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出门在外也不愁World J Gastroenterol
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14-1219/R& World
J Gastroenterol& 2008
28;14(24): &&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&
&&&&RAPID COMMUNICATION
Isolation and biological analysis of tumor stem cells from
pancreatic adenocarcinoma Peng
Huang, Chun-You Wang, Shan-Miao Gou, He-Shui Wu, Tao Liu, Jiang-Xin
Peng Huang, Chun-You Wang, Shan-Miao Gou, He-Shui Wu,
Tao Liu, Jiang-Xin Xiong,
Department of Pancreatic Surgery, Union Hospital, Tongji Medical
College, Huazhong University of Science and Technology, Wuhan
430022, Hubei Province, China
Author contributions:
Huang P and Wang CY contributed
Huang P, Wang
CY, Gou SM, Wu HS, Liu T and Xiong JX d Huang P
and Gou SM pe Wang CY provided new
reagents/ Huang P and Huang P and Wang
CY wrote the paper.
Supported by
The National Natural Science Foundation of China, No.
Correspondence to: Chun-You Wang,
Department of Pancreatic Surgery, Union Hospital, Tongji Medical
College, Huazhong University of Science and Technology, Wuhan
430022, Hubei Province, China.
Telephone:
November 19, 2007&
February 16, 2008
February 23, 2008
Published online:
June 28, 2008
To explore the method of isolation and biological analysis of tumor
stem cells from pancreatic adenocarcinoma cell line PANC-1.
The PANC-1 cells were cultured in Dulbecco modified eagle medium F12
(1:1 volume) (DMEM-F12) supplemented with 20% fetal bovine serum (FBS).
Subpopulation cells with properties of tumor stem cells were
isolated from pancreatic adenocarcinoma cell line PANC-1 according
to the cell surface markers CD44 and CD24 by flow cytometry. The
proliferative capability of these cells in vitro were estimated by
3-[4,5-dimehyl-2-thiazolyl]-2, 5-diphenyl-2H-tetrazolium bromide (MTT)
method. And the tumor growth of different subpopulation cells which
were injected into the hypodermisof right and left armpit of nude
mice was studied, and expression of CD44 and CD24 of the CD44+CD24+
cell-formed nodules and PANC-1 cells were detected by
avidin-biotin-peroxidase complex (ABC) immunohistochemical staining.
The 5.1%-17.5% of sorted PANC-1 cells expressed the cell surface
marker CD44, 57.8% -70.1% expressed CD24, only 2.1%-3.5% of cells
were CD44+ CD24+. Compared with CD44-CD24-
cells, CD44+CD24+ cells had a
lower growth rate in vitro. Implantation of 104 CD44-CD24-
cells in nude mice showed no evident tumor growth at
wk 12. In contrast, large tumors were found in nude mice implanted
with 103 CD44+CD24+ cells at wk 4
(2/8), a 20-fold increase in tumorigenic potential (P & 0.05
or P & 0.01). There was no obvious histological difference
between the cells of the CD44+CD24+
cell-formed nodules and PANC-1 cells.
CONCLUSION:
CD44 and CD24 may be used as the cell surface markers for isolation
of pancreatic cancer stem cells from pancreatic adenocarcinoma cell
line PANC-1. Subpopulation cells CD44+CD24+
have properties of tumor stem cells. Because cancer stem cells are
thought to be responsible for tumor initiation and its recurrence
after an initial response to chemotherapy, it may be a very
promising target for new drug development.
(C) 2008 The WJG Press. All rights reserved.
Key words:
Identification
Peer reviewers:
Minoti V Apte, Associate Professor, Pancreatic Research Group, South
Western Sydney Clinical School, The University of New South Wales.
Liverpool, NSW 2170, Australia
Huang P, Wang CY, Gou SM, Wu
HS, Liu T, Xiong JX. Isolation and biological analysis of tumor stem
cells from pancreatic adenocarcinoma.
World J Gastroenterol
): & Available from: URL: //3903.asp&
DOI: http://dx.doi.org/10.3748/wjg.14.3903
INTRODUCTION
Pancreatic carcinoma is an obstinate disease that is
difficult to deal with. Though pancreatic cancer accounts for only
2%-3% of all cancers, it is the fourth most frequent cause of cancer
death in industrialized countries[1]. It is estimated in
the United States in 1998 that at least 29&# new cases of
pancreatic cancer will be diagnosed[2]. Unfortunately,
only 18% will survive one year after diagnosis, the five-year
survival rate is 4%.
