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Sent on Saturday, 2008 Sep 20.
Search brain cancer
Click on the following url to view complete results in pubmed. (Results may change over time.)
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==================== Entrez pubmed Results ======================
Items 1 - 5 of 46
1: J Neuropathol Exp Neurol. 2008 Sep 16; [Epub ahead of print]
Accumulation of HtrA2/Omi in Neuronal and Glial Inclusions in Brains With
alpha-Synucleinopathies.
Kawamoto Y, Kobayashi Y, Suzuki Y, Inoue H, Tomimoto H, Akiguchi I, Budka H,
Martins LM, Downward J, Takahashi R.
From the Department of Neurology (Y. Kawamoto, Y. Kobayashi, HI, HT, RT),
Faculty of Medicine, Kyoto University; Department of Neurology (Y. Kawamoto),
Seijinnkai Rakusaisimizu Hospital, Kyoto; and Department of Degenerative
Neurological Diseases (YS), National Institute of Neuroscience, National Center
of Neurology and Psychiatry, Tokyo, Japan; Center of Neurological and
Cerebrovascular Diseases (IA), Koseikai Takeda Hospital, Kyoto, Japan; Institute
of Neurology (HB), Medical University of Vienna, Vienna, Austria; Cell Death
Regulation Laboratory (LMM), MRC Toxicology Unit, Leicester, UK; and Signal
Transduction Laboratory (JD), Cancer Research UK London Research Institute,
London, UK.
HtrA2/Omi is a mitochondrial serine protease that is released into the cytosol
and promotes apoptotic processes by binding to several members of the inhibitors
of apoptosis protein family. HtrA2/Omi knockout mice show a parkinsonian
phenotype, and mutations in the gene encoding HtrA2/Omi have been identified as
susceptibility factors for Parkinson disease (PD). These results suggest that
HtrA2/Omi may be involved in the pathogenesis of PD. We performed
immunohistochemical studies of HtrA2/Omi on brains from patients with
alpha-synuclein-related disorders, including PD, dementia with Lewy bodies
(DLB), and multiple-system atrophy (MSA); patients with other neurodegenerative
diseases; and controls. HtrA2/Omi is expressed in normal brain tissue, and there
was some anti-HtrA2/Omi immunostaining of neurons in normal brains as well as
those with other neurodegenerative diseases. In PD and DLB brains, both classic
(i.e. brainstem-type) and cortical Lewy bodies were intensely immunostained;
pale bodies were also strongly immunopositive for HtrA2/Omi. In MSA brains,
numerous glial cytoplasmic inclusions, neuronal cytoplasmic inclusions, and
dystrophic neurites were also intensely immunoreactive for HtrA2/Omi. These
results suggest that widespread accumulation of HtrA2/Omi may occur in
pathologic alpha-synuclein-containing inclusions in brains with PD, DLB, or MSA
and that HtrA2/Omi may be associated with the pathogenesis of
alpha-synucleinopathies.
PMID: 18800009 [PubMed - as supplied by publisher]
2: Hum Pathol. 2008 Sep 15; [Epub ahead of print]
Nestin expression correlates with nerve and retroperitoneal tissue invasion in
pancreatic cancer.
Kawamoto M, Ishiwata T, Cho K, Uchida E, Korc M, Naito Z, Tajiri T.
Surgery for Organ and Biological Regulation (Department of Surgery I), Graduate
School of Medicine, Nippon Medical School, Tokyo 113-8603, Japan; Department of
Pathology, Integrative Oncological Pathology, Nippon Medical School, Tokyo
113-8602, Japan.
Nestin was first described as an intermediate filament protein expressed in
neuroepithelial stem cells. Nestin expression has also been reported in brain
tumors, schwannomas, gastrointestinal stromal tumors, and melanomas. In the
pancreas, Nestin expression has been detected in exocrine and mesenchymal cells,
including stellate cells, pericytes, and endothelial cells. In the present
study, we examined Nestin expression in human pancreatic ductal adenocarcinoma
and sought to determine its role in this malignancy. Reverse
transcription-polymerase chain reaction analysis demonstrated the presence of
Nestin mRNA in all 10 tested pancreatic cancer cell lines, and quantitative
reverse transcription-polymerase chain reaction revealed that Nestin mRNA levels
were highest in PANC-1 cells and lowest in PK-8 cells. Immunofluorescent
analysis revealed that Nestin localized in the outer cytoplasm of PANC-1 cells.
Nestin immunoreactivity was present in the cancer cells in 20 (33.3%) of 60
cancer cases, and its expression was confirmed by in situ hybridization. Nestin
expression was also increased in peripheral nerve fibers adjacent to cancer
cells and in peripheral nerve fibers invaded by cancer cells.
Clinicopathologically, there was a statistically significant association between
Nestin expression in pancreatic cancer cells and nerve invasion (P = .010) and
the presence of cancer cells in the tumor resection margins (P = .003).
