Table of Contents
1
UI - 11770927
AU - Smith MM; Strottmann JM
TI -
Imaging of the optic nerve and visual pathways.
SO - Semin Ultrasound CT MR 2001 Dec;22(6):473-87
AD - Department of Radiology, Medical College of Wisconsin, Milwaukee 53226,
USA. mmsmith@mcw.edu
The visual pathway extends from the globes anteriorly to the occipital
cortex posteriorly. A wide variety of disease processes may produce
visual dysfunction. Because the optic nerve is a fiber tract of the
brain covered by meninges, it can be affected by many of the same
pathologic processes that occur in the brain and meninges. Physical
examination and diagnostic tests of visual function performed by the
clinician can frequently identify the anatomic location of the causative
lesion in the patient with vision loss. This enables the radiologist to
optimize the imaging evaluation of the patient. This article reviews the
normal anatomy of the optic nerve and visual pathways, presents computed
tomography (CT) and magnetic resonance (MR) imaging techniques for
evaluation of these structures, and discusses the pathologic processes
intrinsic to the optic nerve and visual pathways.
2
UI - 11792751
AU - Plath T; Peters M; Detjen K; Welzel M; von Marschall Z; Radke C;
TI -
Wiedenmann B; Rosewicz S
Overexpression of pRB in human pancreatic carcinoma cells: function in
chemotherapy-induced apoptosis.
SO - J Natl Cancer Inst 2002 Jan 16;94(2):129-42
AD - T. Plath, M. Peters, K. Detjen, M. Welzel, Z. von Marschall, B.
Wiedenmann, S. Rosewicz (Department of Hepatology and Gastroenterology),
C. Radke (Department of Pathology), Charite, Campus Virchow-Klinikum,
Humboldt-University, Berlin, Germany.
BACKGROUND: Human pancreatic adenocarcinomas are highly resistant to
chemotherapy. The p16 tumor-suppressor protein is inactivated in more
than 90% of human pancreatic cancers. The p16 protein transcriptionally
inhibits expression of retinoblastoma tumor-suppressor gene pRB. The pRB
protein transcriptionally inhibits expression of the p16 gene. Because
pRB normally prevents apoptosis, we investigated whether pRB is involved
in resistance to chemotherapy-induced apoptosis in pancreatic cancer
cells. METHODS: pRB expression was examined by immunohistochemistry in
106 human pancreatic tissue specimens. The human pancreatic tumor cell
line Capan-1 (pRB+/p16-) was stably transfected with p16 to functionally
inactivate pRB. pRB gene expression was examined by western and northern
blot analyses, and pRB function was assessed by electrophoretic mobility
shift assays and promoter transactivation studies for the transcription
factor E2F. Changes in cell sensitivity to chemotherapy were measured by
assays for cytotoxicity and apoptosis. RESULTS: pRB was overexpressed in
pancreatic ductal adenocarcinomas but was hardly detectable in other
pancreatic malignancies, chronic pancreatitis, or nontransformed human
pancreatic tissue. Expression of p16 in Capan-1 cells resulted in the
loss of pRB gene and protein expression concomitant with increased
activity of the transcription factor E2F, which was not detected in
wild-type or control-transfected Capan-1 cells. Wild-type and
control-transfected Capan-1 cells were resistant to chemotherapy-induced
apoptosis, but pRB-depleted (i.e., p16-transfected) Capan-1 cells were
highly sensitive. The effect was specific to pRB depletion because two
other human pancreatic cancer cell lines that retained high pRB
expression after p16 transfection were resistant to chemotherapy-induced
apoptosis. CONCLUSIONS: Overexpression of pRB is associated with human
pancreatic duct-cell cancer and may allow pancreatic cancer cells to
evade chemotherapy-induced apoptosis.
3
UI - 11642725
AU - Cavallotti I; De Luca L; D'Aponte A; De Falco M; Acanfora F; Visciano
TI -
ML; Gualdiero L; De Luca B; Baldi A; De Luca A
Expression of the retinoblastoma-related p107 and Rb2/p130 genes in
human placenta: an immunohistochemical study.
SO - Histol Histopathol 2001 Oct;16(4):1057-60
AD - Institute of Topographical Anatomy, School of Medicine, Second
University of Naples, Italy.
It has been proposed that tumor suppressor genes may have a role in the
mechanisms of proliferation and differentiation during human placental
development. The Retinoblastoma gene family is a well known family of
tumor suppressor genes. Many studies have pointed out a role of this
family not only in cell cycle progression, but also during development
and differentiation. On the light of these observations we have
investigated the immunohistochemical expression pattern of the
Retinoblastoma family members, p107 and Rb2/p130 in human placenta
samples in first trimester and full-term placental sections. p107 and
pRb2/p130 showed the most abundant expression levels during the first
trimester of gestation and progressively declined to being barely
detectable in the placenta by late gestation. These results indicate
that the expression of the above genes is modulated during placental
development and suggest a mechanism for controlling trophoblast
proliferation.
