Disease relevance of Dnm3os

• The data reveal an unexpected capability of CD4 T cells, whereby, proinflammatory CD4+ T cells, apparently responding to bacterial infection of dysplastic skin lesions, can inadvertently enhance neoplastic progression to invasive cancer [1].
• The tumor microenvironment, which includes inflammatory cells, vasculature, extracellular matrix, and fibroblasts, is a critical mediator of neoplastic progression and metastasis [2].
• Further study delineated stages of transformation zone carcinogenesis, including formation of hyperplastic lower uterine glands and emergence of multiple foci of squamous metaplasia from individual stem-like glandular reserve cells, followed by neoplastic progression of metaplasia to dysplasia and squamous cancer [3].
• These findings show that expression of calcyclin is related to metastasis of human melanoma cell lines in nude mice and emphasize the role of this family of calcium-binding proteins in neoplastic progression as was reported for the mouse homologue of calcyclin and other members of the same family [4].
• Neoplastic progression of a low grade regressive squamous cell carcinoma, MC-T11, was also achieved in this system after in vitro exposure to ABP, N-OH-ABP, or N-OH-AABP [5].

High impact information on Dnm3os

• Proliferation, senescence, and neoplastic progression of beta cells in hyperplasic pancreatic islets [6].
• HPV16 mice deficient in CD4+ T cells were found to have delayed neoplastic progression and a lower incidence of tumors [1].
• Activation of gastrin by beta-catenin may therefore represent an early event in colorectal tumorigenesis and may contribute significantly toward neoplastic progression [7].
• Rearrangement of the int-1 and int-2 regions of mouse chromosomes was compared in the C3H and BALB/cfC3H hyperplastic alveolar nodule and its hyperplastic outgrowth (HPO) model systems by examining the DNA of the different stages of the neoplastic progression, with use of the Southern blot technique [8].
• Studies on sections representing different stages of neoplastic progression showed disruption in the antibody-staining pattern in urothelium and, in all cases, a strong distinct staining of invasive tumor areas and metastatic secondary tumors [9].

Chemical compound and disease context of Dnm3os

• The ability of salicylate to induce cell cycle arrest and apoptosis and, in particular, the increased sensitivity of cells at later stages of neoplastic progression may be mechanistically important in the chemopreventive action of aspirin toward colorectal cancer [10].
• Continual estrogen-induced proliferation might be viewed by in vivo and in vitro mechanisms by which squamous cells as well as glandular cells in cervix and vagina became permissive for neoplastic progression in HPV-18 URR E6/E7 transgenic mice and their molecular systems [11].
• Finally, further alteration in morphology and the appearance of a 177k cell surface protein were associated with the development of metastasis ability, in an early stage; loss of fibronectin and the ability to grow as macrocolonies in increasing concentrations of deoxyglucose appeared as associated to more advanced stages of neoplastic progression [12].

Biological context of Dnm3os

• We show that expression of the Dnm3 and Dnm3os transcripts overlaps during embryogenesis and in adult tissues, except that Dnm3 is most highly expressed in adult brain and testis and expressed at lower levels in embryos, whereas the antisense transcript is most strongly expressed in embryos and gravid uterus [13].
• To better understand the molecular mechanism of multistage carcinogenesis, we have attempted to identify putative oncogenes and/or tumor suppressor genes involved in preneoplastic-to-neoplastic progression of mouse epidermal JB6 variants [14].
• To test the hypothesis that elevated expression of TIMP-1 functionally regulates epithelial carcinogenesis, we introduced a human TIMP-1 transgene into K14-HPV16 transgenic mice and assessed neoplastic progression [15].
• Neoplastic progression of human and rat intestinal cell lines after transfer of the ras and polyoma middle T oncogenes [16].
• Matrix metalloproteinases (MMPs) regulate ductal morphogenesis, apoptosis, and neoplastic progression in mammary epithelial cells [17].

Anatomical context of Dnm3os

• Both Dnm3 and Dnm3os are downregulated in branchial arch tissue of Twist-null embryos [13].
• The goal of this study was to further understand the mechanism of action of tumor promotion during early neoplastic progression of human stratified epithelium [18].
• 12-O-tetradecanoylphorbol-13-acetate induces clonal expansion of potentially malignant keratinocytes in a tissue model of early neoplastic progression [18].
• It is apparent that the expression of intermediate filaments throughout neoplastic progression is best studied by use of an in vivo model system in parallel with culture studies [19].
• Synergism of v-myc and v-Ha-ras in the in vitro neoplastic progression of murine lymphoid cells [20].