Nestin-positive cases exhibited similar survival after resection by comparison
with Nestin-negative cases, irrespective of whether they were given adjuvant
therapy. These findings indicate that Nestin expression in pancreatic cancer
cells may contribute to nerve and stromal invasion in this malignancy.
PMID: 18799194 [PubMed - as supplied by publisher]
3: Pediatr Blood Cancer. 2008 Sep 17; [Epub ahead of print]
Epidemiology and clinical risk factors predisposing to thromboembolism in
children with cancer.
Athale U, Siciliano S, Thabane L, Pai N, Cox S, Lathia A, Khan A, Armstrong A,
Chan AK.
Division of Hematology/Oncology, Department of Pediatrics, McMaster University,
Hamilton, Ontario, Canada.
PURPOSE: The prevalence and risk factors for thromboembolism (TE) in children
with cancer are largely unknown. This retrospective cohort study aims to
determine the epidemiology of TE and to identify potential risk factors for TE
in children with cancer. METHODS: We used logistic regression to determine the
association of age (<10 years vs. >/=10 years), gender, type of cancer, presence
or absence of intra-thoracic disease (mediastinal mass or any primary or
metastatic pulmonary disease), type of central venous line (CVL) and
CVL-dysfunction (difficulty of blood draw, infusion or documented CVL infection)
on the risk of developing TE. RESULTS: Fifty-seven of 726 patients [7.9%; 95%
confidence intervals (CI); 6.0,10.0] developed TE; children with brain tumors (n
= 201) had significantly lower prevalence of TE (0.5%; P < 0.001). Older
patients had increased risk of developing TE compared to younger patients [Odds
ratios (OR) 1.8; 95% CI; 1.0,3.2; P = 0.036]. Children with acute lymphoblastic
leukemia (ALL) (OR 4.6; 95% CI; 1.8, 12.3; P = 0.002), lymphoma (OR 3.8; 95% CI;
1.3, 11.1; P = 0.016), and sarcoma (OR 4.3; 95% CI; 1.4, 13.3; P = 0.012) had an
increased risk of TE. Subgroup analyses showed that patients with
CVL-dysfunction and intra-thoracic disease had a higher prevalence of TE
compared to those without CVL-dysfunction (22.8% vs. 8.8%; 95% CI; 4.0, 24.3; P
= 0.006) and intra-thoracic disease (18.0% vs. 6.1%; 95% CI; 2.4, 21.4; P =
0.02). CONCLUSIONS: TE is common in children with cancer. Age and type of cancer
are independent risk factors for TE in children with non-CNS cancers.
CVL-dysfunction and intra-thoracic disease are significantly associated with the
diagnosis of TE. Pediatr. Blood Cancer (c) 2008 Wiley-Liss, Inc.
PMID: 18798556 [PubMed - as supplied by publisher]
4: Cancer. 2008 Sep 17;113(S7):1953-1968 [Epub ahead of print]
Brain tumor epidemiology: Consensus from the Brain Tumor Epidemiology
Consortium.
Bondy ML, Scheurer ME, Malmer B, Barnholtz-Sloan JS, Davis FG, Il'yasova D,
Kruchko C, McCarthy BJ, Rajaraman P, Schwartzbaum JA, Sadetzki S, Schlehofer B,
Tihan T, Wiemels JL, Wrensch M, Buffler PA; On behalf of the Brain Tumor
Epidemiology Consortium Members of the Brain Tumor Epidemiology Consortium (in
alphabetical order): Phyllis Adatto, MPH (M. D. Anderson Cancer Center), Jill
Barnholtz-Sloan, PhD (Case Comprehensive Cancer Center), Fabienne Bauchet
(Groupe de Neuro-Oncologie du Languedoc-Roussillon), Luc Bauchet, MD (Hopital
Gui de Chauliac), Melissa Bondy, PhD (M. D. Anderson Cancer Center), Jennifer
Brusstar (The Tug McGraw Foundation), Patricia Buffler, PhD (University of
California, Berkeley), Mary Ann Butler, PhD (CDC/NIOSH), Elizabeth Cardis, PhD
(IARC), Tania Carreon-Valencia, PhD (CDC/NIOSH), Jeffrey Chang, PhD (University
of California, San Francisco), Anand Chokkalingam, PhD (University of
California, Berkeley), Charles Cobbs, MD (CPMC Research Institute), Jimmy Efrid,
PhD (University of Hawaii), Paul Graham Fisher, MD (Stanford University), James
Gurney, PhD (University of Michigan), Trisha Hartge, PhD (NCI/NIH), Dora
Il'yasova, PhD (Duke University Medical Center), Alice Kang (University of
California, Berkeley), Carol Kruchko (Central Brain Tumor Registry of the United
States), Amy Kyle, PhD (University of California, Berkeley), Rose Lai, MD
(Columbia University), Sharon Lamb (National Brain Tumor Foundation), Ching Lau,
MD, PhD (Baylor College of Medicine), Beatrice Malmer, MD (Umea University),
Bridget McCarthy, PhD (University of Illinois at Chicago), Roberta
McKean-Cowdin, PhD (University of Southern California), Eckart Meese, PhD
(University of Saarland), Catherine Metayer, PhD (University of California,
Berkeley), Dominique Michaud, SD (Imperial College London), Isis Mikhail, MD,
