; Kuriyama N; Jenkins RB; Israel MA
Prognostic significance of an apoptotic index and
apoptosis/proliferation ratio for patients with high-grade astrocytomas.
SO - Neuro-oncol 2002 Jul;4(3):179-86
AD - The Preuss Laboratory for Molecular Neuro-Oncology, Brain Tumor Research
Center, University of California-San Francisco, San Francisco, CA 94143,
USA.
We evaluated the association of spontaneous apoptosis and an
apoptosis/proliferation index with survival to determine the potential
of such measures to serve as predictive markers for patients with
glioblastoma multiforme (GBM). We examined the extent of spontaneous
apoptosis in tumors from newly diagnosed patients, 75 with GBM and 21
with anaplastic astrocytoma, who were entered on treatment protocols of
the North Central Cancer Treatment Group. In the group of GBM patients,
those with a higher apoptotic index tended to live longer ( P = 0.04;
Cox proportional hazards model including performance score, age, and
extent of resection in a multivariate model). We found that the
apoptotic index values for anaplastic astrocytoma patients tended to be
lower than those in the GBM patients, although with small sample sizes,
the result was not statistically significant ( P = 0.1). We also
examined expression of the Ki-67 cell proliferation antigen
immunohistochemically using the MIB-1 monoclonal antibody. Ki-67
expression did not provide additional information regarding the survival
of patients with GBM. In this group of GBM patients, those patients with
higher apoptotic index/proliferation ratios had a better prognosis than
did those with a low ratio ( P < 0.021, same model as above). These
findings suggest that both apoptosis and a cell death/cell proliferation
ratio are associated with patient survival, and they may be useful for
either the clinical evaluation of patients with GBM or the
stratification of patients for treatment evaluation.
20
UI - 12068298
AU - Taylor MD; Liu L; Raffel C; Hui CC; Mainprize TG; Zhang X; Agatep R;
TI -
Chiappa S; Gao L; Lowrance A; Hao A; Goldstein AM; Stavrou T; Scherer
SW; Dura WT; Wainwright B; Squire JA; Rutka JT; Hogg D
Mutations in SUFU predispose to medulloblastoma.
SO - Nat Genet 2002 Jul;31(3):306-10
AD - Division of Neurosurgery, The Arthur and Sonia Labatt Brain Tumour
Research Centre, Toronto, Canada.
The sonic hedgehog (SHH) signaling pathway directs the embryonic
development of diverse organisms and is disrupted in a variety of
malignancies. Pathway activation is triggered by binding of hedgehog
proteins to the multipass Patched-1 (PTCH) receptor, which in the
absence of hedgehog suppresses the activity of the seven-pass membrane
protein Smoothened (SMOH). De-repression of SMOH culminates in the
activation of one or more of the GLI transcription factors that regulate
the transcription of downstream targets. Individuals with germline
mutations of the SHH receptor gene PTCH are at high risk of
developmental anomalies and of basal-cell carcinomas, medulloblastomas
and other cancers (a pattern consistent with nevoid basal-cell carcinoma
syndrome, NBCCS). In keeping with the role of PTCH as a tumor-suppressor
gene, somatic mutations of this gene occur in sporadic basal-cell
carcinomas and medulloblastomas. We report here that a subset of
children with medulloblastoma carry germline and somatic mutations in
SUFU (encoding the human suppressor of fused) of the SHH pathway,
accompanied by loss of heterozygosity of the wildtype allele. Several of
these mutations encode truncated proteins that are unable to export the
GLI transcription factor from nucleus to cytoplasm, resulting in the
activation of SHH signaling. SUFU is a newly identified tumor-suppressor
gene that predisposes individuals to medulloblastoma by modulating the
SHH signaling pathway through a newly identified mechanism.
21
UI - 12087206
AU - Kim TH; Joh JH; Kim MY; Kim YM; Han KS
TI -
Fetal pericallosal lipoma: US and MR findings.
SO - Korean J Radiol 2002 Apr-Jun;3(2):140-3
AD - Department of Radiology, Sejong Heart Institute, Sejong General
Hospital, Pucheon, Kyunggido, Korea. fetalus@naver.com
We report a case of fetal pericallosal lipoma occurring at the anterior
interhemispheric fissure and associated with agenesis of the corpus
callosum. During targeted prenatal ultrasonography at 26 weeks'
gestation, the lesion was seen as a highly echogenic mass. MR imaging
performed at 35 weeks' gestation and during the postnatal period
revealed a pericallosal fatty mass and agenesis of the corpus callosum.