This is because by the time a patient exhibits
symptoms, and the cancer is diagnosed, it is no longer in its early
stage[3-5]. The main conventional treatments for
pancreatic cancer are surgery, radiation therapy and chemotherapy.
Despite advances in surgical and medical therapy, little effect has
been made on the mortality rate of this disease. According to
Bjerkvig et al[6], the capacity of a tumor to grow
and propagate is dependent on a small subset of cells (so-called
tumor stem cells), tumor stem cells are immature cells that can
replicate or self-renew, and are able to differentiate or grow into
all the cells that an organism or particular organ system need. It
has profound implications to understand how tumors evolve and how we
treat tumors. If we can destroy these tumor stem cells, it will be
possible to treat the patients successfully. However, it is
difficult to purify tumor stem cells because of lack of specific
cell surface markers in solid tumors. Recently, it was reported that
cancer stem cells existed in some solid malignancies, including
breast[7], brain[8,9], prostate[10],
and lung cancers[11]. Thus, we deduced that pancreatic
cancer might contain its own stem cells responsible for its
metastasis and recurrence. To prove this hypothesis, we isolated
subpopulation cells that have characteristics of tumor stem cells
according to markers CD44 and CD24 by flow cytometry from pancreatic
adenocarcinoma cell line PANC-1, and explore their biological
characteristics. This study was to identify the method of isolation
of pancreatic tumor stem cells and the ability of propagation of the
tumor stem cells in vitro and in vivo.
MATERIALS AND METHODS
Experimental materials
Male nude mice, aged 6-8 wk and weighing 20 ± 2 g,
were provided by the Experimental Animal Center, Hubei Center for
Disease Control and Prevention, China. The nude mice were caged
individually under specific pathogen free (SPF) conditions. Human
pancreatic adenocarcinoma cell line PANC-1 was obtained from
American Type Culture Collection, Manassas, Virginia, the Dulbecco
modified eagle medium F12 (1:1 volume) (DMEM-F12) from Hyclone,
Wuhan, China, the fetal bovine serum from Sijiqing, Hangzhou, China,
trypsin from Sigma-Aldrich, Shanghai, China, the epidermal growth
factor (EGF), basic fibroblast growth factor (b-FGF), insulin-transferrin-selenium
solution (ITS) and trypsin from Sigma-Aldrich, Shanghai, China and
PE anti-human CD44 and FITC anti-human CD24 were purchased from
American Ancell.
Cell culture
cells were cultured in incubator filled with 5% CO2 at
37℃. The PANC-1 cells were cultured in DMEM-F12 (1:1 volume)
supplemented with 20% fetal bovine serum (FBS), penicillin (1 × 105
U/L) and streptomycin (100 mg/L).
Flow cytometric analysis
Cells were dissociated by trypsin-EDTA solution (trypsin,
0.25%; EDTA, 0.02%) for 2-5 min at 37℃, transferred to a 5-mL tube,
washed twice with PBS with 2% heat-inactivated calf serum (HICS; 5
min at 1000 r/min), resuspended in 100 mL (per 106 cells)
of PBS, then were counted. PE anti-human CD44 and (or) FITC
anti-human CD24 (appropriate dilution per antibody) were added and
incubated for 30 min at 4℃, and then washed twice with PBS. Flow
cytometry was performed on a FACS, and data were analyzed with the
Cell Quest software (B.D., America). Using forward and side scatter
profile, debris and dead cells were gated out. Cells were routinely
sorted twice, and& reanalyzed for purity. Then CD44+,
cells, CD44+CD24+ and CD44-CD24-and
unsorted cells were obtained.
Estimation of proliferative capability of cells in
CD44+CD24+, CD44-CD24-
and unsorted cells were diluted to a density of about 104
cells/mL with serum-free medium (SFM), a mixture of DMEM-F12
containing 10 ng/mL fibroblast and 20 ng/mL epidermal growth
factors, 5 kg/mL insulin,
2.75 mg/mL transferrin, 2.75 ng/mL selenium (insulin-transferrin-selenium
solution), penicillin (1 × 105 U/L) and streptomycin (100
mg/L). The 200-mL/well diluted cell suspension was plated to 96-well
culture dishes. The wells with 2 × 103 cells were
observed everyday under an Olympus CKX41 the images were
captured using an Olympus C5050Z camera. Each group was set up with
five duplicate holes. Their OD values were measured with
spectrophotometer at 490 nm by 3-[4,5-dimehyl-2-thiazolyl]-2,
5-diphenyl-2H-tetrazolium bromide (MTT) method, and a 96-well plate
was determined every 24h. The mean value was obtained and a growth
curve was drawn.
