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Accelerated apoptosis and low bcl-2 expression associated with neuroendocrine differentiation predict shortened survival in operated large cell carcinoma of the lung.

https://arctichealth.org/en/permalink/ahliterature20816
Source
Pathol Oncol Res. 1999;5(3):179-86
Publication Type
Article
Date
1999
Author
A K Eerola
H. Ruokolainen
Y. Soini
H. Raunio
P. Pääkkö
Author Affiliation
University of Oulu, Department of Pathology Kajaanintie 52 D, Oulu, FIN-90401, Finland.
Source
Pathol Oncol Res. 1999;5(3):179-86
Date
1999
Language
English
Publication Type
Article
Keywords
Adult
Aged
Apoptosis
Blotting, Western
Carcinoma, Neuroendocrine - metabolism - mortality - pathology - surgery
Carcinoma, Non-Small-Cell Lung - metabolism - mortality - pathology - surgery
Cell Differentiation
Cyclin D1 - metabolism
Female
Follow-Up Studies
Humans
Immunohistochemistry
Lung Neoplasms - metabolism - mortality - pathology - surgery
Male
Membrane Proteins - metabolism
Middle Aged
Necrosis
Neoplasm Proteins - metabolism
Prognosis
Proto-Oncogene Proteins - metabolism
Proto-Oncogene Proteins c-bcl-2 - metabolism
Survival Rate
bcl-2 Homologous Antagonist-Killer Protein
bcl-2-Associated X Protein
Abstract
In order to test the hypothesis that increased apoptotic activity is connected with neuroendocrine differentiation and low differentiation degree in large cell carcinoma (LCLC) and is regulated by bcl-2 family proteins, we analysed the extent of apoptosis and tumor necrosis and their relation to the expression of bcl-2, bax, bak and mcl-1 in 35 LCLCs, of which 20 were classified as large cell neuroendocrine lung carcinomas (LCNEC) and 15 as large cell non-neuroendocrine lung carcinomas (LCNNEC). The extent of apoptosis was determined by detecting and counting the relative and absolute numbers of apoptotic cells and bodies using in situ 3 -end labelling of the apoptotic DNA. The extent and intensity of expression of the bcl-2, bax, bak and mcl-1 proteins were studied by immunohistochemistry. Also the relative volume density of necrosis was evaluated and correlated with the other parameters. Finally, all the parameters were evaluated as prognostic markers and correlated with data on the survival of the patients. Relatively high apoptotic indices were seen in both tumor types (average for both 2.53%, range 0.09 27.01%). Significantly higher bcl-2 and bak indices were detected more often in LCNECs than in LCNNECs. Immunohistochemically detected bax, bcl-2 and bak expression was independent of apoptotic index in both tumor types, while there was a statistically significant positive association between mcl-1 expression and apoptotic index in LCNNEC but not in LCNEC. There was a statistically significant association between high apoptotic index and shortened survival in LCLC. However, no association was found between tumor stage and apoptosis. The patients with LCNEC and low bcl-2 protein expression had a significantly shorter survival time than those with high bcl-2 indices. There was also a clear association between shortened survival and necrotic LCNNEC. LCLCs show relatively high apoptotic activity, which is associated with shortened survival. The expression of bcl-2, bak and mcl- 1 is associated with neuroendocrine differentiation in LCLC. Finally, our results support some previous reports suggesting that bcl-2 expression in combination with some other markers involved in apoptosis and/or proliferation may be of prognostic value in cases of lung carcinoma with neuroendocrine differentiation.
PubMed ID
10491014 View in PubMed
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Age dependence of tumor genetics in unfavorable neuroblastoma: arrayCGH profiles of 34 consecutive cases, using a Swedish 25-year neuroblastoma cohort for validation.

https://arctichealth.org/en/permalink/ahliterature114056
Source
BMC Cancer. 2013;13:231
Publication Type
Article
Date
2013
Author
Cihan Cetinkaya
Tommy Martinsson
Johanna Sandgren
Catarina Träger
Per Kogner
Jan Dumanski
Teresita Díaz de Ståhl
Fredrik Hedborg
Author Affiliation
Department of Immunology, Genetics and Pathology, Rudbeck Laboratory, Uppsala University, Uppsala SE-751 85, Sweden.