22
UI - 12112531
AU - Actor B; Cobbers JM; Buschges R; Wolter M; Knobbe CB; Reifenberger G;
TI -
Weber RG
Comprehensive analysis of genomic alterations in gliosarcoma and its two
tissue components.
SO - Genes Chromosomes Cancer 2002 Aug;34(4):416-27
AD - Abteilung Molekulare Genetik, Deutsches Krebsforschungszentrum,
Heidelberg, Germany.
Gliosarcoma is a variant of glioblastoma multiforme characterized by two
components displaying gliomatous or sarcomatous differentiation. We
investigated 38 gliosarcomas for aberrations of tumor-suppressor genes
and proto-oncogenes that are commonly altered in glioblastomas.
Amplification of CDK4, MDM2, EGFR, and PDGFRA were found in 11% (4/35),
8% (3/38), 8% (3/38), and 3% (1/35) of the tumors, respectively. Nine of
38 gliosarcomas (24%) carried TP53 mutations. PTEN mutations were
identified in 45% (9/20) of the investigated tumors. Twenty gliosarcomas
were analyzed by comparative genomic hybridization (CGH). Chromosomal
imbalances commonly detected were gains on chromosomes 7 (15/20; 75%), X
(4/20; 20%), 9q, and 20q (3/20, 15% each); and losses on chromosomes 10
and 9p (7/20, 35% each), and 13q (3/20, 15%). Five different high-level
amplifications were mapped to 4q12-q21 (1 case), 6p21 (1 case), 7p12 (2
cases), proximal 12q (4 cases), and 14q32 (1 case) by CGH. Southern blot
and/or differential PCR analyses identified amplification of PDGFRA
(4q12), CCND3 (6p21), EGFR (7p12), CDK4 (12q14) and/or MDM2
(12q14.3-q15), and AKT1 (14q32.3) in the respective tumors. Separate
analysis of the gliomatous and sarcomatous components of eight
gliosarcomas by CGH after microdissection and universal DNA
amplification revealed that both components shared 57% of the
chromosomal imbalances detected. Taken together, our data indicate that
the genomic changes in gliosarcomas closely resemble those found in
glioblastomas. However, the number of chromosomes involved in imbalances
in gliosarcomas was significantly lower than that in glioblastomas,
indicating a higher genomic stability in gliosarcomas. In addition, we
provide further support for the hypothesis that the gliomatous and
sarcomatous components are derived from a single precursor cell clone,
which progressed into subclones with distinct morphological features
during tumor evolution. According to our data, gain/amplification of
genes on proximal 12q may facilitate the development of a sarcomatous
phenotype. Copyright 2002 Wiley-Liss, Inc.
23
UI - 12135196
AU - Chuang SS; Lee PS; Lin CN; Tsai TC; Chio CC; Que J; Huang CT
TI -
Primary brain lymphoma: a report of eight cases from a medical center in
southern Taiwan.
SO - Zhonghua Yi Xue Za Zhi (Taipei) 2002 Apr;65(4):172-9
AD - Department of Pathology, Chi-Mei Medical Center, Tainan, Taiwan, ROC.
BACKGROUND: Primary brain lymphoma (PBL) in Taiwan has been reported
only in three series with very limited immunophenotypic
characterization. METHODS: We retrospectively studied PBL cases with
history review, immunohistochemistry, and in situ hybridization (ISH)
for Epstein-Barr virus-encoded mRNA (EBER) from a single institution in
southern Taiwan during 1989-2000. RESULTS: We found eight cases of PBL
including four males and four females with mean age of 64.1 years and
median of 63.0. The major presenting symptoms were headache, poor
memory, slurred speech, and hemiplegia in three patients each. All
patients had stage I solitary tumor. Half of the patients received tumor
excision, the other half, stereotactic biopsy. Seven cases were of
diffuse large B-cell type (DLBL), with expression of bcl-2 in six cases.
