Received today!
Virchows Arch. 2013 Nov 19. [Epub ahead of print]
Cancer stem cell characteristics, ALDH1 expression in the invasive front of
nasopharyngeal carcinoma.
Luo WR, Yao KT.
Cancer Research Institute, Southern Medical University, 1838 Guangzhou Road
North, Guangzhou, 510515, Guangdong, People's Republic of China,
The invasive tumor front underlies the biological aggressiveness and
epithelial-mesenchymal transition (EMT) in various human malignances. However,
the molecular and biological characteristics of invasive tumor front in NPC have
rarely been described. Additionally, the features of cancer stem cells (CSCs) in
the invasive front of tumors and its correlation with EMT also remain elusive.
Our study was to investigate the expression of CSCs marker aldehyde dehydrogenase
1 (ALDH1) in the invasive front of nasopharyngeal carcinoma (NPC) and its
clinical significance. Immunohistochemistry was mainly used to detect ALDH1
expression in the invasive front of NPC. The relationship between ALDH1
expression and EMT-associated markers was also examined. ALDH1 expression in the
invasive front correlated strongly with lymphatic invasion (p
This is connected with the subjet, I guess
Science. 2013 Dec 6;342(6163):1243259. doi: 10.1126/science.1243259.
Single-cell metabolomics: analytical and biological perspectives.
Zenobi R.
Department of Chemistry and Applied Biosciences, ETH Zürich, CH-8093 Zürich,
Switzerland.
There is currently much interest in broad molecular profiling of single cells; a
cell's metabolome-its full complement of small-molecule metabolites-is a direct
indicator of phenotypic diversity of single cells and a nearly immediate readout
of how cells react to environmental influences. However, the metabolome is very
difficult to measure at the single-cell level because of rapid metabolic
dynamics, the structural diversity of the molecules, and the inability to amplify
or tag small-molecule metabolites. Measurement techniques including mass
spectrometry, capillary electrophoresis, and, to a lesser extent, optical
spectroscopy and fluorescence detection have led to impressive advances in
single-cell metabolomics. Even though none of these methodologies can currently
measure the metabolome of a single cell completely, rapidly, and
nondestructively, progress has been sufficient such that the field is witnessing
a shift from feasibility studies to investigations that yield new biological
insight. Particularly interesting fields of application are cancer biology, stem
cell research, and monitoring of xenobiotics and drugs in tissue sections at the
single-cell level.
PMID: 24311695 [PubMed - in process]
This has a connection to the subject, I guess
Stem Cells. 2012 Feb;30(2):292-303. doi: 10.1002/stem.791.
Epithelial and mesenchymal subpopulations within normal basal breast cell lines
exhibit distinct stem cell/progenitor properties.
Sarrio D, Franklin CK, Mackay A, Reis-Filho JS, Isacke CM.
Author information:
Breakthrough Breast Cancer Research Centre, The Institute of Cancer Research,
London, United Kingdom. [email protected]
It has been proposed that epithelial-mesenchymal transition (EMT) in mammary
epithelial cells and breast cancer cells generates stem cell features, and that
the presence of EMT characteristics in claudin-low breast tumors reveals their
origin in basal stem cells. It remains to be determined, however, whether EMT is
an inherent property of normal basal stem cells, and if the presence of a
mesenchymal-like phenotype is required for the maintenance of all their stem cell
properties. We used nontumorigenic basal cell lines as models of normal stem
cells/progenitors and demonstrate that these cell lines contain an epithelial
subpopulation ("EpCAM+," epithelial cell adhesion molecule positive
[EpCAM(pos)]/CD49f(high)) that spontaneously generates mesenchymal-like cells
("Fibros," EpCAM(neg)/CD49f(med/low)) through EMT. Importantly, stem
cell/progenitor properties such as regenerative potential, high aldehyde
dehydrogenase 1 activity, and formation of three-dimensional acini-like
structures predominantly reside within EpCAM+ cells, while Fibros exhibit
invasive behavior and mammosphere-forming ability. A gene expression profiling
meta-analysis established that EpCAM+ cells show a luminal progenitor-like
expression pattern, while Fibros most closely resemble stromal fibroblasts but
not stem cells. Moreover, Fibros exhibit partial myoepithelial traits and strong
similarities with claudin-low breast cancer cells. Finally, we demonstrate that
Slug and Zeb1 EMT-inducers control the progenitor and mesenchymal-like phenotype
in EpCAM+ cells and Fibros, respectively, by inhibiting luminal differentiation.
In conclusion, nontumorigenic basal cell lines have intrinsic capacity for EMT,
but a mesenchymal-like phenotype does not correlate with the acquisition of
global stem cell/progenitor features. Based on our findings, we propose that EMT
in normal basal cells and claudin-low breast cancers reflects aberrant/incomplete
myoepithelial differentiation.
