Breast Cancer Microenvironment and the Metastatic Process

Breast Cancer ◽  
2017 ◽  
pp. 39-48
Author(s):  
George Sflomos ◽  
Cathrin Brisken
2019 ◽  
Author(s):  
Shahan Mamoor

Differential gene expression analysis of multiple datasets, in mice and in men revealed that transcripts of the olfactomedin-like family are differentially expressed in metastases, both in patients with breast cancer and in genetically engineered mouse models of breast cancer. The expression of olfactomedin-like genes was perturbed in metastases to the bone, brain and the lung, suggesting that these molecules function in the metastatic process rather than having tissue-specific associations with the site of dissemination. The olfactomedin-like family may play a role in the progression of breast cancer from frank tumor to colonization of distant organ sites.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Matthew R. Swiatnicki ◽  
Eran R. Andrechek

AbstractThe E2F family of transcription factors is important for many cellular processes, from their canonical role in cell cycle regulation to other roles in angiogenesis and metastasis. Alteration of the Rb/E2F pathway occurs in various forms of cancer, including breast cancer. E2F1 ablation has been shown to decrease metastasis in MMTV-Neu and MMTV-PyMT transgenic mouse models of breast cancer. Here we take a bioinformatic approach to determine the E2F1 regulated genomic alterations involved in the metastatic cascade, in both Neu and PyMT models. Through gene expression analysis, we reveal few transcriptome changes in non-metastatic E2F1−/− tumors relative to transgenic tumor controls. However investigation of these models through whole genome sequencing found numerous differences between the models, including differences in the proposed tumor etiology between E2F1−/− and E2F1+/+ tumors induced by Neu or PyMT. For example, loss of E2F1 within the Neu model led to an increased contribution of the inefficient double stranded break repair signature to the proposed etiology of the tumors. While the SNV mutation burden was higher in PyMT mouse tumors than Neu mouse tumors, there was no statistically significant differences between E2F WT and E2F1 KO mice. Investigating mutated genes through gene set analysis also found a significant number of genes mutated in the cell adhesion pathway in E2F1−/− tumors, indicating this may be a route for disruption of metastasis in E2F1−/− tumors. Overall, these findings illustrate the complicated nature of uncovering drivers of the metastatic process.


2021 ◽  
Vol 22 (5) ◽  
pp. 2267
Author(s):  
Roni H. G. Wright ◽  
Miguel Beato

Despite global research efforts, breast cancer remains the leading cause of cancer death in women worldwide. The majority of these deaths are due to metastasis occurring years after the initial treatment of the primary tumor and occurs at a higher frequency in hormone receptor-positive (Estrogen and Progesterone; HR+) breast cancers. We have previously described the role of NUDT5 (Nudix-linked to moiety X-5) in HR+ breast cancer progression, specifically with regards to the growth of breast cancer stem cells (BCSCs). BCSCs are known to be the initiators of epithelial-to-mesenchyme transition (EMT), metastatic colonization, and growth. Therefore, a greater understanding of the proteins and signaling pathways involved in the metastatic process may open the door for therapeutic opportunities. In this review, we discuss the role of NUDT5 and other members of the NUDT family of enzymes in breast and other cancer types. We highlight the use of global omics data based on our recent phosphoproteomic analysis of progestin signaling pathways in breast cancer cells and how this experimental approach provides insight into novel crosstalk mechanisms for stratification and drug discovery projects aiming to treat patients with aggressive cancer.


2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Sidar Bagbudar ◽  
Hasan Karanlik ◽  
Neslihan Cabioglu ◽  
Aysel Bayram ◽  
Kamuran Ibis ◽  
...  

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Begüm Utz ◽  
Rita Turpin ◽  
Johanna Lampe ◽  
Jeroen Pouwels ◽  
Juha Klefström

Abstract Breast cancer is the most common form of cancer in women. Despite significant therapeutic advances in recent years, breast cancer also still causes the greatest number of cancer-related deaths in women, the vast majority of which (> 90%) are caused by metastases. However, very few mouse mammary cancer models exist that faithfully recapitulate the multistep metastatic process in human patients. Here we assessed the suitability of a syngrafting protocol for a Myc-driven mammary tumor model (WAP-Myc) to study autochthonous metastasis. A moderate but robust spontaneous lung metastasis rate of around 25% was attained. In addition, increased T cell infiltration was observed in metastatic tumors compared to donor and syngrafted primary tumors. Thus, the WAP-Myc syngrafting protocol is a suitable tool to study the mechanisms of metastasis in MYC-driven breast cancer.


2019 ◽  
Vol 39 (8) ◽  
pp. 4031-4041 ◽  
Author(s):  
WATARU GOTO ◽  
SHINICHIRO KASHIWAGI ◽  
YUKA ASANO ◽  
KOJI TAKADA ◽  
KATSUYUKI TAKAHASHI ◽  
...  

Adipocyte ◽  
2020 ◽  
Vol 9 (1) ◽  
pp. 313-325
Author(s):  
Frank L. Lombardi ◽  
Naser Jafari ◽  
Kimberly A. Bertrand ◽  
Lauren J. Oshry ◽  
Michael R. Cassidy ◽  
...  

PLoS ONE ◽  
2017 ◽  
Vol 12 (3) ◽  
pp. e0174126 ◽  
Author(s):  
Jiwoo Lee ◽  
Bok Sil Hong ◽  
Han Suk Ryu ◽  
Han-Byoel Lee ◽  
Minju Lee ◽  
...  

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