Table of Contents
1
UI - 11840325
AU - Lasorella A; Uo T; Iavarone A
TI -
Id proteins at the cross-road of development and cancer.
SO - Oncogene 2001 Dec 20;20(58):8326-33
AD - Department of Neurology, Developmental and Molecular Biology, Albert
Einstein College of Medicine, Bronx, NY 10461, USA.
A large body of evidence has been accumulated that demonstrates dominant
effects of Id proteins on different aspects of cellular growth.
Generally, constitutive expression of Id not only blocks cell
differentiation but also drives proliferation. In some settings, it is
sufficient to render cells immortal or induce oncogenic transformation.
The participation of Id proteins in advanced human malignancy, where
they are frequently deregulated, has been dramatically bolstered by the
recent discovery that Id exert pivotal contributions to many of the
essential alterations that collectively dictate malignant growth.
Relentless proliferation associated with self-sufficiency in growth
signals and insensitivity to growth inhibitory signals, sustained
neoangiogenesis, tissue invasiveness and migration capabilities of tumor
cells all share dependency on the unlimited availability of Id proteins.
It is remarkable that many of these features recapitulate those
physiologically propelled by Id proteins to support normal development.
We propose that the participation of Id in multiple fundamental traits
of cancer may be the basis for unprecedented therapeutic opportunities.
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.
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