Abstract B22: Capturing L1 retrotransposon-mediated DNA transductions in endometriosis associated ovarian cancers as a way to track tumor development

Author(s):  
Zhouchunyang Xia ◽  
Dawn Cochrane ◽  
Michael Anglesio ◽  
Winnie Yang ◽  
Miguel Alcaide ◽  
...  
2018 ◽  
Author(s):  
Kate Lawrenson ◽  
Marcos A.S. Fonseca ◽  
Felipe Segato ◽  
Janet M. Lee ◽  
Rosario I. Corona ◽  
...  

AbstractHistorically, high-grade serous ovarian cancers (HGSOCs) were thought to arise from ovarian surface epithelial cells (OSECs) but recent data implicate fallopian tube secretory epithelial cells (FTSECs) as the major precursor. We performed transcriptomic and epigenomic profiling to characterize molecular similarities between OSECs, FTSECs and HGSOCs. Transcriptomic signatures of FTSECs were preserved in most HGSOCs reinforcing FTSECs as the predominant cell-of-origin; though an OSEC-like signature was associated with increased chemosensitivity (Padj= 0.03) and was enriched in proliferative-type tumors, suggesting a dualistic model for HGSOC origins. More super-enhancers (SEs) were shared between FTSECs and HGSOCs than between OSECS and HGSOCs (P< 2.2 × 10−16). SOX18, ELF3 and EHF transcription factors (TFs) coincided with HGSOC SEs and represent putative novel drivers of tumor development. Our integrative analyses support a predominantly fallopian origin for HGSOCs and indicate tumorigenesis may be driven by different TFs according to cell-of-origin.


Cancers ◽  
2021 ◽  
Vol 13 (20) ◽  
pp. 5040
Author(s):  
Maja Sabol ◽  
Jean Calleja-Agius ◽  
Riccardo Di Di Fiore ◽  
Sherif Suleiman ◽  
Sureyya Ozcan ◽  
...  

Rare ovarian cancers (ROCs) are OCs with an annual incidence of fewer than 6 cases per 100,000 women. They affect women of all ages, but due to their low incidence and the potential clinical inexperience in management, there can be a delay in diagnosis, leading to a poor prognosis. The underlying causes for these tumors are varied, but generally, the tumors arise due to alterations in gene/protein expression in cellular processes that regulate normal proliferation and its checkpoints. Dysregulation of the cellular processes that lead to cancer includes gene mutations, epimutations, non-coding RNA (ncRNA) regulation, posttranscriptional and posttranslational modifications. Long non-coding RNA (lncRNA) are defined as transcribed RNA molecules, more than 200 nucleotides in length which are not translated into proteins. They regulate gene expression through several mechanisms and therefore add another level of complexity to the regulatory mechanisms affecting tumor development. Since few studies have been performed on ROCs, in this review we summarize the mechanisms of action of lncRNA in OC, with an emphasis on ROCs.


Author(s):  
U.I. Heine ◽  
G.R.F. Krueger ◽  
E. Munoz ◽  
A. Karpinski

Infection of newborn mice with Moloney leukemia virus (M-MuLV) causes a T-cell differentiation block in the thymic cortex accompanied by proliferation and accumulation of prethymic lymphoblasts in the thymus and subsequent spreading of these cells to generate systemic lymphoma. Current evidence shows that thymic reticular epithelial cells (REC) provide a microenvironment necessary for the maturation of prethymic lymphoblasts to mature T-lymphocytes by secretion of various thymic factors. A change in that environment due to infection of REC by virus could be decisive for the failure of lymphoblasts to mature and thus contribute to lymphoma development.We have studied the morphology and distribution of the major thymic cell populations at different stages of tumorigenesis in Balb/c mice infected when newborn with 0.2ml M-MuLV suspension, 6.8 log FFU/ml. Thymic tissue taken at 1-2 weekly intervals up to tumor development was processed for light and electron microscopy, using glutaraldehyde-OsO4fixation and Epon-Araldite embedding.


Author(s):  
S.K. Aggarwal ◽  
J. San Antonio

Cisplatin (cis-dichlorodiammineplatinum(II)) a potent antitumor agent is now available for the treatment of testicular and ovarian cancers. It is however, not free from its serious side effects including nephrotoxicity, gastro intestinal toxicity, myelosuppression, and ototoxicity. Here we now report that the drug produces peculiar bloating of the stomach in rats and induces acute ulceration.Wistar-derived rats weighing 200-250 g were administered cisplatin(9 mg/kg) ip as a single dose in 0.15 M NaCl. After 3 days the animals were sacrificed by decapitation. The stomachs were removed, the contents analyzed for pepsin and acidity. The inner surface was examined with a dissecting microscope after a moderate stretching for ulcers. Affected areas were fixed and processed for routine electron microscopy and enzyme cytochemistry.The drug treated animals kept on food and water consistently showed bloating and lesions (Fig. 1) with a frequency of 6-70 ulcers in the rumen section of the stomachs.


1998 ◽  
Vol 5 (1) ◽  
pp. 82A-82A
Author(s):  
A MUNKARAH ◽  
L BAZZETT ◽  
F QURESHI ◽  
S JACQUES ◽  
R MORRIS ◽  
...  

2003 ◽  
Vol 31 (5) ◽  
pp. 539-548 ◽  
Author(s):  
Veera Näyhä ◽  
Jaakko Laitakari ◽  
Frej Stenbäck
Keyword(s):  

2014 ◽  
Vol 68 (1) ◽  
pp. 8-15
Author(s):  
Lena Kakasheva-Mazhenkovska ◽  
Vesna Janevska ◽  
Gordana Petrushevska ◽  
Liljana Spasevska ◽  
Neli Basheska

Abstract The stroma of the neoplasm is a highly complex structure built by: specialized mesenchymal cells typical for each tissue surroundings, cancer associated fibroblast/myofibroblast, congenital or acquired immune cells, vascular network with endothelial cells and pericytes, mastocytes, macrophages, leukocytes and adipocytes, all together incorporated in the extracellular matrix. Each neoplasm produces its own unique microenvironment where the tumor grows and modifies. Although most of the cells of the host in the stroma have compulsory tumor suppressor ability, the stroma is changing during the malignant process and it even promotes growth, invasion and metastasis. Genetic changes that occur during the development of the cancer, which are guided by the malignant cells lead to changes in the stroma of the host that will overtake it and adjust it to their own needs. In the early stages of the tumor development and invasion, the basal membrane is degraded and the stroma becomes active and contains an increased number of fibroblasts, inflammatory infiltrate and newly composed capillaries which come into direct contact with the tumor cells. These changes lead to cancer invasion.


Sign in / Sign up

Export Citation Format

Share Document