Transplantation of cells into nude mice
resuspension, CD44+, CD44-,
CD24+, CD24-,
CD44+CD24+, CD44-CD24-
and unsorted cells were diluted to a density of about
5 × 106 to 5 × 103 cells/mL with SCM. The
cells (0.1 mL) were injected into the hypodermis of right and left
armpit of nude mice. The mice were maintained in a specific
pathogen-free room under constant temperature and humidity.
Immunohistochemical staining of CD44 and CD24
All samples of the CD44+CD24+
cell-formed nodules were placed into 10% formalin immediately,
processed with routine histological procedures, and embedded in
paraffin. Serial sections were cut 5 mm thick, and parts of them
were stained with hematoxylin and eosin for routine histological
observation under light microscope. The others were used for
immunohistochemical examination for the CD44 and CD24. After
deparaffinization (hydration), sections were treated sequentially
with normal goat serum, anti-human CD44 polyclonal antibody (1:200)
or anti-human CD24 polyclonal antibody (1:200), biotin-labeled goat
anti-mouse IgG, and avidin-biotin-peroxidase complex (ABC). The
sites of peroxidase binding were demonstrated by the
diaminobenzidine method. Sections were then counterstained with
hematoxylin for microscopic examination. Similar procedures were
done for the PANC-1 cells. The numbers and areas of CD44-positive
and CD24-positive foci & 0.2 mm in diameter and the total areas of
the examined sections were measured using a Olympus C5050Z digital
camera, Adobe Photoshop version 7.0, and Image-Pro Plus version 6.0.
Statistical analysis
Data were expressed as means ± SD, and were analyzed
with SPSS 12.0, P & 0.05 was considered significant in
difference.
Presence of CD44 and CD24 on cell surface of
pancreatic carcinoma cell lines
determine the presence of CD44 and CD24 on the cell surface of the
PANC-1 cells, flow cytometric analysis was made. The cell surface
markers CD44 and CD24 were chosen as a starting point based on prior
work on breast cancer stem cells, in which CD44+CD24-/lowLineage
tumorigenic cells generated tumors histologically similar to primary
breast tumors when as few as 100 cells were transplanted, whereas
tens of thousands of bulk unsorted cancer cells were needed to form
tumors in NOD/SCID mice[7]. CD44 and CD24 have been
identified as the stem cell surface markers, which act as adhesive
molecules with multiple signaling functions[12-14]. As
shown in , 5.1%- 17.5% of sorted PANC-1 cells expressed the
cell surface marker CD44, and 57.8%-70.1% expressed CD24. When
expression of multiple surface markers was examined, only 2.1%-3.5%
of cells were CD44+ CD24+ (Figure 1).
Proliferation potential of cells in vitro
To evaluate the proliferation ability of cells in
vitro, the CD44+CD24+, CD44-CD24-
and unsorted cells were cultured in SCM in 96-well culture dishes,
their OD values were measured with spectrophotometer at 490nm by MTT
method. Compared with CD44-CD24-
cells, CD44+CD24+ cells had a lower growth
rate and longer doubling time in vitro. For the former, the
index growth trend appeared at the 5th day, while the latter
appeared at the day 7 ().
Establishment of xenografts
To test the capability of tumor initiation, we
injected cells into the hypodermis of right and left armpit of nude
mice. When unsorted PANC-1 cells (5 × 103) were injected,
no tumor growth was found at wk 12 while 104 cells were
injected, one of six mice developed tumors. For cancer cells sorted
for the markers CD44 and CD24, expression of individual markers
identified cell populations with enhanced tumorigenic potential. For
example, injection of 5 × 103 CD44+ cells
would occasionally form a tumor (1 of 6 animals), whereas no tumor
was observed with CD44-
cells until at least 5 × 104 cells were injected (1 of 10
animals). Six of 10 animals developed tumors when injected with 5 ×
104 CD44+ cells, representing a 10-fold
increase in tumorigenic potential compared with marker negative
cells (P = 0.029). Similar results were obtained with CD24+.