They were all negative for CD5, CD10, bcl-6, and EBER. The eighth
patient had anaplastic large cell lymphoma (ALCL) of T-cell phenotype
with expression of cytotoxic markers and was positive for EBER. Two were
lost to follow up. The median follow-up time for the remaining six was
11.2 months (range, 5.5 - 25.0). They all received radiotherapy with
initial complete remission. Two died of the disease, another of
cardiopulmonary failure, and the other of stroke or recurrence. The
remaining two were free of disease for 9.6 and 25.0 months after
radiotherapy alone. The 1-year survival rate was 60%. CONCLUSIONS: We
have fully characterized eight cases of PBL, including seven DLBLs and
one ALCL, in southern Taiwan that occurred in an older age group. Old
age, immunophenotype (bcl-2-positivity and bcl-6-negativity), and lack
of systemic chemotherapy were probably responsible for the shorter
survival as compared to other studies. Radiotherapy seems to be
effective for inducing complete remission and even long-term survival in
some patients, however, systemic chemotherapy should be administered to
prevent recurrence and to achieve long-term survival.
24
UI - 11855573
AU - Pobereskin LH
TI -
The completeness of brain tumour registration in Devon and Cornwall.
SO - Eur J Epidemiol 2001;17(5):413-6
AD - Department of Neurosurgery, Derriford Hospital, Plymouth, UK.
louis.pobereskin@phnt.swest.nhs.uk
OBJECTIVES: To determine ascertainment rates for primary brain tumours
and examine factors influencing those rates. DESIGN: Comparison of a
clinical database with official figures from the Regional Cancer
Intelligence Unit. RESULTS: Of 1480 potential cases 52% appeared in the
registry. Only two-thirds of patients operated upon were registered and
less than one-third of those who were not operated appeared in the
registry. Independent predictors of registration were having had an
operation, 5.47 (4.19-7.17) (odds ratio (95% CI)), being over 60 years
of age, 1.62 (1.26-2.07), and having a tumour requiring radiotherapy,
2.52 (1.74-3.66). CONCLUSIONS: There is asymmetric registration of
primary brain tumours in Devon and Cornwall with under registration of
more benign tumours in younger patients. If similar problems exist
across the United Kingdom, this could have a negative influence on
survival rates, and international comparisons of such rates should be
performed with caution.
25
UI - 12111801
AU - Ray SK; Patel SJ; Welsh CT; Wilford GG; Hogan EL; Banik NL
TI -
Molecular evidence of apoptotic death in malignant brain tumors
including glioblastoma multiforme: upregulation of calpain and
caspase-3.
SO - J Neurosci Res 2002 Jul 15;69(2):197-206
AD - Department of Neurology, Medical University of South Carolina,
Charleston, South Carolina 29425, USA.
Cell death in the core of human brain tumors is triggered by hypoxia and
lack of nutrients, but the mode of cell death whether necrosis or
apoptosis is not clearly defined. To identify the role of apoptosis in
brain tumor cell death, we investigated macromolecular (RNA and protein)
synthesis and activity in the central to peripheral region of benign
[desmoplastic infantile ganglioglioma (DIG) and transitional meningioma
(TMG)] and malignant [ependymoma (END), anaplastic astrocytoma (APA),
and glioblastoma multiforme (GBM)] brain tumors derived from five
patients who had not received previously radiotherapy or chemotherapy.
Normal brain tissue (NBT) served as control. RT-PCR analysis of tumor
tissues covering central to peripheral regions detected mRNA
overexpression of pro-apoptotic gene bax in malignant tumors, indicating
a commitment to apoptosis. The mRNA expression of calpain (a
Ca(2+)-dependent cysteine protease) and calpastatin (endogenous calpain
inhibitor) was altered resulting in an elevated calpain/calpastatin
ratio. Calpain content and activity were increased, suggesting a role
for calpain in cell death. In the mitochondria-dependent death pathway,
caspase-9 and caspase-3 were also overexpressed in tumors. The increased
caspase-3 activity cleaved poly(ADP-ribose) polymerase (PARP). Agarose
gel electrophoresis detected a mixture of random and internucleosomal
DNA fragmentation in malignant brain tumors. Overexpression of
pro-apoptotic bax, upregulation of calpain and caspase-3, and occurrence
of internucleosomal DNA fragmentation are now presented indicating that
one mechanism of cell death in malignant brain tumors is apoptosis, and
that enhancement of this process therapeutically may promote decreased
tumor growth. Copyright 2002 Wiley-Liss, Inc.
26
UI - 12134179
AU - Sood S; Sharma NK; Nada M; Dutt A; Nagpal RC
TI -
Correlation between CT scan and automated perimetry in supratentorial
tumors.
