Chemistry: molecular biology and microbiology – Measuring or testing process involving enzymes or... – Involving antigen-antibody binding – specific binding protein...
Reexamination Certificate
1999-10-26
2003-04-22
Stucker, Jeffrey (Department: 1648)
Chemistry: molecular biology and microbiology
Measuring or testing process involving enzymes or...
Involving antigen-antibody binding, specific binding protein...
C435S007100, C435S007800, C435S007920, C435S007940, C435S007950, C436S514000, C530S388800, C530S388850
Reexamination Certificate
active
06551789
ABSTRACT:
TECHNICAL FIELD
The present invention relates to immunological receptors and ligands, and more particularly to monoclonal receptors raised to polypeptides who whose amino acid residue sequences correspond to sequences of retroviral oncoprotein ligands.
BACKGROUND ART
Retroviruses are viruses that contain a single strand of RNA as the genetic material rather than DNA. The single-stranded RNA genome of each of these viruses gives rise to a double-stranded DNA molecule after the virus infects a susceptible host. This DNA replica of the viral genome then introduces itself permanently into a chromosome of the successfully infected cell and replicates in that host chromosome.
The retroviruses discussed hereinafter and in the claims may be further defined as being replication-defective retro-viruses. Thus, these viruses do not themselves contain a gene encoding the reverse transcriptase usually required to permit the viral RNA genome to be translated into a DNA that can be introduced into a chromosome of the infected host. Rather, the retro-viruses discussed hereinafter typically must be complimented in their infection by a so-called helper virus that is replication-competent. That second virus contains the gene that encodes the reverse transcriptase enzyme that incorporates the genomic materials from both viruses into the successfully infected host cells to transform those cells.
For ease in understanding, the replication-defective retroviruses will be discussed hereinafter and in the claims merely as retroviruses with the understanding that they are replication-defective and require the assistance of a helper virus for successful infection and transformation of host cells. This usage of the term retrovirus is known in the art and has been used in the art as such without further explanation.
Some members of the retrovirus family are highly oncogenic as judged by their ability to cause the formation of solid tumors within a short period of time after being inoculated into the host. These viruses can also cause “cancerous” changes in cells grown and cultured in the laboratory; such changes are called “transformations” and provide a reliable in vitro biological assay for oncogenic viruses. Several such viruses have been isolated from chickens, turkeys, mice, rats, cats and monkeys.
A single gene, the oncogene, located on the genome of these highly oncogenic viruses is responsible for the tumorgenic potential of the virus. In the case of several viruses, the protein products of their oncogenes, referred to herein as oncoproteins, have been immunologically identified by taking advantage of the fact that serum from an animal bearing a virus-induced tumor contains antibodies directed against those oncoproteins.
A rapidly growing body of evidence indicates that the oncogenes of retroviruses are closely related to and are derived from specific genetic loci in the normal cellular genetic information of all vertebrates.
Interest in oncogenes has steadily risen in the last decade. Although RNA tumor viruses have been implicated as the causative agents of experimentally induced neoplasia in chickens for over 50 years, it was not until the mid 1970s that mechanisms of virally induced neoplasia began to emerge [Bishop (1983)
Ann. Rev. Biochem
. 52:301-54]. According to one such mechanism, replication-competent avian viruses and defective mammalian viruses had captured cellular genes that provided the viruses with a transforming potential.
Molecular hybridization studies using specific nucleic acid probes, followed by genetic cloning of viral oncogenes and their cellular relatives by recombinant DNA technology, have established the kinship between retroviral oncogenes (v-onc) and cellular oncogenes (c-onc) found in all normal vertebrate cells. Molecular analysis of the several retroviruses thus far isolated has revealed more than two dozen different oncogenes. In most cases, a corresponding cellular to the retroviral oncogene or oncoprotein has been isolated.
For example, the human EJ or T24 bladder carcinoma oncogene was identified as the homolog of the transforming gene of Harvey murine sarcoma virus (ras
Ha
) and also of the BALB sarcoma virus (bas) [Parada et al.,
Nature
, 297, 474-478 (1982); Der et al.,
Proc. Natl. Acad. Sci USA
, 79, 3627-3634 (1982); and Santos et al.,
Nature
, 298, 343-347 (1982)]. In addition, the oncogene of the human carcinoma cell line LX-1 was found to be homologous to the transforming gene of Kirsten strain of murine sarcoma virus (ras
Ki
) [Der et al., above]. Still further, the v-onc for a c-onc designated fps of avian origin is represented at least twice among a limited number of avian retrovirus isolates; its mammalian cognate designated fes in feline species is found in two different strains of feline sarcoma viruses.
The homology [Doolittle et al., (1983)
Science
221:275-277; Waterfield et al., (1983)
Nature
304:35-39] between the gene product of the sis oncogene and one of the chains of platelet-derived growth factor provided the most solid link between malignant transformation by oncogenes and stimulation of normal cell division by growth factors. This identity between oncogene products and growth factors and cellular receptors was further substantiated with sequence analysis of the epidermal growth factor cellular receptor [Downward et al., (1984)
Nature
307, 521-527; Ullrich et al., (1984)
Nature
309:418-425] that was found to be the normal homologue of erb B. Furthermore, immunological cross-reactivity of fms antibodies with colony stimulating factor-1 receptor [Sherr et al., (1985)
Cell
:665-676] as well as protein kinase homology with the insulin-receptor [Ullrich et al., (1985)
Nature
:313, 756-761] and platelet derived growth factor receptor [Yarden et al., (1986)
Nature
323; 226-232] indicated the kinase activity of many of the sequenced oncogenes would be important in the signal transduction of several growth factors.
Sequencing of oncogenes captured by retroviruses or identified via transfection experiments greatly extended the number of kinase family members. [Hunter et al., (1985)
Ann. Rev. Biochem
. 54:897-930.] This sequence analysis suggested the number of kinase-related proteins would be large and the family members could be divided into subgroups based upon sequence homology and overall structural similarities. The kinase family can be conveniently divided into gene products that do or do not have extracellular (hormone/growth factor) binding domains.
The close similarity between the kinase portion of src and yes has been apparent for several years. [Kitamura et al., (1982)
Nature
297:205-208.] Recently, sequencing of additional genes has extended this homology to fgr, [Naharro et al., (1984)
Science
222;63-66] lck, [Marth et al., (1985)
Cell
43:393-404. syn, [Semba et al., (1986)
Proc. Natl. Acad. Sci. USA
83:5459-5463] and lyn [Yamanashi et al., (1987)
Mol. and Cell Biol
. 1:237-243]. All six of these genes encode proteins of approximately the same size 55-65 kd, and the genes share intron/exon borders indicating they evolved from the same ancestral proto-oncogene. However, each gene is located on a separate chromosome and expresses different proteins in different tissues.
Many additional kinase family members can also be placed into subgroups. Mos [Van Beveran et al., (1981)
Nature
289:258-262] is closely related to pim-1 [Selten et al., (1986)
Cell
46:603-611], one of the preferred integration sites of Moloney leukemia virus. Abl [Reddy et al., (1983)
Proc. Natl. Acad. Sci. USA
80:3623-3627] is closely related to arg [Kruh et al., (1986)
Science
234:1545-1547]. Fes [Hampe et al., (1982)
Cell
30:775-785] and fps [Shibuya et al., (1982)
Cell
30:787-795]. represent the mammalian and avian counterparts of the same gene.
Similarly, raf [Sutrave et al., (1984)
Nature
309:85-88] and mil [Mark et al.
Fitting Thomas
Northrup Thomas E.
Stucker Jeffrey
The Scripps Research Institute
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