Injection of CD44+CD24+ cells resulted in an
enhanced tumorigenic potential compared with single marker sorted
cells. More tumors formed with injection of as few as 103
cells, and no tumor formed in marker-negative cells until at least 5
× 104 cells were injected. The sorted cell population
with the highest tumorigenic potential was those expressing CD44 and
CD24. For example, injection of 104 CD44-CD24-
cells in nude mice found no tumor growth at wk 12. In
contrast, nude mice injected with 103 CD44+CD24+
cells had large tumors at wk 4 (2 of 8), a 20-fold increase in
tumorigenic potential (P & 0.05 or P & 0.01) (). There was no obvious histological difference between the CD44+CD24+
cell-formed nodules and PANC-1 cells.
CD44- and CD24- positive
numbers and areas
For sections stained with hematoxylin and eosin,
tumor cells with variable shape from polygon, spindle to irregular
were seen under light microscope. The total CD44-
positive and CD24- positive numbers and areas in the
examined sections were measured using an Olympus C5050Z digital
camera, Adobe Photoshop version 7.0, and Image-Pro Plus version 6.0.
There was no significant difference in quantitative values of CD44+
and CD24+ cells between the formed nodules and the PANC-1
cells (P & 0.05) ().
DISCUSSION
The theory of tumor stem cells[15,16]
indicates that tumor cells have heterogeneity, i.e., the majority of
cells in the tumor have lost the growth potential, only a small
subset of cells have the capability of the infinite proliferation,
the differentiation and the formation of cloning in vitro.
The initial isolation and identification of tumor stem cells was
first proved in hematological malignancies. The CD34+CD38-
phenotype cells (5% of the cancer cells) with obvious
proliferation, differentiation and self-renewal ability were
purified from the blood of the patients with acute myeloid leukemia[17,18].
In 2003, researchers found that only a small subset of human breast
cancer cells, with the phenotype CD44+CD24-,
formed new tumors in NOD/SCID mice[7]. These breast
cancer-initiating cells can be isolated and propagated in vitro
as extensively proliferating, clonal, nonadherent spherical
clusters& are able to differentiate along different mammary
epithelial lineages[19]. A small population of
cancer-initiating cells (also called cancer stem cells) was later
found in several malignancies, including brain[8],
prostate[10], liver[20,21], lung[22],
melanoma[23], and colon tumors[24,25].
Although there is increasing evidence that a rare
population of undifferentiated cells is responsible for tumor
formation and maintenance, little work has been done on the
identification of pancreatic cancer special surface markers or on
isolation of pancreatic tumor-initiating cells. Based on studies in
breast cancer[7] and pancreatic adenocarcinoma[16],
we identified cells with the characteristics of tumor stem cells
according to the cell surface markers CD44 and CD24 by flow
cytometry from pancreatic adenocarcinoma cell line PANC-1. Tumor
stem cells have the capability to maintain themselves in culture in
an undifferentiated state, initiate tumor growth after
xenotransplantation in mice, and differentiate into cancers that are
phenotypically indistinguishable from the original tumor. We found
that 5.1%-17.5% of sorted PANC-1 cells expressed the cell surface
marker CD44, 57.8%-70.1% expressed CD24, and only 2.1%-3.5% of cells
were CD44+CD24+. To take a small subset of
cells and put it in the organism and see if it regenerates the
original tissues is the classic definition of a stem cell. We
injected cells into the hypodermis of the right and left armpit of
nude mice to test the capability of tumor initiation. When 5 × 103
unsorted PANC-1 cells were injected into nude mice, no tumor grew at
wk 12 unless at least 104 cells were injected. For cancer
cells sorted for the markers CD44 and CD24, injection of 5 × 103
CD44+ cells would form a tumor, whereas no tumor was
observed with CD44-cells
until at least 5 × 104 cells were injected. Similar
results were obtained with CD24+. The sorted cell
population with the highest tumorigenic potential was those cells
expressing CD44 and CD24. For instance, injection of 104
CD44-CD24-
cells into nude mice, no tumor growth was evident at
wk 12. In contrast, nude mice injected with 103 CD44+CD24+
cells had large tumors at wk 4. Moreover, the CD44+CD24+
cells maintained the ability to engraft and reproduce the same
histological and antigenic pattern of the PANC-1. In addition,
compared with CD44-CD24- cells in vitro,
CD44+CD24+ cells had a lower growth rate. The
reason is that tumor stem cells are similar to stem cells, which& is
in relatively static group of cells, and besides other primates, the
stem cell pool proliferates once a year[26]. For the CD44+CD24+
cells, there were biological behaviors of the lower proliferative
index and the faster tumor growth rate in vivo. It is
self-contradictory. The reason awaits& further studies. In addition,
there was no obvious histological difference between the CD44+CD24+
cell-formed nodules and PANC-1 cells.
