Chemistry: molecular biology and microbiology – Animal cell – per se ; composition thereof; process of... – Primate cell – per se
Reexamination Certificate
2000-12-07
2004-05-04
Mosher, Mary E. (Department: 1642)
Chemistry: molecular biology and microbiology
Animal cell, per se ; composition thereof; process of...
Primate cell, per se
C435S325000, C435S366000
Reexamination Certificate
active
06730514
ABSTRACT:
BACKGROUND OF THE INVENTION
1. Field of the Invention
This invention relates to a stable human oral cancer cell carcinoma cell line suitable for understanding the differences in the tumorigenic pathways implicated in the development and progression of oral squamous cell carcinoma obtained from the floor of the mouth of a chronic tobacco consumer.
2. Background of the Related Art
Oral cancer ranks as the sixth most common globally and is a major cause of cancer-related morbidity and mortality. The aetiology of betel and tobacco related oral cancer is considerably different to that resulting from smoking of tobacco. Exposure of the oral mucosa of habitual betel quid chewers to a plethora of carcinogenic constituents of tobacco and areca nut causes multiple genotoxic insults at the site bolus application, often resulting in the development of clinically distinct premalignant lesions, leukoplakia or erthroplakia, which undergo malignant transformation. Established human oral cancer cell lines are widely used to study the mechanism implicated in oral tumorigenesis. The human oral cancer cell lines available in Cell Repositories and Culture Collections around the world have been established from the Western or Japanese population and resulting from smoking of tobacco. In this respect, reference is made to Table 1.
TABLE 1
REPORTED HEAD AND NECK
SQUAMOUS CARCINOMA CELL LINES
CELL LINE
Site
Study subject
Reference
SCC-40
SP
Keratins
Wu et. al. 1982
SqCC/Y1
B
Retinoids;
Reiss, et. al. 1985
differentiation
HLC-1
L
Cytogenetics
Hauser-Urfer et. al.
HTC-1
T
HTC-2
T
CAL-27
T
Establishment:
Gioanni et. al. 1988
chemotheraphy
CAL-33
T
HN11
FOM
Establishment:
Meghji et. al. 1988
cytokiness
HN12
H
HN15
FOM
HSC-2
FOM
Establishment;
Momose et. al. 1989
metastasis
HSC-3
T
HSC-4
T
HST-1
PE(T)
Establishment
Nakano et. al. 1989
ZA
Ln(P)
Oncogenes
Todokoro et. al. 1989
R105
FOM
Establishment-
Crooijmans et. al. 1990
differentiation
T87/rc
E
SCC-83-01-82
NS
Oncogenes-
Shuler et. al. 1890
tumorigenicity
Ca9-22
G
Rikimaru et. al. 1990
H103
T
Establishment
Prime et. al. 1990
H157
B
H314
FOM
H191
T
H140
B
H357
T
H376
FOM
H400
A
H413
B
H440
FOM
MH85
M
Epidermal
Yoneda et. al. 1991
growth factor
UT-SCC-1A
G
Radiotheraphy
Pekkola et. al. 1991
HOC605
LN(P)
Epidermal
Rikimaru et. al. 1992
growth factor
HOC815
LN(Mn)
HOC815
LN(T)
HOC927
LN(T)
T1/CUHK
T
Establishment
Chew et. al. 1992
T2/CUHK
T
SCCKN
Oral
Establishment:
Urade et. al. 1992
chemotheraphy
SCCTF
Oral
EVSCC1
A
p53
Somers et. al. 1992
EVSCC3
T
EVSCC4
FOM
JHU-011-SCC
R(L)
Interferons:
Scher et. al. 1993
integrins
JHU-220-SCC
L
JHU-022-SCC
Ln(L)
HNSCC28
L
Radiobiology:
Cowan et. al. 1993
cytogenetics
HNSCC167
To
HNSCC151
T
HNSCC135
HP
HNSCC294
T
HNSCC143
O
Tu-138
G
Gene therapy,
Liu et. al. 1994
p53
Tu-177
L
H-1
G
Establishment
Harada et. al. 1993
KOSC-2
FOM
Establishment:
Inagaki et. al. 1994
p53
KOSC-3
G
MISK81-5
Ln(oral)
Establishment
Matsuo et. al. 1994
GCSF
FS-1
M
Establishment:
Fukiage et. al. 1994
immunobiology
OSC-1
T
Establishment-
Osaki et. al. 1994
tumorigenicity
OSC-2
Ln(G)
OSC-3
Ln(G)
OSC-4
T
OSC-5
T
OSC-6
T
OSC-7
T
MSK-922
L
p53 expression
Xu et. al. 1994
MSK-921
T
MSK-QLL1
T
MSK-QLL2
L
MDA-686Ln
Ln(T)
MDA-686Tu
T
MDA-886Ln
Ln(L)
MDA-1186
L
MDA-1386Ln
Ln(H)
MDA-1586
L
MDA-1686
B
MDA-1986
Ln(T)
UT-SCC-1A
G
Radiosesitivity
Pekkolo-Heino et. al. 1994
UT-SCC-1B
Met(G)
UT-SCC-2
FOM
UT-SCC-4
L
UT-SCC-5
T
UT-SCC-6A
L
UT-SCC-6B
Met(L)
UT-SCC-8
L
UT-SCC-9
L
BICR3
A
Tumor
Edington et. al. 1995
progression
BICR6
H
BICR10
B
BICR16
R(T)
BICR18
Met(L)
BICR22
Met(T)
BICR31
T
BICR56
T
BICR63
T
BICR68
T
BICR78
A
BICR82
M
A. alveolus; B. buccal mucosa; E. epiglottis; FOM. floor of mouth; G. gingiva, H. hypopharynx; HD. hard Palate; L. Larynx; M. maxilla; Mn. Mandible; O. oropharynx; P. palate; SP. soft palate; T. tongue; To. tonsil; LN 0. Lymph node metastasis (primary site); Met0. metastasis (primary site); PE0. Pleural effusion (primary Site); R0. recurrence (primary site); NS. not stated.
