scholarly journals MYC gene amplification is often acquired in lethal distant breast cancer metastases of unamplified primary tumors

2011 ◽  
Vol 25 (3) ◽  
pp. 378-387 ◽  
Author(s):  
Aatur D Singhi ◽  
Ashley Cimino-Mathews ◽  
Robert B Jenkins ◽  
Fusheng Lan ◽  
Stephanie R Fink ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Amplification ◽  
Primary Tumors ◽  
Breast Cancer Metastases ◽  
Cancer Metastases ◽  
Myc Gene

High concordance of HER-2/neu gene amplification and overexpression in hematogeneous breast cancer metastases

2005 ◽  
Vol 23 (16_suppl) ◽  
pp. 626-626
Author(s):  
R. Simon ◽  
A. Kaur ◽  
P. Schraml ◽  
H. Novotny ◽  
M. Mirlacher ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Amplification ◽  
Breast Cancer Metastases ◽  
Cancer Metastases ◽  
High Concordance ◽  
Her 2

scholarly journals SNX9 promotes metastasis by enhancing cancer cell invasion via differential regulation of RhoGTPases

2016 ◽  
Vol 27 (9) ◽  
pp. 1409-1419 ◽  
Author(s):  
Nawal Bendris ◽  
Karla C. Williams ◽  
Carlos R. Reis ◽  
Erik S. Welf ◽  
Ping-Hung Chen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cell ◽  
Cell Invasion ◽  
Cancer Metastasis ◽  
Breast Cancer Metastasis ◽  
Primary Tumors ◽  
Multifunctional Protein ◽  
Breast Cancer Metastases ◽  
Cancer Metastases

Despite current advances in cancer research, metastasis remains the leading factor in cancer-related deaths. Here we identify sorting nexin 9 (SNX9) as a new regulator of breast cancer metastasis. We detect an increase in SNX9 expression in human breast cancer metastases compared with primary tumors and demonstrate that SNX9 expression in MDA-MB-231 breast cancer cells is necessary to maintain their ability to metastasize in a chick embryo model. Conversely, SNX9 knockdown impairs this process. In vitro studies using several cancer cell lines derived from a variety of human tumors reveal a role for SNX9 in cell invasion and identify mechanisms responsible for this novel function. We show that SNX9 controls the activation of RhoA and Cdc42 GTPases and also regulates cell motility via the modulation of well-known molecules involved in metastasis, namely RhoA-ROCK and N-WASP. In addition, we find that SNX9 is required for RhoGTPase-dependent, clathrin-independent endocytosis, and in this capacity can functionally substitute to the bona fide Rho GAP, GTPase regulator associated with focal adhesion kinase (GRAF1). Taken together, our data establish novel roles for SNX9 as a multifunctional protein scaffold that regulates, and potentially coordinates, several cellular processes that together can enhance cancer cell metastasis.

scholarly journals Breast cancer metastases are molecularly distinct from their primary tumors

Oncogene ◽  
2007 ◽  
Vol 27 (15) ◽  
pp. 2148-2158 ◽  
Author(s):  
M Vecchi ◽  
S Confalonieri ◽  
P Nuciforo ◽  
M A Viganò ◽  
M Capra ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Primary Tumors ◽  
Breast Cancer Metastases ◽  
Cancer Metastases

Liver Surgery for Breast Cancer Metastases

2009 ◽  
Vol 69 (05) ◽  
Author(s):  
EC Schest ◽  
H Cerwenka ◽  
A El-Shabrawi ◽  
H Bacher ◽  
HJ Mischinger
Keyword(s):  
Breast Cancer ◽  
Liver Surgery ◽  
Breast Cancer Metastases ◽  
Cancer Metastases

Deprivation of the vitamin D receptor (VDR) fuels breast cancer metastases to bone

2019 ◽  
Author(s):  
K Horas ◽  
M Abraham ◽  
F Jakob ◽  
R Ebert ◽  
G Maier ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Vitamin D ◽  
Vitamin D Receptor ◽  
Breast Cancer Metastases ◽  
Cancer Metastases

Olfactomedin-like 2A, 2B and 3 are differentially expressed in breast cancer metastases.

2019 ◽  
Author(s):  
Shahan Mamoor
Keyword(s):  
Breast Cancer ◽  
Genetically Engineered ◽  
Differentially Expressed ◽  
Genetically Engineered Mouse Models ◽  
Breast Cancer Metastases ◽  
Multiple Datasets ◽  
Cancer Metastases ◽  
Distant Organ ◽  
Metastatic Process ◽  
Differential Gene

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.

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