above results showed that CD44 and CD24 may be used as markers for
isolation of pancreatic cancer stem cells from pancreatic
adenocarcinoma cell line PANC-1, subpopulation cells CD44+CD24+
have the characteristics of tumor stem cells. The purification and
other biological behaviors of pancreatic adenocarcinoma stem cells
need to be further studied in the future.
Background
Pancreatic carcinoma is an obstinate disease that is difficult to
deal with. Though pancreatic cancer accounts for only 2%-3% of all
cancers, it is the fourth most frequent cause of cancer deaths in
industrialized countries. Unfortunately, only 18% will survive one
year after diagnosis, the five-year survival rate is only 4%.
Conventional main treatments for pancreatic cancer are surgery,
radiation therapy and chemotherapy. Despite advances in surgical and
medical therapy, little effect has been achieved on the mortality
rate of this disease.
Research frontiers
initial isolation and identification of tumor stem cells was first
proved in hematological malignancies. The CD34+CD38-
phenotype cells (5% of the cancer cells) with obvious proliferation,
differentiation and self-renewal ability had been purified from the
blood of the patients with acute myeloid leukemia. Researchers have
discovered a small population of cancer-initiating cells (also
called cancer stem cells) in several malignancies, including brain,
prostate, liver, lung, melanoma, and colon tumors.
Innovations and breakthroughs
authors isolated pancreatic adenocarcinoma cell line PANC-1
according to the cell surface markers CD44 and CD24 by flow
cytometry, obtained subpopulation cells which have properties of
tumor stem cells, and identified the ability of propagation of the
tumor stem cells
Applications
Because cancer stem cells are thought to be responsible for tumor
initiation and its recurrence after an initial response to
chemotherapy, it may be a very promising target for new drug
development.
Peer review
study corroborates a recent publication in the pancreas reporting
that a subpopulation of Panc1 cells can propagate to form spheres
and that these cells express stem cell markers such as CD44. The
study is very interesting.
ACKNOWLEDGMENT
thank our colleagues from the Research Laboratory of General
Surgery, Union Hospital, Wuhan, for their technical assistance.
REFERENCES
1&&&&& Bardeesy N, DePinho RA. Pancreatic cancer biology and
genetics. Nat Rev Cancer 2002; 2: 897-909&
2&&&&& Murphy SL. Deaths: final data for 1998. Natl Vital
Stat Rep 2000; 48: 1-105&
3&&&&& Cameron JL, Crist DW, Sitzmann JV, Hruban RH, Boitnott
JK, Seidler AJ, Coleman J. Factors influencing survival after
pancreaticoduodenectomy for pancreatic cancer. Am
J Surg 1991; 161: 120-124; discussion 124-125&
4&&&&& Niederhuber JE, Brennan MF, Menck HR. The National
Cancer Data Base report on pancreatic cancer. Cancer 1995;
5&&&&& Jemal A, Thomas A, Murray T, Thun M. Cancer
statistics, 2002. CA Cancer J Clin 2002; 52: 23-47&
6&&&&& Bjerkvig R, Tysnes BB, Aboody KS, Najbauer J, Terzis AJ. Opinion:
the origin of the cancer stem cell: current
controversies and new insights. Nat Rev Cancer
2005; 5: 899-904&
7&&&&& Al-Hajj M, Wicha MS, Benito-Hernandez A, Morrison SJ,
Clarke MF. Prospective identification of tumorigenic breast
cancer cells. Proc Natl Acad Sci USA 2003;
8&&&&& Singh SK, Clarke ID, Terasaki M, Bonn VE, Hawkins C,
Squire J, Dirks PB. Identification of a cancer stem cell in human
brain tumors. Cancer Res 2003; 63:
9&&&&& Galli R, Binda E, Orfanelli U, Cipelletti B, Gritti A,
De Vitis S, Fiocco R, Foroni C, Dimeco F, Vescovi A. Isolation and
characterization of tumorigenic, stem-like neural
precursors from human glioblastoma. Cancer Res 2004; 64:
10&&& Collins AT, Berry PA, Hyde C, Stower MJ,
Maitland NJ. Prospective identification of tumorigenic prostate
cancer stem
cells. Cancer Res 2005; 65: &
11&&& Kim CF, Jackson EL, Woolfenden AE,
Lawrence S, Babar I, Vogel S, Crowley D, Bronson RT, Jacks T.