Presently, there are no oral cancer cell lines resulting from chewing of tobacco. Majority of the studies on oral carcinogenesis have been carried out using tissue specimens (biopsy or surgically resected oral premalignant and malignant lesions) or cell lines resulting from smoking of tobacco. Majority of the studies on oral carcinogenesis has been carried out using tissue specimens (biopsy or surgically resected oral premalignant and malignant lesions) or cell lines resulting from smoking of tobacco. The recent awareness of inherited nature of some cancers, ethnic groups, existence of cancer families and importance of surveillance of high risk individuals using cancer susceptibility genes as markers emphasizes the need to establish oral cancer cell lines resulting from chewing of tobacco to provide a much needed model for oral tumorigenesis. The existing oral cancer cell lines are from tobacco smokers and thus are not suitable for studies pertaining to cancer susceptibility originating from chewing of tobacco. It may be argued that these studies could be carried in human oral cancer tissue specimens. However, in-depth studies carried out by the applicants have shown that the availability of the tissue specimen poses a major constraint on the work. Often the biopsy/FNAC specimens yield insufficient number of tumor cells for detailed molecular analysis. Furthermore, the yield of RNA from biopsy/surgically resected tissue specimens may be low reducing the feasibility of conducting studies aimed at identification of genes that are differentially expressed in different stages of oral tumorigenesis by Differential Display Reverse Transcription Polymerase Chain Research (DDRT-PCR). Hence, the non-availability of an experimental model system for tobacco induced oral cancer is a major obstacle in understanding the mechanism underlying oral tumorigenesis. Establishment of human oral cancer cell lines from betel and tobacco consumers is of utmost importance to provide an in vitro experimental model system for oral tumorigenesis.
OBJECTS OF THE INVENTION
An object of this invention is to propose a human oral cancer line established and propogated in vitro from the oral squamous cell curcinome obtained from the floor of mouth of a chronic tobacco consumer.
Another object of this invention is to propose a human oral squamous cell carcinoma cell line from the floor of the mouth of a habitual tobacco consumer for the study of genetic/molecular alterations involved in development and progression of an environmental carcinogen induced malignancy.
Still another object of this invention is to propose a human oral cancer line established and propagated in vitro from the oral squamous cell curcinome obtained from the floor of mouth of a chronic tobacco consumer for indentifying novel targets for use as diagnostic/prognostic markers and designing new therapeutic strategies for more effective management of cancer patients.
Yet another object of this invention is to propose a human oral cancer line established and propogated in vitro from the oral squamous cell carcinoma obtained from the floor of mouth of a chronic tobacco consumer which may be advantageously used for various applications as described hereinbelow.
SUMMARY OF THE INVENTION
According to this invention there is provided human oral cancer cell line established and propagated in vitro from oral squamous cell carcinoma obtained from the mouth of a chronic tobacco consumer, wherein said cell line AMOS-III has the following marker profile:
a. positive for tumor suppressor gene product, p53; marker of invasion and metastasis, ets-1; ternary complex factors, Net and elk; retinoic acid receptors, RXR∝; RAR∝; anti-apoptotic protein and chaperone, HSP 70; epithelial specific antigen, ESA; human cytokeratin, CK 14, cell cycle regulatory protein, p21; Oncogene cyclin D1, heat shock protein, HSP90; transcription factor, ets-2; proliferation marker; Ki67.
b. Negative for human papilloma virus, HPV E6; mesenchymal cells marker, Vimentin; Low level of expression of oncogene MDM2, the p53 suppressor protein.
Further according to this
Kaur Jatinder
Ralhan Ranju
Mosher Mary E.
Schneller Marina V.
Venable
Yu Misook
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