Source
BMC Cancer. 2013;13:231
Date
2013
Language
English
Publication Type
Article
Keywords
Adolescent
Age Factors
Base Sequence
Child
Child, Preschool
Chromosome Aberrations
Chromosomes, Human, Pair 11 - genetics
Chromosomes, Human, Pair 12 - genetics
DNA Copy Number Variations
Gene Amplification
Gene Expression Profiling
Humans
Infant
Neuroblastoma - genetics
Nuclear Proteins - genetics
Oligonucleotide Array Sequence Analysis
Oncogene Proteins - genetics
Registries
Sequence Deletion
Sweden
Abstract
Aggressive neuroblastoma remains a significant cause of childhood cancer death despite current intensive multimodal treatment protocols. The purpose of the present work was to characterize the genetic and clinical diversity of such tumors by high resolution arrayCGH profiling.
Based on a 32K BAC whole-genome tiling path array and using 50-250K Affymetrix SNP array platforms for verification, DNA copy number profiles were generated for 34 consecutive high-risk or lethal outcome neuroblastomas. In addition, age and MYCN amplification (MNA) status were retrieved for 112 unfavorable neuroblastomas of the Swedish Childhood Cancer Registry, representing a 25-year neuroblastoma cohort of Sweden, here used for validation of the findings. Statistical tests used were: Fisher's exact test, Bayes moderated t-test, independent samples t-test, and correlation analysis.
MNA or segmental 11q loss (11q-) was found in 28/34 tumors. With two exceptions, these aberrations were mutually exclusive. Children with MNA tumors were diagnosed at significantly younger ages than those with 11q- tumors (mean: 27.4 vs. 69.5 months; p=0.008; n=14/12), and MNA tumors had significantly fewer segmental chromosomal aberrations (mean: 5.5 vs. 12.0; p
Notes
Cites: Nucleic Acids Res. 2002 Feb 15;30(4):e1511842121
Cites: Nat Rev Cancer. 2003 Mar;3(3):203-1612612655
Cites: BMC Genomics. 2004 Sep 20;5:7015380028
Cites: Cancer Genet Cytogenet. 2004 Oct 15;154(2):131-715474148
Cites: Science. 1984 Jun 8;224(4653):1121-46719137
Cites: Hum Genet. 1991 Apr;86(6):562-62026421
Cites: Med Pediatr Oncol. 1992;20(4):292-3001608350
Cites: EMBO J. 1993 Dec 15;12(13):5083-78262051
Cites: Eur J Cancer. 1995;31A(4):520-37576957
Cites: Cancer. 1997 May 15;79(10):2028-359149032
Cites: J Clin Oncol. 2005 Apr 1;23(10):2280-9915800319
Cites: N Engl J Med. 2005 Nov 24;353(21):2243-5316306521
Cites: Bioinformatics. 2006 Apr 15;22(8):1024-616455749
Cites: Genes Chromosomes Cancer. 2007 Dec;46(12):1098-10817823929
Cites: Oncogene. 2007 Nov 22;26(53):7432-4417533364
Cites: Hum Mutat. 2008 Mar;29(3):398-40818058796
Cites: Bioinformatics. 2008 Mar 15;24(6):751-818204059
Cites: BMC Genomics. 2008;9:35318664255
Cites: J Clin Oncol. 2009 Jan 10;27(2):289-9719047291
Cites: Clin Cancer Res. 2006 Jun 1;12(11 Pt 1):3368-7316740759
Cites: Cancer Genet Cytogenet. 2007 Jan 15;172(2):127-3817213021
Cites: Genes Chromosomes Cancer. 2007 Oct;46(10):936-4917647283
Cites: J Clin Oncol. 2009 Mar 1;27(7):1026-3319171713
Cites: Hematol Oncol Clin North Am. 2010 Feb;24(1):65-8620113896
Cites: Oncogene. 2010 Feb 11;29(6):865-7519901960
Cites: Proc Natl Acad Sci U S A. 2010 Mar 2;107(9):4323-820145112
Cites: Clin Cancer Res. 2010 Jun 1;16(11):2971-820406844
Cites: N Engl J Med. 2010 Jun 10;362(23):2202-1120558371
Cites: J Clin Oncol. 2010 Jul 1;28(19):3122-3020516441
Cites: Cell. 2011 Mar 4;144(5):646-7421376230
Cites: Cancer. 2011 Sep 15;117(18):4286-9321387264
Cites: Nature. 2012 Mar 29;483(7391):589-9322367537
PubMed ID
23656755 View in PubMed
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Age-related deficit in load-induced skeletal muscle growth.