Copyright © 2011 AlphaMed Press.
PMID: 22102611 [PubMed - indexed for MEDLINE]
Nat Med. 2013 Dec 1. doi: 10.1038/nm.3418. [Epub ahead of print]
Self-renewal as a therapeutic target in human colorectal cancer.
Kreso A(1), van Galen P(2), Pedley NM(3), Lima-Fernandes E(4), Frelin C(5), Davis
T(6), Cao L(6), Baiazitov R(6), Du W(6), Sydorenko N(6), Moon YC(6), Gibson L(3),
Wang Y(3), Leung C(3), Iscove NN(7), Arrowsmith CH(8), Szentgyorgyi E(9),
Gallinger S(10), Dick JE(11), O'Brien CA(12).
Author information:
(1)1] Princess Margaret Cancer Centre, University Health Network, Toronto, Ontario,
Canada. [2] Department of Molecular Genetics, University of Toronto, Toronto,
Ontario, Canada.
(2)Princess Margaret Cancer Centre, University Health Network, Toronto, Ontario,
Canada.
(3)1] Princess Margaret Cancer Centre, University Health Network, Toronto, Ontario,
Canada. [2] Department of Laboratory Medicine and Pathobiology, University of
Toronto, Toronto, Ontario, Canada.
(4)Structural Genomics Consortium, Toronto, Ontario, Canada.
(5)1] Princess Margaret Cancer Centre, University Health Network, Toronto, Ontario,
Canada. [2] Department of Medical Biophysics, University of Toronto, Toronto,
Ontario, Canada.
(6)PTC Therapeutics, South Plainfield, New Jersey, USA.
(7)1] Princess Margaret Cancer Centre, University Health Network, Toronto, Ontario,
Canada. [2] Department of Medical Biophysics, University of Toronto, Toronto,
Ontario, Canada. [3] Department of Immunology, University of Toronto, Toronto,
Ontario, Canada.
(8)1] Princess Margaret Cancer Centre, University Health Network, Toronto, Ontario,
Canada. [2] Structural Genomics Consortium, Toronto, Ontario, Canada. [3]
Department of Medical Biophysics, University of Toronto, Toronto, Ontario,
Canada.
(9)Department of Pathology, Toronto General Hospital, Toronto, Ontario, Canada.
(10)1] Department of Surgery, Toronto General Hospital, Toronto, Ontario, Canada. [2]
Fred Litwin Centre for Cancer Genetics, Samuel Lunenfeld Research Institute,
Mount Sinai Hospital, Toronto, Ontario, Canada.
(11)1] Princess Margaret Cancer Centre, University Health Network, Toronto, Ontario,
Canada. [2] Department of Molecular Genetics, University of Toronto, Toronto,
Ontario, Canada. [3].
(12)1] Princess Margaret Cancer Centre, University Health Network, Toronto, Ontario,
Canada. [2] Department of Laboratory Medicine and Pathobiology, University of
Toronto, Toronto, Ontario, Canada. [3] Department of Surgery, Toronto General
Hospital, Toronto, Ontario, Canada. [4].
Tumor recurrence following treatment remains a major clinical challenge. Evidence
from xenograft models and human trials indicates selective enrichment of
cancer-initiating cells (CICs) in tumors that survive therapy. Together with
recent reports showing that CIC gene signatures influence patient survival, these
studies predict that targeting self-renewal, the key 'stemness' property unique
to CICs, may represent a new paradigm in cancer therapy. Here we demonstrate that
tumor formation and, more specifically, human colorectal CIC function are
dependent on the canonical self-renewal regulator BMI-1. Downregulation of BMI-1
inhibits the ability of colorectal CICs to self-renew, resulting in the
abrogation of their tumorigenic potential. Treatment of primary colorectal cancer
xenografts with a small-molecule BMI-1 inhibitor resulted in colorectal CIC loss
with long-term and irreversible impairment of tumor growth. Targeting the
BMI-1-related self-renewal machinery provides the basis for a new therapeutic
approach in the treatment of colorectal cancer.
PMID: 24292392 [PubMed - as supplied by publisher]
Natalie Turner held an e-eso lecture on: 'Metabolomics in Cancer. A bench to bedside Interaction', on sept 5, 2013, registering in e-eso and accessing CME activities is free. Have a good week. Best regards. Salut
According to many papers, ALDH1 activity is restricted to stem cell population in both healthy and tumor stem cells. Additionally, colony formation ability in vitro also should be assessed. I think the best way to prove that your cells are cancer stem cells is to use in vivo assays. Engrafment in mice e.g. is the best and exact method. Some researchers used chemotherapeutic agents to distinguish cancer stem cells and non-stem cells. Strategy is that if your cancer cells are stems than they should be resistant to those agents comparing with non-stems.
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