Qualitative histological differences between transplacentally-induced lung tumors in young and aging mice

Anderson, Lucy M.; Budinger, John M.

doi:10.1016/0304-3835(81)90093-8

Cited by 11 publications

(5 citation statements)

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“…A better control might be to use puri ed alveolar epithelial cells from control mice ( although connexin expression was reported to change rapidly in these preparations after isolation [ 5] ) or a nontransformed lung epithelial cell line [ 4]. The second possibility is that in ammation, which increases Cx43 expression in lung [ 6] and is present in mouse lung adenomas [ 7], could have increased Cx43 expression relative to nonin ammatory control lung. Besides this paradoxical difference in Cx43 expression between uninvolved lung and lung adenomas, the strong decrease in Cx43 expression in malignant lung tumors ( which also contain predominantly 1 cell type ) suggests that it is involved in lung tumor progression.…”

Section: Gjic and Connexin Expression Are Highly Decreased In Human Amentioning

confidence: 96%

“…( A ) Nuclear run-on assay was performed by hybridizing 32 P-labeled nascent mRNA transcripts from E9 and E10 cells to Cx32 cDNA, Cx43 cDNA, glyceraldehyde phosphate-3-dehydrogenase ( GAPDH ) cDNA, or pBSIIKS 1 plasmid ( 2 m g each ) previously spotted by dot-blotting onto nylon membranes. ( B ) A Cx43 promoter-luciferase reporter gene construct, pGL2Cx43 [7] ( 3 m g per plate ) and pSV2 gal ( Promega; 0.3 m g per plate ) were transfected into E9 and E10 cells and 48 hours later, luciferase and -galactosidase activities were determined in cell extracts. Luciferase activity was corrected for transfection ef ciency by normalization to -galactosidase activity for each sample and was signi cantly greater in E10 cells ( * P < .05, mean SD, n H 4 ).…”

Section: Mechanisms Of Decreased Cx43 Expression and Gjicmentioning

confidence: 99%

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DEFECTIVE GAP JUNCTIONAL INTERCELLULAR COMMUNICATION IN LUNG CANCER: Loss of an Important Mediator of Tissue Homeostasis and Phenotypic Regulation

Ruch¹,

Porter²,

Koffler³

et al. 2001

Experimental Lung Research

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Gap junctions provide direct pathways for the exchange of molecules and ions between neighboring cells, a process known as gap junctional intercellular communication (GJIC). This GJIC is important for homeostasis and regulation of mitosis, differentiation, and apoptosis. Gap junctions are present in lung airway and alveolar epithelial cells and, in addition to the above roles, might coordinate ciliary beating and surfactant secretion. GJIC is decreased in human and mouse lung carcinoma cells because of reduced expression of the gap junction protein, connexin43 (Cx43), and defects in signal transduction pathways that mediate Cx43 function. This reduced GJIC is important in the behavior of lung carcinoma cells because forced expression of Cx43 in lung carcinoma cells inhibits their growth and tumorigenicity. In this report, we summarize our studies on the role of GJIC in lung neoplasia.

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Section: Gjic and Connexin Expression Are Highly Decreased In Human Amentioning

confidence: 96%

Section: Mechanisms Of Decreased Cx43 Expression and Gjicmentioning

confidence: 99%

DEFECTIVE GAP JUNCTIONAL INTERCELLULAR COMMUNICATION IN LUNG CANCER: Loss of an Important Mediator of Tissue Homeostasis and Phenotypic Regulation

Ruch¹,

Porter²,

Koffler³

et al. 2001

Experimental Lung Research

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“…Kauffman (1981 and Anderson and Budinger (1981) have already presented evidence that such as sequence is not necessarily involved in the development of transplacentally induced lung tumours. The finding in our experiments that the papillary tumours appear earlier than the alveolar ones shows definitely that papillary tumours do not need to have an alveolar precursor; it further indicates that the two lung tumour types may indeed be different entities as proposed by Kauffman et al (1979).…”

Section: Discussionmentioning

confidence: 99%

“…For the interpretation and further analysis of effects of the H-2 complex on alveolar and papillary tumours it is important to know whether a progression of alveolar type tumours to papillary type tumours as proposed by Kimura (1973) occurs. Kauffman (1981) and Anderson and Budinger (1981) have already presented evidence that such as sequence is not necessarily involved in the development of transplacentally induced lung tumours. The finding in our experiments that the papillary tumours appear earlier than the alveolar ones shows definitely that papillary tumours do not need to have an alveolar precursor; it further indicates that the two lung tumour types may indeed be different entities as proposed by Kauffman et al (1979).…”

Section: Discussionmentioning

confidence: 99%

Multiple genes in the H‐2 complex affect differently the number and growth rate of transplacentally induced lung tumours in mice

Oomen

Démant

Hart

et al. 1983

Intl Journal of Cancer

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Although several studies have demonstrated that the H-2 haplotypes influence susceptibility to both spontaneous and carcinogen induced lung tumours in mice, little is known about the nature of their action. In this study, we analysed the effects of four haplotypes (a, h2, h4, b) with a C57BL/10ScSn background on the histological type of the tumours, their incidence, numbers and size. The tumours were studied in 8 and 16 week old progenies of mothers which were injected on the 15th day of pregnancy with N-ethyl-N-nitrosourea. Even with the limited number of haplotypes tested, our data show that the effect of H-2 genotype is both genetically and biologically complex. Lung tumours of the alveolar type were detected in appreciable numbers only in a and h2 mice, indicating that their incidence is controlled by gene(s) to the left of I-E. On the other hand, tumours of the papillary type were present in all streams in approximately the same numbers, but their size differed between strains, being largest in a mice, intermediate in h2 and h4 mice, and smallest in b mice. Moreover, in contrast to a, h2 and h4 mice, in b mice the average tumour size did not increase in the time interval between the age of 8 and 16 weeks. Apparently, several MHC genetic factors are responsible for the control of growth and incidence of the transplacentally induced lung tumours. At least one factor maps to the left of I-E, other(s) to the right of S. It is possible that these genes act through different mechanisms, since they affect the numbers of alveolar tumours, but with papillary tumours their main effect is on their size (growth intensity).

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“…In chronic interstitial pneumonia of human lung, with continuous type II cell proliferation as indicated by proliferating cell nuclear antigen staining, there was minimal apoptosis [43]. Other possibile in¯uences on tumor size, remaining to be investigated, are necrosis, cell enlargement in the absence of mitosis [44], and tumor cell shedding [45].…”

Section: DI Is Sc Cu Us Ss Si Io On Nmentioning

confidence: 99%

Ki-ras and the Characteristics of Mouse Lung Tumors

et al. 2000

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Qualitative histological differences between transplacentally-induced lung tumors in young and aging mice

Cited by 11 publications

References 10 publications

DEFECTIVE GAP JUNCTIONAL INTERCELLULAR COMMUNICATION IN LUNG CANCER: Loss of an Important Mediator of Tissue Homeostasis and Phenotypic Regulation

DEFECTIVE GAP JUNCTIONAL INTERCELLULAR COMMUNICATION IN LUNG CANCER: Loss of an Important Mediator of Tissue Homeostasis and Phenotypic Regulation

Multiple genes in the H‐2 complex affect differently the number and growth rate of transplacentally induced lung tumours in mice

Ki-ras and the Characteristics of Mouse Lung Tumors

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