4
UI - 11719516
AU - Strobeck MW; Reisman DN; Gunawardena RW; Betz BL; Angus SP; Knudsen KE;
TI -
Kowalik TF; Weissman BE; Knudsen ES
Compensation of BRG-1 function by Brm: insight into the role of the core
SWI-SNF subunits in retinoblastoma tumor suppressor signaling.
SO - J Biol Chem 2002 Feb 15;277(7):4782-9
AD - Department of Cell Biology, University of Cincinnati College of
Medicine, Vontz Center for Molecular Studies, Cincinnati, Ohio
45267-0521, USA.
The BRG-1 subunit of the SWI-SNF complex is involved in chromatin
remodeling and has been implicated in the action of the retinoblastoma
tumor suppressor (RB). Given the importance of BRG-1 in RB function,
germ line BRG-1 mutations in tumorigenesis may be tantamount to RB
inactivation. Therefore, in this study we assessed the behavior of cells
harboring discrete BRG-1 alleles for the RB-signaling pathway. Using
p16ink4a, an upstream activator of endogenous RB, or a constitutively
active RB construct (PSM-RB), we determined that the majority of tumor
lines with germ line defects in BRG-1 were sensitive to RB-mediated cell
cycle arrest. By contrast, A427 (lung carcinoma) cells were resistant to
expression of p16ink4a and PSM-RB. Analysis of the SWI-SNF subunits in
the different tumor lines revealed that A427 are deficient for BRG-1 and
its homologue, Brm, whereas RB-sensitive cell lines retained Brm
expression. Similarly, the RB-resistant SW13 and C33A cell lines were
also deficient for both BRG-1/Brm. Reintroduction of either BRG-1 or Brm
into A427 or C33A cells restored RB-mediated signaling to cyclin A to
cause cell cycle arrest. Consistent with this compensatory role, we
observed that Brm could also drive expression of CD44. We also
determined that loss of these core SWI-SNF subunits renders SW13 cells
resistant to activation of the RB pathway by the chemotherapeutic agent
cisplatin, since reintroduction of either BRG-1 or Brm into SW13 cells
restored the cisplatin DNA-damage checkpoint. Together, these data
demonstrate that Brm can compensate for BRG-1 loss as pertains to RB
sensitivity.
5
UI - 11801265
AU - Finger PT; Harbour JW; Karcioglu ZA
TI -
Risk factors for metastasis in retinoblastoma.
SO - Surv Ophthalmol 2002 Jan-Feb;47(1):1-16
AD - The New York Eye Cancer Center, New York, NY, USA.
Children with retinoblastoma typically survive their cancer due to
advances in early diagnosis and treatment. Despite this success, risk
factors persist for metastasis that are thought to be related to patient
age, sex, laterality, treatment, genetics, histopathology, and
extraocular extension. This review has found that invasion of the uvea,
orbit, and optic nerve continue to be the most important predictors of
metastatic retinoblastoma. Bilaterality and delays in diagnosis are also
important factors. We examine molecular and genetic studies that offer
the potential of predicting which tumors are likely to metastasize,
which will recur within the eye, and which will undergo senescence. In
this review, we describe which clinical evaluations, genetic studies,
and histopathologic evaluations of retrieved specimens are currently
used widely. This review has been performed to help those caring for
patients with retinoblastoma and to aid informed consent.
6
UI - 11821358
AU - Dockerty JD; Draper G; Vincent T; Rowan SD; Bunch KJ
TI -
Case-control study of parental age, parity and socioeconomic level in
relation to childhood cancers.
SO - Int J Epidemiol 2001 Dec;30(6):1428-37
AD - 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 environmental risk factor.
7
UI - 11836727
AU - Carlos LL; Roberto RL; Victor TG; Carlos HG; Eduardo LP
TI -
Risk of dying of retinoblastoma in Mexican children.
SO - Med Pediatr Oncol 2002 Mar;38(3):211-3
AD - National Institute of Pediatrics (Instituto Nacional de Pediatria,
Departamento de Oncologia), Oncology Department, Mexico City.
8
UI - 11861365
AU - Chen D; Pajovic S; Duckett A; Brown VD; Squire JA; Gallie BL
TI -
Genomic amplification in retinoblastoma narrowed to 0.6 megabase on
chromosome 6p containing a kinesin-like gene, RBKIN.
