Detection of extracellular tumor-associated nucleic acid in...

Chemistry: molecular biology and microbiology – Measuring or testing process involving enzymes or... – Involving nucleic acid

Reexamination Certificate

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C435S091100, C435S091200, C536S022100, C536S023100, C536S024300, C536S024310, C536S024320, C536S024330

Reexamination Certificate

active

06630301

ABSTRACT:

BACKGROUND OF THE INVENTION
1. Field of the Invention
This invention relates to methods for detecting specific extracellular nucleic acid in plasma or serum fractions of human or animal blood associated with neoplastic, pre-malignant or proliferative disease. Specifically, the invention relates to detection of nucleic acid derived from mutant oncogenes or other tumor-associated DNA, and to methods of detecting and monitoring extracellular mutant oncogenes or tumor-associated DNA found in the plasma or serum fraction of blood using DNA enrichment methods, wherein enrichment-based extraction methods are used prior to amplification and/or detection, or wherein enrichment for the nucleic acid of interest occurs during amplification, in particular through use of a restriction endonuclease. In particular, the invention relates to the detection, identification, or inference of the existence of premalignant neoplasms or tissue in humans or other animals without cancer, wherein the neoplasm contains a mutation that is associated with the neoplasm, through detection of the mutated nucleic acid associated with the neoplasm in plasma or serum fractions.
2. Description of the Related Art
Neoplastic disease, including most particularly that collection of diseases known as cancer, is a significant part of morbidity and mortality in adults in the developed world, being surpassed only by cardiovascular disease as the primary cause of adult death. Although improvements in cancer treatment have increased survival times from diagnosis to death, success rates of cancer treatment are more closely related to early detection of neoplastic disease that enable aggressive treatment regimes to be instituted before either primary tumor expansion or metastatic growth can ensue. A particularly favorable prognosis is achieved if premalignant tissue can be eradicated prior to progression to cancer.
Oncogenes are normal components of every human and animal cell, responsible for the production of a great number and variety of proteins that control cell proliferation, growth regulation, and cell death. Although well over one hundred oncogenes have been described to date with nearly all identified at the deoxyribonucleic acid (DNA) sequence level. It is likely that a large number of oncogenes remain to be discovered.
Mutations in DNA occur as the result of inborn (inherited) genetic errors or acquired (somatic) mutations, often as a result of environmental insults, and have long been recognized as playing a causative role in the development of neoplastic disease. Within the last twenty years the sites of such mutations have been recognized to be within oncogenes, including tumor suppressor genes, and similar tumor-related gene regions including those with DNA microsatellite alterations and hypermethylated genes. Mutation of these genes have been found to be an intrinsic and crucial component of premalignant and malignant growth in both animals and humans. Many malignant tumors or cell lines derived from the m have been shown to contain one or more mutated oncogenes, and it is possible that every tumor contains at least one mutant oncogene.
Mutated oncogenes are therefore markers of malignant or premalignant conditions. It is also known that other non-oncogenic portions of the genome may be altered in the neoplastic state. Nucleic acid based assays can detect both oncogenic and non-oncogenic DNA, whether mutated or non-mutated.
In particular, nucleic acid amplification methods (for example, the polymerase chain reaction) allow the detection of small numbers of mutant molecules among a background of normal ones. While alternate means of detecting small numbers of tumor cells (such as flow cytometry) have generally been limited to hematological malignancies (Dressler and Bartow, 1989
, Semin. Diag. Pathol
. 6: 55-82), nucleic acid amplification assays have proven both sensitive and specific in identifying malignant cells and for predicting prognosis following chemotherapy (Fey et al., 1991
, Eur. J. Cancer
27: 89-94).
Various nucleic acid amplification strategies for detecting small numbers of mutant molecules in solid tumor tissue have been developed, particularly for the ras oncogene (Chen and Viola, 1991
, Anal. Biochem
. 195: 51-56; Kahn et al., 1991
, Oncogene
6: 1079-1083; Pellegata et al., 1992
, Anticancer. Res
. 12: 1731-1736; Stork et al., 1991
, Oncogene
6: 857-862). For example, one sensitive and specific method identifies mutant ras oncogene DNA on the basis of failure to cleave a restriction site at the crucial 12th codon (Kahn et al., 1991, ibid.). Similar protocols can be applied to detect any mutated region of DNA in a neoplasm, allowing detection of other oncogene DNA or tumor-associated DNA. Since mutated DNA can be detected not only in the primary cancer but in both precursor lesions and metastatic sites (Dix et al., 1995
, Diagn. Molec. Pathol
. 4: 261-265; Oudejans et al., 1991
, Int. J. Cancer
49: 875-879), nucleic acid amplification assays' provide a means of detecting and monitoring cancer both early and late in the course of disease.
While direct analysis of neoplastic tissue is frequently difficult or impossible (such as in instances of occult, unrecognized disease), peripheral blood is easily accessible and amenable to nucleic acid-based assays such as those mentioned above. Many studies have used nucleic acid amplification assays to analyze the peripheral blood of patients with cancer in order to detect intracellular DNA extracted from circulating cancer cells in patients, including one study which detected the intracellular ras oncogene from circulating pancreatic cancer cells (Tada et al., 1993
, Cancer Res
. 53: 2472-4). However, it must be emphasized that these studies attempt to use nucleic acid-based amplification assays to detect extracted intracellular DNA within circulating cancer cells. The assay is performed on the cellular fraction of the blood from patients having cancer using the cell pellet or cells within whole blood, and the serum or plasma fraction is conventionally ignored or discarded prior to analysis. Since such an approach requires the presence of metastatic circulating cancer cells (for non-hematologic tumors), it is of limited clinical use in patients with early cancers, and it is not useful in the detection of non-hematologic non-invasive neoplasms or pre-malignant states.
It was known in the prior art that small but significant amounts of normal DNA circulate in the blood of healthy people (Fedorov et al., 1986
, Bull. Exp. Biol. Med
. 102: 1190-2; Leon et al., 1977
, Cancer Res
. 37: 646-50), and this amount has been found to increase in cancer states (Shapiro et al., 1983
, Cancer
51: 2116-20: Stroun et al., 1989
, Oncology
46: 318-322). The prior art contains disclosure that mutant oncogene DNA could be detected in peripheral blood plasma or serum of cancer patients (see, for example, Sorenson et al;, 1994
, Cancer Epidemiology, Biomarkers & Prevention
3: 67-71; Vasioukhin et al., 1994
, Br. J. Haematol
. 86: 774-9; Vasyukhin et al., in Verna & Shamoo (eds),
Biotechnology Today
, Ares-Serono Symposia Publications, pp. 141-150). Mutant ras oncogenes have been demonstrated in plasma or serum using polymerase chain reaction. However, these reports have also been. generally limited to patients with advanced cancer or known neoplastic or proliferative disease.
We have recognized that nucleic acid amplification assays can detect tumor-associated extracellular mutated DNA, including oncogene DNA, in the plasma or serum fraction of blood of humans without clinically-diagnosed cancer or known disease (see U.S. Ser. No. 08/818,058 filed Mar. 14, 1997, now U.S. Pat. No. 6,156,504, issued Dec. 5, 2000, incorporated by reference), and that this can be accomplished in a clinically useful manner.
SUMMARY OF THE INVENTION
The present invention relates to detection of specific extracellular nucleic acid in plasma or serum in human or animals without cancer which are associated with neoplastic, preneoplastic or proliferative disease or conditions. Specifically,

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