Associations of Dnm3os with chemical compounds

• Although aberrant integrin expression has been documented in many epithelial tumors, little is known about how integrins influence neoplastic progression [21].
• Associated effects of bromocriptine on neoplastic progression of mouse mammary preneoplastic hyperplastic alveolar nodule line C4 and on hyperplastic alveolar nodule-infiltrating and splenic lymphocyte function [22].
• Tumorigenic transformation and neoplastic progression of human uroepithelial cells after exposure in vitro to 4-aminobiphenyl or its metabolites [5].
• The effects of estradiol on neoplastic progression of estrogen-receptor-positive MCF10AT cells in the orthotopic site were examined in ovariectomized female nude mice that received subcutaneous administration of implants of 17beta-estradiol or placebo pellets [23].
• Synergy of IL-7 and v-Ha-ras in the in vitro neoplastic progression of murine pre-B cells [24].

Regulatory relationships of Dnm3os

• Pdcd4 mRNA was also expressed at greater levels in the less progressed keratinocytes of another mouse skin neoplastic progression series [25].
• Using a novel transgenic mouse model of spontaneous mammary carcinoma, we show here that the IL-12/pulse IL-2 combination can induce rapid and complete regression of well-established autochthonous tumor in a setting where the host immune system has been conditioned by the full dynamic process of neoplastic progression and tumorigenesis [26].
• Thus, in view of evidence that tumors can derive from tissue stem cells and that tumors harbor "cancer stem cells," aberrant K-ras expression could promote neoplastic progression by increasing their capacity for self-renewal [27].
• Expression of keratin and vimentin intermediate filaments in rabbit bladder epithelial cells at different stages of benzo[a]pyrene-induced neoplastic progression [19].

Other interactions of Dnm3os

• A 6-kb antisense transcript (Dnm3os) contained within an intron of the mouse Dnm3 gene has been identified in a screen for genes that may be regulated by the basic helix-loop-helix transcription factor Twist during mouse development [13].
• The tissue inhibitor of metalloproteinases-3 (TIMP-3) gene is specifically down-regulated in neoplastic cells of the mouse JB6 progression model, suggesting a role for TIMP-3 inactivation in neoplastic progression [28].
• We investigated the hypothesis that there are significant alterations in the levels of apoptotic protein as well as p21 protein expression in the neoplastic progression associated with Barrett's metaplasia [29].
• In the epidermis of transgenic mice in which expression of the HPV16 E6 and E7 oncogenes are targeted to basal keratinocytes, neoplastic progression occurs and is marked by an expansion of c-myc expressing basal-like cells [30].
• These observations, together with our recent finding attributing AP-1 non-responsiveness to Erk deficiency in a clonal line of transformation resistant (P-) cells, argue for a requirement for Erks1 and/or 2 activation in AP-1 transactivation in the mouse JB6 neoplastic progression model, and suggest the utility of Erks as a prevention target [31].

Analytical, diagnostic and therapeutic context of Dnm3os

• A cell culture model system has been used to study the susceptibility of cells to apoptotic cell death during different stages of neoplastic progression [32].
• In this study, we examined the relationship between C-CAM expression during human prostate development and neoplastic progression by immunohistochemical staining of frozen sections [33].
• The intratracheal inoculation and xenotransplantation of human-derived cell lines offers a time-saving alternative to the s.c. inoculation assay for tumorigenicity and is at the same time a potentially valuable approach to studying preneoplastic and neoplastic progression with human cell subpopulations [34].
• A combination of immunologic tests, cell culture studies, and tumorigenicity assays indicates that alpha-melanocyte-stimulating hormone, which is overproduced by melanotroph tumors, attenuates neoplastic progression by decreasing cell proliferation and inducing apoptosis [35].
• Using immunohistochemistry and RT-PCR, we show that Rhamm, a protein with an important role in wound healing and neoplastic progression, is also expressed at high levels in aggressive fibromatosis [36].

References