SO - Cancer Res 2002 Feb 15;62(4):967-71
AD - Division of Cancer Informatics, Ontario Cancer Institute/Princess
Margaret Hospital, University Health Network, Toronto, M5G 2M9 Canada.
All retinoblastomas (RBs) show genomic changes in addition to loss of
both RB1 alleles. Quantitative-multiplex PCR analysis identified in 41
of 70 (59%) RBs a 0.6-Mb minimal region of chromosome 6p22 gain from
which we cloned the human kinesin gene, RBKIN/KIF13A, by rapid
amplification of retinal cDNA. RBKIN is expressed ubiquitously in adult
tissues, at low levels in fetal tissues, and at high levels in RB.
Antisense RBKIN oligonucleotide reduced the growth rate of RB cell
lines. RBKIN and/or another closely linked gene are candidate oncogenes
contributing to malignant progression of RB.
9
UI - 7569348
AU - Shields JA; Shields CL; Eagle RC Jr; Barrett J; De Potter P
TI -
Endogenous endophthalmitis simulating retinoblastoma. The 1993 David and
Mary Seslen Endowment Lecture.
SO - Retina 1995;15(3):213-9
AD - Ocular Oncology Service, Wills Eye Hospital, Thomas Jefferson
University, Philadelphia, Pennsylvania 19107, USA.
BACKGROUND: Among conditions that can simulate retinoblastoma,
endogenous endophthalmitis is quite rare. METHODS: Case records of six
children with unusual forms of endogenous endophthalmitis, all of whom
were referred to the authors because retinoblastoma was a strong
diagnostic consideration, were reviewed. The clinical features that may
help differentiate atypical endophthalmitis from retinoblastoma were
investigated. RESULTS: The final diagnosis in these cases included
idiopathic subretinal abscess, streptococcal endophthalmitis, idiopathic
retinovitreal abscess, cytomegalovirus endophthalmitis, Candida
endophthalmitis, and meningococcal endophthalmitis. All of the affected
children presented primarily with ocular findings without serious
systemic infection. Although these conditions closely simulated
retinoblastoma, they were more likely to have signs of concurrent or
prior inflammation. CONCLUSION: Differentiation between infectious
conditions and retinoblastoma can sometimes be difficult, but clues as
to the diagnosis can be obtained from careful clinical examination.
10
UI - 11867572
AU - Van Aken EH; Papeleu P; De Potter P; Bruyneel E; Philippe J; Seregard S;
TI -
Kvanta A; De Laey JJ; Mareel MM
Structure and function of the N-cadherin/catenin complex in
retinoblastoma.
SO - Invest Ophthalmol Vis Sci 2002 Mar;43(3):595-602
AD - Department of Ophthalmology, Laboratory of Experimental Cancerology,
Ghent University Hospital, De Pintelaan 185, B-9000 Gent, Belgium.
PURPOSE: To identify in human retinoblastoma and normal retinal tissue
the type of cadherin, its relationship with cytoplasmic catenins, and
its participation in invasion. METHODS: The cadherin/catenin complex was
characterized in surgical retinoblastoma specimens from five patients
and human retinas from four donor eyes by immunocytochemistry, flow
cytometry, and coimmunoprecipitation with antibodies against N-cadherin,
alpha-catenin, and beta-catenin, followed by Western blot analysis or
autoradiography. Y79 and WERI-Rb-1 retinoblastoma cell lines serve the
evaluation of the cadherin/catenin complex in aggregation and collagen
type I invasion in vitro. The association of the cadherin/catenin
complex with the cytoskeleton was examined by an antibody-capping assay.
RESULTS: In retinoblastoma and normal retina N-cadherin associated with
alpha-catenin and beta-catenin but not E- or P-cadherin. The
N-cadherin/catenin complex formed a regular, linear, and continuous
honeycomb pattern in normal retina that was irregular, clustered, and
interrupted in retinoblastoma. The N-cadherin/catenin complex was found
also in the retinoblastoma cell lines WERI-Rb and Y79, in which it also
showed an irregular pattern. Both cell lines were invasive in collagen
type I, and invasion was inhibited by the GC-4 antibody, which
functionally neutralizes N-cadherin. Less GC-4 antibody was needed to
inhibit invasion of Y79 cells, which expressed N-cadherin at a lower
level, than to inhibit invasion of WERI-Rb-1 cells. In both cell lines,
antibody capping of the N-cadherin/catenin complex indicated that its
linkage with the cytoskeleton were weak or absent. CONCLUSIONS:
Retinoblastoma cells, in contrast with normal retina, express an
N-cadherin/catenin complex that is irregularly distributed and weakly
linked to the cytoskeleton. In retinoblastoma, this complex acts as an
invasion promoter.
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