scholarly journals EMP2 is a novel therapeutic target for endometrial cancer stem cells

Oncogene ◽  
2017 ◽  
Vol 36 (42) ◽  
pp. 5793-5807 ◽  
Author(s):  
M H Kiyohara ◽  
C Dillard ◽  
J Tsui ◽  
S R Kim ◽  
J Lu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Endometrial Cancer ◽  
Cancer Stem Cells ◽  
Therapeutic Target ◽  
Novel Therapeutic

Abstract A54: STAT3 as a novel therapeutic target in human breast cancer stem cells

2009 ◽  
Author(s):  
Li Lin ◽  
Brian Hutzen ◽  
Zhengang Peng ◽  
Huey‐Jen Lin ◽  
Pui‐Kai Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Therapeutic Target ◽  
Human Breast Cancer ◽  
Breast Cancer Stem Cells ◽  
Human Breast ◽  
Novel Therapeutic

Abstract 2510: Iron control is a novel therapeutic target of cancer stem cells

2016 ◽  
Author(s):  
Toshiaki Ohara ◽  
Takayuki Ninomiya ◽  
Kazuhiro Noma ◽  
Hajime Kashima ◽  
Yuki Katsura ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Therapeutic Target ◽  
Novel Therapeutic

scholarly journals Novel therapeutic target for cancer stem cells in hepatocellular carcinoma

2012 ◽  
Vol 19 (6) ◽  
pp. 600-605 ◽  
Author(s):  
Hiroaki Nagano ◽  
Hideshi Ishii ◽  
Shigeru Marubashi ◽  
Naotsugu Haraguchi ◽  
Hidetoshi Eguchi ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Therapeutic Target ◽  
Novel Therapeutic

scholarly journals The Alox5 gene is a novel therapeutic target in cancer stem cells of chronic myeloid leukemia

Cell Cycle ◽  
2009 ◽  
Vol 8 (21) ◽  
pp. 3488-3492 ◽  
Author(s):  
Yaoyu Chen ◽  
Dongguang Li ◽  
Shaoguang Li
Keyword(s):  
Stem Cells ◽  
Chronic Myeloid Leukemia ◽  
Cancer Stem Cells ◽  
Therapeutic Target ◽  
Myeloid Leukemia ◽  
Novel Therapeutic

Breast Cancer Stem Cells: A Novel Therapeutic Target

2013 ◽  
Vol 13 (1) ◽  
pp. 7-15 ◽  
Author(s):  
Sudeshna Gangopadhyay ◽  
Argha Nandy ◽  
Pooja Hor ◽  
Ashis Mukhopadhyay
Keyword(s):  
Breast Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Therapeutic Target ◽  
Breast Cancer Stem Cells ◽  
Novel Therapeutic

Aberrant Hedgehog Signaling Represents a Novel Therapeutic Target in B Cell Lymphomas.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 3582-3582
Author(s):  
Qiuju Wang ◽  
Craig Peacock ◽  
Kortney Hensley ◽  
Sarah Brennan ◽  
Akil Merchant ◽  
...  
Keyword(s):  
Stem Cells ◽  
Multiple Myeloma ◽  
Cancer Stem Cells ◽  
B Cell ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Therapeutic Target ◽  
Self Renewal ◽  
Hh Signaling ◽  
Novel Therapeutic

Abstract Aberrant self-renewal is a hallmark of cancer and is central to the initiation, maintenance and relapse of clinical disease. The cellular processes responsible for self-renewal have not been delineated in most human cancers, but it is likely that conserved pathways required for the regulation of normal stem cells are involved. Notably several highly conserved signaling pathways that regulate stem cell fate decisions during embryonic development, such as Notch, Hedgehog (Hh) and Wingless (Wnt), are inappropriately activated in a wide variety of human cancers. We recently demonstrated that the Hh signaling pathway is required for the maintenance of cancer stem cells in the plasma cell malignancy, multiple myeloma. Since myeloma stem cells phenotypically resemble normal B cells, we hypothesized that aberrant Hh signaling is a feature of other B cell malignancies. We studied established human cell lines derived from patients with classical Hodgkin lymphoma (L428, KM-H2), diffuse large B cell NHL (HT, Pfeiffer, RL, and Hs 602), and mantle cell NHL (Granta 519, Jeko-1, Rec-1) and found that expression of the Hh signaling pathway components PATCHED (PTCH), SMOOTHENED (SMO), and GLI1, 2 or 3 by RT-PCR was markedly elevated compared to normal B cells in the majority of cell lines from each subtype of lymphoma. In order to examine the functional role of Hh signaling on human lymphomas, cells were treated with recombinant human sonic Hh ligand (SHh) or the naturally occurring inhibitor of SMO, cyclopamine, followed by evaluation of clonogenic growth in methylcellulose. Resulting colony formation was significantly increased in response to activating SHh ligand, whereas treatment with cyclopamine significantly inhibited clonogenic recovery. Similarly, the inhibition of pathway signaling by neutralizing anti-Hh antibodies limited colony formation suggesting that ligand binding by PTCH was required for pathway activation similar to other non-Gorlins tumors such as small cell lung cancer, pancreatic carcinoma, and metastatic prostate cancer that lack mutation of pathway components. Furthermore, we examined the activity of a novel semi-synthetic cyclopamine analogue, IPI-609, and found that it also limited clonogenic lymphoma growth. The effects of IPI-609 were highly specific as the clonogenic recovery of cell lines lacking expression of Hh pathway components was not affected by treatment. Our previous studies in multiple myeloma have suggested that cancer stem cells can be identified by their relatively higher activity of the intracellular enzyme retinaldehyde dehydrogenase (ALDH) similar to normal hematopoietic and neural stem cells. We found that high ALDH activity could also identify rare cell populations with greater clonogenic growth potential compared to ALDHlow/neg cells in the majority of lines and treatment with cyclopamine or IPI-609 significantly reduced the relative proportion of ALDHhigh cells. Therefore, the Hh signaling pathway may represent a novel therapeutic target in human lymphomas. Moreover, novel Hh inhibitors, such as IPI-609, may inhibit highly clonogenic lymphoma cancer stem cells responsible for disease relapse.

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