DrPH (NCI/NIH), Lloyd Morgan (Central Brain Tumor Registry of the United
States), Beth Mueller, PhD (Fred Hutchinson Cancer Research Center), Michael
Murphy, PhD (University of Oxford), John Neuberger, DrPH (University of Kansas),
Manuela Orjuela, MD (Columbia University), Harriet Patterson, MPH (National
Brain Tumor Foundation), Susan Preston-Martin, PhD (University of Southern
California), Preetha Rajaraman, PhD (NCI/NIH), Steve Rappaport, PhD (University
of California, Berkeley), Avima Ruder, PhD (CDC/NIOSH), Siegal Sadetzki, MD
(Gertner Institute), Michael Scheurer, PhD (BaylorCollege of Medicine), Brigitte
Schlehofer, PhD (German Cancer Research Center), Joerg Schlehofer, MD (German
Cancer Research Center), Judith Schwartzbaum, PhD (Ohio State University), Jenni
Spezeski, MPH (National Brain Tumor Foundation), Tarik Tihan, MD (University of
California, San Francisco), Rob Tufel, MPH (National Brain Tumor Foundation),
Kevin Urayama, MPH (University of California, Berkeley), Joseph Wiemels, PhD
(University of California, San Francisco), John Wiencke, PhD (University of
California, San Francisco), Margaret Wrensch, PhD (University of California, San
Francisco)..
Department of Epidemiology, The University of Texas M. D. Anderson Cancer
Center, Houston, Texas.
Epidemiologists in the Brain Tumor Epidemiology Consortium (BTEC) have
prioritized areas for further research. Although many risk factors have been
examined over the past several decades, there are few consistent findings,
possibly because of small sample sizes in individual studies and differences
between studies in patients, tumor types, and methods of classification.
Individual studies generally have lacked samples of sufficient size to examine
interactions. A major priority based on available evidence and technologies
includes expanding research in genetics and molecular epidemiology of brain
tumors. BTEC has taken an active role in promoting understudied groups, such as
pediatric brain tumors; the etiology of rare glioma subtypes, such as
oligodendroglioma; and meningioma, which, although it is not uncommon, has only
recently been registered systematically in the United States. There also is a
pressing need for more researchers, especially junior investigators, to study
brain tumor epidemiology. However, relatively poor funding for brain tumor
research has made it difficult to encourage careers in this area. In this
report, BTEC epidemiologists reviewed the group's consensus on the current state
of scientific findings, and they present a consensus on research priorities to
identify which important areas the science should move to address. Cancer
2008;113(7 suppl):1953-68. (c) 2008 American Cancer Society.
PMID: 18798534 [PubMed - as supplied by publisher]
5: Am J Med Genet A. 2008 Sep 16; [Epub ahead of print]
Two new patients with Curry-Jones syndrome with trichoblastoma and
medulloblastoma suggest an etiologic role of the sonic hedgehog-patched-GLI
pathway.
Grange DK, Clericuzio CL, Bayliss SJ, Berk DR, Heideman RL, Higginson JK, Julian
S, Lind A.
Division of Genetics and Genomic Medicine, Department of Pediatrics, Washington
University School of Medicine, St. Louis, Missouri.
Curry-Jones syndrome (OMIM #601707) is a rare multiple malformation disorder of
unknown etiology, associated with brain and skull abnormalities, polysyndactyly,
and defects of the eyes, skin and gastrointestinal tract. We report on two new
cases of Curry-Jones syndrome with previously unreported features, including
benign and malignant neoplasms. The first patient had typical features of
Curry-Jones syndrome as well as multiple intra-abdominal smooth muscle
hamartomas and trichoblastoma of the skin. The second patient was born with
occipital meningoceles and developed a desmoplastic medulloblastoma. Routine
lymphocyte karyotype, GLI3 gene analysis and Patched (PTCH) gene analysis on
both patients and chromosome microarray analysis on the first patient were
normal. We review the previously reported cases of Curry-Jones syndrome and
compare our patients' findings. In view of the association of trichoblastoma
with basal cell carcinoma and desmoplastic medulloblastoma with nevoid basal
cell carcinoma syndrome (NBCCS) and PTCH mutations, we hypothesize that
Curry-Jones syndrome is caused by malfunction of an element in the sonic
hedgehog pathway. (c) 2008 Wiley-Liss, Inc.
PMID: 18798318 [PubMed - as supplied by publisher]