SO - Neurol India 2002 Jun;50(2):158-61
AD - Department of Ophthalmology, Pt. B.D. Sharma Postgraduate Institute of
Medical Sciences, Rohtak, 124001, India.
An attempt was made to correlate various types of visual field defects
on automated perimetry with the findings of computed tomography in 44
patients of supratentorial tumors. All the patients above the age of 10
years were subjected to complete neurological examination including
investigations like plain X-rays and CT scan, however, MRI and
angiography were performed wherever indicated. Ocular examination
particularly pertaining to neuro-ophthalmological profile was carried
out with special emphasis on automated perimetry on Humphrey field
analyser. The results indicated that automated perimetry was capable of
reliably detecting and quantitating the visual field defects and thus
established the location of the tumor in 72% patients when compared to
CT scan. Hence, any patient with neuro-ophthalmic features should be
subjected to automated perimetry for early diagnosis and probable
location of intracranial space occupying lesion affecting visual
pathways.
27
UI - 11839067
AU - Alavi A; Reivich M
TI -
Guest editorial: the conception of FDG-PET imaging.
SO - Semin Nucl Med 2002 Jan;32(1):2-5
28
UI - 12037449
AU - Noble JP; Boisnic S; Branchet-Gumila MC; Poisson M
TI -
Palmar erythema: cutaneous marker of neoplasms.
SO - Dermatology 2002;204(3):209-13
AD - Consultation de Medecine, Hopital Pitie-Salpetriere, Paris, France.
BACKGROUND: Acral erythema on the palms is observed in several
conditions. However, the relationship with malignant tumors has only
been reported exceptionally. It should be noted that tumors produce
angiogenic mediators. OBJECTIVE: These mediators might promote palmar
erythema (PE), and the aim of the present study was to investigate the
vasodilation of palmar skin capillaries and angiogenesis, mainly with
tumors of the central nervous system. METHODS: In a prospective study of
107 patients affected by brain tumors, we assessed PE clinically and the
rate of dilated vessels histologically. We also evaluated the mean
surface of the lumen of capillaries on skin biopsies and brain tumors.
RESULTS: 6.5% of the patients had an important erythema and 18.5% had
slight and/or localized PE. In the skin biopsies, the rate of dilated
vessels and the mean surface of the lumen of capillaries were higher
than in normal skin. Moreover, the intensity of palmar redness was
related to the increase in these vascular changes in the
histopathological slices of brain tumors. The intensity also depended on
the type of tumor and on its growth. CONCLUSION: The results of the
present study strongly suggest that acral erythema is associated with
malignant tumors and that the intensity of erythema and the vascular
changes of brain tumors are related, probably due to angiogenic factors.
Copyright 2002 S. Karger AG, Basel
29
UI - 11880547
AU - Lopez de Mesa R; Lopez de Cerain Salsamendi A; Ariznabarreta LS;
TI -
Abinzano MJ; Patino-Garcia A
Measurement and analysis of the chemotherapy-induced genetic instability
in pediatric cancer patients.
SO - Mutagenesis 2002 Mar;17(2):171-5
AD - Laboratory and Department of Pediatrics, University of Navarra, E-31080
Pamplona, Spain.
Bleomycin sensitivity has been proven to be a useful biomarker for
environmental carcinogenesis and tumor genetic instability. We have
previously reported a significant increase in the chromosomal
aberrations induced by chemotherapy regimens. This study aimed to test
whether there is an inherent increased genetic instability in cancer
patients at diagnosis, to determine the increase and time course of the
chemotherapy-induced instability and to test whether bleomycin
sensitivity can be used as a predictor of tumor evolution or relapse.
The analysis included 99 pediatric cancer patients with four different
tumor types (Ewing's sarcoma, osteosarcoma, lymphoma and CNS tumors) and
25 controls. Blood samples (n = 171) were obtained before and at the end
of treatment, during clinical remission and at relapse and bleomycin
tests on lymphocyte cultures were performed. We detected a significant
increase (P = 0.004) in mutagen sensitivity in patients at the end of
treatment compared with untreated patients, regardless of the tumor
type. In both the longitudinal and cross-sectional analyses maximal and
similar values of mutagen sensitivity were found in patients during
treatment (1.84 +/- 0.82) and at relapse (1.78 +/- 0.52); minimum and
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