https://arctichealth.org/en/permalink/ahliterature89394
Source
J Gerontol A Biol Sci Med Sci. 2009 Jun;64(6):618-28
Publication Type
Article
Date
Jun-2009
Author
Hwee Darren T
Bodine Sue C
Author Affiliation
Department of Neurobiology, Physiology, and Behavior, University of California, Davis, 95616, USA.
Source
J Gerontol A Biol Sci Med Sci. 2009 Jun;64(6):618-28
Date
Jun-2009
Language
English
Publication Type
Article
Keywords
Adaptation, Physiological
Age Factors
Aging - physiology
Animals
Caloric Restriction
Hindlimb - physiology
Hindlimb Suspension - physiology
Male
Models, Animal
Muscle Development - physiology
Muscle Proteins - metabolism
Muscle, Skeletal - growth & development
Proto-Oncogene Proteins c-akt - metabolism
Rats
Rats, Inbred F344
Signal Transduction - physiology
Weight-Bearing - physiology
Abstract
The growth response of ankle flexor and extensor muscles to two models of increased loading, functional overload (FO) and hind-limb reloading following hind-limb suspension, was measured by wet weight in Fisher 344-Brown Norway rats at ages ranging from 6 to 30 months. In response to FO, there was a 40% decrease in absolute growth of the plantaris beginning in middle age. Interestingly, the growth response to FO of 30-month old rats maintained on a 40% calorie-restricted diet improved by more than twofold relative to 30-month old rats on a normal chow diet. Recovery of muscle mass upon reloading following disuse was significantly impaired (reduced 7-16%) in predominantly fast, but not slow, muscles of 30-month relative to 9-month old rats. Initial investigation of the Akt signaling pathway following FO suggests a reduction or delay in activation of Akt and its downstream targets in response to increased loading in old rats.
PubMed ID
19351696 View in PubMed
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Aging alters vascular mechanotransduction: pressure-induced regulation of p70S6k in the rat aorta.

https://arctichealth.org/en/permalink/ahliterature83419
Source
Mech Ageing Dev. 2005 Nov;126(11):1213-22
Publication Type
Article
Date
Nov-2005
Author
Rice K M
Kinnard R S
Wright G L
Blough E R
Author Affiliation
Department of Biological Sciences, Laboratory of Molecular Physiology, Suite 311, Science Building, 1 John Marshall Drive, Marshall University, Huntington, WV 25755-1090, USA.
Source
Mech Ageing Dev. 2005 Nov;126(11):1213-22
Date
Nov-2005
Language
English
Publication Type
Article
Keywords
Aged
Aging - physiology
Animals
Aorta - anatomy & histology - metabolism
Blood Pressure - physiology
Glycogen Synthase Kinase 3 - metabolism
Humans
Intracellular Signaling Peptides and Proteins - metabolism
Male
Mechanotransduction, Cellular - physiology
PTEN Phosphohydrolase - metabolism
Phosphorylation
Protein-Tyrosine-Phosphatase - metabolism
Proto-Oncogene Proteins c-akt - metabolism
Rats
Rats, Inbred F344
Ribosomal Protein S6 Kinases, 70-kDa - metabolism
Abstract
Physical forces are important regulators of vascular structure and function though it is unknown how aging may affect the ability of the vasculature to respond to mechanical stimuli. We investigated the pressure-induced activation of ribosomal S6-kinase (p70S6k) and its pathway-related proteins (Akt, GSK-3beta, SHP-2, PTEN) in aortae from young adult (6 month), aged (30 month), and very aged (36 month) Fischer 344 x Brown Norway F1 hybrid rats. With aging, the aortic tissue content of Akt. SHP-2, and PTEN was significantly increased while total p70S6k and GSK-3beta were unchanged. By comparison, the basal phosphorylation of p70S6k at Thr 389 and Thr 421/Ser 424 was increased ( approximately 40%) and unchanged, respectively, while Akt decreased (approximately 37%), GSK-3beta was unchanged, SHP-2 increased (approximately 73.5%), and PTEN increased (approximately 120%) in the aortae of very aged rats. Acute pressurization of aortae resulted in similar increases in phosphorylation of Akt among the different age groups. By comparison, pressure-induced phosphorylation of p70S6k at Thr 389, GSK-3beta and SHP-2 decreased; whereas, PTEN dephosphorylation was increased in 36-month versus 6-month aortae. The results indicate marked alterations in the p70S6k signaling pathway with aging. The implications of these findings on age-associated vessel remodeling are discussed.