Identification of
bronchioalveolar stem cells in normal lung and lung
cancer. Cell 2005; 121: 823-835&
12&&& Litvinov SV, Velders MP, Bakker HA,
Fleuren GJ, Warnaar SO. Ep-CAM: a human epithelial antigen is a
homophilic cell-
cell adhesion molecule. J Cell Biol 1994;
125: 437-446&
13&&& Ponta H, Sherman L, Herrlich PA. CD44:
from adhesion molecules to signalling regulators. Nat Rev Mol
Cell Biol 2003;
14&&& Weichert
W, Denkert C, Burkhardt M, Gansukh T, Bellach J, Altevogt
P, Dietel M, Kristiansen G. Cytoplasmic CD24
expression in colorectal cancer independently
correlates with shortened patient survival. Clin Cancer Res
15&&& Bjerkvig R, Tysnes BB, Aboody KS,
Najbauer J, Terzis AJ. Opinion: the origin of the cancer stem cell:
controversies and new insights. Nat Rev Cancer
2005; 5: 899-904&
16&&& Li C, Heidt DG, Dalerba P, Burant CF,
Zhang L, Adsay V, Wicha M, Clarke MF, Simeone DM. Identification of
pancreatic
cancer stem cells. Cancer Res 2007; 67:
17&&& Bonnet D, Dick JE. Human acute myeloid
leukemia is organized as a hierarchy that originates from a
hematopoietic cell.
1997; 3: 730-737&
Lapidot T, Sirard C, Vormoor J, Murdoch B, Hoang T, Caceres-Cortes
J, Minden M, Paterson B, Caligiuri MA, Dick JE.
cell initiating human acute myeloid leukaemia after
transplantation into SCID mice.
1994; 367: 645-648&
19&&& Ponti D, Costa A, Zaffaroni N, Pratesi
G, Petrangolini G, Coradini D, Pilotti S, Pierotti MA, Daidone MG.
Isolation and in
vitro propagation of tumorigenic breast cancer cells
with stem/progenitor cell properties. Cancer Res 2005; 65:
20&&& Chiba T, Kita K, Zheng YW, Yokosuka O,
Saisho H, Iwama A, Nakauchi H, Taniguchi H. Side population purified
hepatocellular carcinoma cells harbors cancer stem
cell-like properties. Hepatology 2006; 44: 240-251&
21&&& Suetsugu A, Nagaki M, Aoki H, Motohashi
T, Kunisada T, Moriwaki H. Characterization of CD133+ hepatocellular
carcinoma cells as cancer stem/progenitor cells.
Biochem Biophys Res Commun 2006; 351: 820-824&
22&&& Dome B, Timar J, Dobos J, Meszaros L,
Raso E, Paku S, Kenessey I, Ostoros G, Magyar M, Ladanyi A, Bogos K,
Identification and clinical significance of
circulating endothelial progenitor cells in human non-small cell
lung cancer.
Cancer Res
2006; 66: &
Grichnik JM, Burch JA, Schulteis RD, Shan S, Liu J, Darrow
TL, Vervaert CE, Seigler HF. Melanoma, a tumor based on a
mutant stem cell? J Invest Dermatol 2006;
126: 142-153&
O'Brien CA, Pollett A, Gallinger S, Dick JE. A human colon
cancer cell capable of initiating tumour growth in
immunodeficient mice. Nature 2007; 445:
Ricci-Vitiani L, Lombardi DG, Pilozzi E, Biffoni M, Todaro M,
Peschle C, De Maria R. Identification and expansion of
human colon-cancer-initiating cells. Nature
2007; 445: 111-115&
Dunnwald M, Chinnathambi S, Alexandrunas D, Bickenbach JR.
Mouse epidermal stem cells proceed through the cell
cycle. J Cell Physiol 2003; 195:
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E-Editor: Zhang WB
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