scholarly journals Human Mammary Tumor Virus, Human Papilloma Virus, and Epstein-Barr Virus Infection Are Associated With Sporadic Breast Cancer Metastasis

2020 ◽  
Vol 14 ◽  
pp. 117822342097638
Author(s):  
Mohammad Al Hamad ◽  
Ismail Matalka ◽  
Mazhar Salim Al Zoubi ◽  
Ivana Armogida ◽  
Rawan Khasawneh ◽  
...  

Background: Viral cause of sporadic breast cancer (SBC) has been suggested based on the experimental murine model of mammary tumor caused by mouse mammary tumor virus (MMTV), Epstein-Barr virus (EBV), and human papillomavirus (HPV). While some studies have demonstrated the presence of viral sequences of MMTV, HPV, and EBV in breast cancer cells, others failed. These contradictions may be attributed to the geographical distribution of breast cancer incidence and/or technical variations. In the current study, we aimed to investigate the correlation of MMTV, HPV, and EBV infections with the development of breast cancer in Jordanian patients. Methods: One hundred SBC tissue samples were subjected to laser capture microdissection for the selection of tumor cells populations. Fluorescence polymerase chain reaction (PCR) was used to detect the presence of the MMTV env-like sequences. Real-time PCR was used for HPV and EBV detection, and EBV was further confirmed by chromogen in situ hybridization (CISH). Results: Mouse mammary tumor virus, HPV, and EBV were detected in SBC in 11%, 21%, and 23%, respectively. Only 3 of 52 (5.7%) positive cases demonstrated multiple virus infections. However, 49 of 52 (94%) of the positive cases revealed the presence of 1 type of viral sequences. Consequently, 52% of the studied breast cancer cases were infected with at least 1 type of the aforementioned viruses. Conclusions: The current cohort suggests that MMTV, HPV, and EBV have a potential role in the development of breast cancer and adding more reasons to proceed with the quest of a possible viral origin of breast cancer.

2013 ◽  
Vol 3 (1) ◽  
Author(s):  
Abigail Morales-Sánchez ◽  
Tzindilú Molina-Muñoz ◽  
Juan L. E. Martínez-López ◽  
Paulina Hernández-Sancén ◽  
Alejandra Mantilla ◽  
...  

2015 ◽  
Vol 29 (10) ◽  
pp. 1468-1485 ◽  
Author(s):  
Cecilia J. Proietti ◽  
Franco Izzo ◽  
María Celeste Díaz Flaqué ◽  
Rosalía Cordo Russo ◽  
Leandro Venturutti ◽  
...  

Abstract Accumulated findings have demonstrated the presence of bidirectional interactions between progesterone receptor (PR) and the ErbB family of receptor tyrosine kinases signaling pathways in breast cancer. We previously revealed signal transducer and activator of transcription 3 (Stat3) as a nodal convergence point between said signaling pathways proving that Stat3 is activated by one of the ErbBs' ligands, heregulin (HRG)β1 via ErbB2 and through the co-option of PR as a signaling molecule. Here, we found that HRGβ1 induced Stat3 recruitment to the promoters of the progestin-regulated cell cycle modulators Bcl-XL and p21CIP1 and also stimulated Stat3 binding to the mouse mammary tumor virus promoter, which carries consensus progesterone response elements. Interestingly, HRGβ1-activated Stat3 displayed differential functions on PR activity depending on the promoter bound. Indeed, Stat3 was required for PR binding in bcl-X, p21CIP1, and c-myc promoters while exerting a PR coactivator function on the mouse mammary tumor virus promoter. Stat3 also proved to be necessary for HRGβ1-induced in vivo tumor growth. Our results endow Stat3 a novel function as a coregulator of HRGβ1-activated PR to promote breast cancer growth. These findings underscore the importance of understanding the complex interactions between PR and other regulatory factors, such as Stat3, that contribute to determine the context-dependent transcriptional actions of PR.


2004 ◽  
Vol 64 (12) ◽  
pp. 4105-4111 ◽  
Author(s):  
Yue Wang ◽  
Jian-Dong Jiang ◽  
Dongping Xu ◽  
Yan Li ◽  
Chunfeng Qu ◽  
...  

1984 ◽  
Vol 33 (3) ◽  
pp. 305-308 ◽  
Author(s):  
P. H. Levine ◽  
R. Mesa-Tejada ◽  
I. Keydar ◽  
F. Tabbane ◽  
S. Spiefelman ◽  
...  

Oncology ◽  
2002 ◽  
Vol 62 (1) ◽  
pp. 78-84 ◽  
Author(s):  
Hirobumi Mizunuma ◽  
Kyotaro Kanazawa ◽  
Shigeto Ogura ◽  
Shin Otsuka ◽  
Hideo Nagai

2008 ◽  
Vol 80 (8) ◽  
pp. 1447-1451 ◽  
Author(s):  
Hidetoshi Fukuoka ◽  
Masako Moriuchi ◽  
Hiroshi Yano ◽  
Takeshi Nagayasu ◽  
Hiroyuki Moriuchi

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