PubMed ID
16087221 View in PubMed
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Aging influences multiple incidices of oxidative stress in the aortic media of the Fischer 344/NNiaxBrown Norway/BiNia rat.

https://arctichealth.org/en/permalink/ahliterature82960
Source
Free Radic Res. 2006 Feb;40(2):185-97
Publication Type
Article
Date
Feb-2006
Author
Rice K M
Preston D L
Walker E M
Blough E R
Author Affiliation
Marshall University, Department of Biological Sciences, Huntington, WV 2755-1090, USA.
Source
Free Radic Res. 2006 Feb;40(2):185-97
Date
Feb-2006
Language
English
Publication Type
Article
Keywords
Aging - physiology
Animals
Aorta - metabolism
Cell Proliferation
Ethidium - chemistry
Genes, src
JNK Mitogen-Activated Protein Kinases - metabolism
Ki-67 Antigen - metabolism
Mitogen-Activated Protein Kinases - metabolism
Multienzyme Complexes
NF-kappa B - genetics - metabolism
Oxidative Stress
Phenanthridines - chemistry
Phosphorylation
Protein-Serine-Threonine Kinases
Proteins - chemistry - metabolism
Proto-Oncogene Proteins c-bcl-2 - metabolism
Rats
Rats, Inbred BN
Rats, Inbred F344
TNF Receptor-Associated Factor 2 - metabolism
bcl-2-Associated X Protein - metabolism
Abstract
Here, we determine the influence of aging on multiple markers of oxidative stress in the aorta of adult (6-month), aged (30-month) and very aged (36-month) Fischer 344/NNiaHSdxBrown Norway/BiNia (F344/NxBN) rats. Compared to adults, increases in as determined by oxidation of hydroethidine (HE) to ethidium (Et) were increased 79.7+/-7.0% in 36-month aortae and this finding was highly correlated with increases in medal thickness (r=0.773, p
PubMed ID
16390828 View in PubMed
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Aging influences multiple indices of oxidative stress in the heart of the Fischer 344/NNia x Brown Norway/BiNia rat.

https://arctichealth.org/en/permalink/ahliterature83665
Source
Redox Rep. 2007;12(4):167-80
Publication Type
Article
Date
2007
Author
Asano Shinichi
Rice Kevin M
Kakarla Sunil
Katta Anjaiah
Desai Devashish H
Walker Ernest M
Wehner Paulette
Blough Eric R
Author Affiliation
Department of Biological Sciences, Marshall University, Huntington, West Virginia 25755-1090, USA.
Source
Redox Rep. 2007;12(4):167-80
Date
2007
Language
English
Publication Type
Article
Keywords
Aging - physiology
Aldehydes - metabolism
Analysis of Variance
Animals
Blood Pressure - physiology
Female
Heart - physiopathology
Heat-Shock Proteins - metabolism
Immunoblotting
Immunohistochemistry
Male
Microscopy, Fluorescence
Mitogen-Activated Protein Kinases - metabolism
Myocardium - metabolism - pathology
Oxidative Stress
Phosphorylation
Proto-Oncogene Proteins c-bcl-2 - metabolism
Rats
Rats, Inbred BN
Rats, Inbred F344
Reactive Oxygen Species - metabolism
Regression Analysis
Signal Transduction - physiology
Superoxides - metabolism
Tyrosine - analogs & derivatives - metabolism
Abstract
We report the influence of aging on multiple markers of oxidative-nitrosative stress in the heart of adult (6-month), aged (30-month) and very aged (36-month) Fischer 344/NNiaHSd x Brown Norway/BiNia (F344/NXBN) rats. Compared to adult (6-month) hearts, indices of oxidative (superoxide anion [O2*-], 4-hydroxy-2-nonenal [4-HNE]) and nitrosative (protein nitrotyrosylation) stress were 34.1 +/- 28.1%, 186 +/- 28.1% and 94 +/- 5.8% higher, respectively, in 36-month hearts and these findings were highly correlated with increases in left ventricular wall thickness (r > 0.669; r > 0.710 and P
PubMed ID
17705987 View in PubMed
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386 records – page 1 of 39.