Establishment of Cell Lines from Colon Carcinoma

2005 ◽  
pp. 67-80
Author(s):  
Robert H. Whitehead
Keyword(s):  
1990 ◽  
Vol 2 (10) ◽  
pp. 345-355 ◽  
Author(s):  
Lizabeth Deutsch Murphy ◽  
Eva M. Valverius ◽  
Maria Tsokos ◽  
Lyn A. Mickley ◽  
Neal Rosen ◽  
...  

2013 ◽  
Vol 28 (3) ◽  
pp. 267-273 ◽  
Author(s):  
Marica Gemei ◽  
Rosa Di Noto ◽  
Peppino Mirabelli ◽  
Luigi Del Vecchio

In colorectal cancer, CD133+ cells from fresh biopsies proved to be more tumorigenic than their CD133– counterparts. Nevertheless, the function of CD133 protein in tumorigenic cells seems only marginal. Moreover, CD133 expression alone is insufficient to isolate true cancer stem cells, since only 1 out of 262 CD133+ cells actually displays stem-cell capacity. Thus, new markers for colorectal cancer stem cells are needed. Here, we show the extensive characterization of CD133+ cells in 5 different colon carcinoma continuous cell lines (HT29, HCT116, Caco2, GEO and LS174T), each representing a different maturation level of colorectal cancer cells. Markers associated with stemness, tumorigenesis and metastatic potential were selected. We identified 6 molecules consistently present on CD133+ cells: CD9, CD29, CD49b, CD59, CD151, and CD326. By contrast, CD24, CD26, CD54, CD66c, CD81, CD90, CD99, CD112, CD164, CD166, and CD200 showed a discontinuous behavior, which led us to identify cell type-specific surface antigen mosaics. Finally, some antigens, e.g. CD227, indicated the possibility of classifying the CD133+ cells into 2 subsets likely exhibiting specific features. This study reports, for the first time, an extended characterization of the CD133+ cells in colon carcinoma cell lines and provides a “dictionary” of antigens to be used in colorectal cancer research.


1985 ◽  
Vol 5 (8) ◽  
pp. 1969-1976
Author(s):  
M D Erisman ◽  
P G Rothberg ◽  
R E Diehl ◽  
C C Morse ◽  
J M Spandorfer ◽  
...  

The structure and expression of the c-myc oncogene were examined in 29 primary human colon adenocarcinomas. Dot blot hybridization of total RNA showed that 21 tumors (72%) had considerably elevated expression of c-myc (5- to 40-fold) relative to normal colonic mucosa. These data were corroborated by Northern blots of polyadenylated RNA, which showed a 2.3-kilobase transcript. Southern analysis of the c-myc locus in these tumors indicated the absence of amplification or DNA rearrangement in a 35-kilobase region encompassing the gene. In a parallel study, elevated expression of c-myc without amplification or DNA rearrangement was also observed in three of six colon carcinoma cell lines examined; in addition, unlike a normal colon cell line control, these three cell lines exhibited constitutive, high-level expression of the gene during their growth in cultures. These results indicate that elevated expression of the c-myc oncogene occurs frequently in primary human colon carcinomas and that the mechanism involved in the regulation of c-myc expression is altered in tumor-derived cell lines.


1981 ◽  
Vol 30 (7) ◽  
pp. 793-798 ◽  
Author(s):  
Gerald W. Crabtree ◽  
Daniel L. Dexter ◽  
Johanna D. Stoeckler ◽  
Todd M. Savarese ◽  
Lucy Y. Ghoda ◽  
...  

1983 ◽  
Vol 47 (3) ◽  
pp. 373-381 ◽  
Author(s):  
M G Brattain ◽  
M E Marks ◽  
J McCombs ◽  
W Finely ◽  
D E Brattain

1989 ◽  
Vol 9 (3) ◽  
pp. 1148-1154
Author(s):  
E Shtivelman ◽  
J M Bishop

The line of human colon carcinoma cells known as COLO320-DM contains an amplified and abnormal allele of the proto-oncogene MYC (DMMYC). Exon 1 and most of intron 1 of MYC have been displaced from DMMYC by a rearrangement of DNA. The RNA transcribed from DMMYC is a chimera that begins with an ectopic sequence of 176 nucleotides and then continues with exons 2 and 3 of MYC. The template for the ectopic sequence represents exon 1 of a gene known as PVT, which lies 50 kilobase pairs downstream of MYC. We encountered three abnormal configurations of MYC and PVT in the cell lines analyzed here: (i) amplification of the genes, accompanied by insertion of exon 1 and an undetermined additional portion of PVT within intron 1 of MYC to create DMMYC; (ii) selective deletion of exon 1 of PVT from amplified DNA that contains downstream portions of PVT and an intact allele of MYC; and (iii) coamplification of MYC and exon 1 of PVT, but not of downstream portions of PVT. We conclude that part or all of PVT is frequently amplified with MYC and that intron 1 of PVT represents a preferred boundary for amplification affecting MYC.


2015 ◽  
Vol 47 (2) ◽  
pp. 773-781 ◽  
Author(s):  
MICHELE LINSALATA ◽  
ANTONELLA ORLANDO ◽  
VALERIA TUTINO ◽  
MARIA NOTARNICOLA ◽  
BENEDETTA D’ATTOMA ◽  
...  

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