Studies of Nucleic Acid Synthesis in Ascites Tumor Cells

LePage, G. A.; Greenlees, Janet; Fernandes, J.F.

doi:10.1111/j.1749-6632.1955.tb36579.x

Cited by 3 publications

(7 citation statements)

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“…Barclay & Garfinkel (427) reported that N-methylformamide, though it stimulated the incorporation of formate into liver nucleic acid, inhibited incorporation into tumor DNA. Davidson & Freeman (428) observed that the alkylating agents : 1,4-bis(methylsulfonyloxy)butane (Myleran), nitrogen mustard, TEM, and triethylenephosphoramide did not affect the incorporation of P3Z into DNA of adenocarcinoma 755, whereas 8-azaguanine and 6-mer captopurine inhibited the process_ A 90 per cent inhibition of the incorpora tion in vitro of glycine-2-C!4 into the nucleic acid purines of the Ehrlich ascites tumor, with very low concentrations of azaserine, has been obtained by LePage et al (429) ; Buchanan has demonstrated that azaserine blocks purine synthesis by preventing subsequent reactions of formyl glycine amide ribotide (430). Balis & Dancis (431) have found that amethopterin inhibits the incorporation of formate into nucleic acid purines and thymine in breis of leukemic spleen, but that in vivo only thymine was inhibited ; similar results with purines in vitro were obtained with mouse leukemias (432) and human granulocytic leukemic cells (433) by Williams & Winzler.…”

Section: Chemotherapymentioning

confidence: 87%

“…A number of studies, including several already mentioned (339,340,341), have determined the effects of various chemotherapeutic agents on the incorporation of labeled precursors into nucleic acids_ Way et al (426) found that x-rays inhibited the incorporation of adenine into DNA, but that 8-azaguanine did not affect its incorporation into DNA or RNA. Barclay & Garfinkel (427) reported that N-methylformamide, though it stimulated the incorporation of formate into liver nucleic acid, inhibited incorporation into tumor DNA.…”

Section: Chemotherapymentioning

confidence: 99%

“…The test systems used were : Sarcoma 180 (323), a spectrum of rat and mouse tumors (324), mammary adenocarcinoma RC (325), transplants of spontaneous mammary adenocarcinomas (326), mam mary adenocarcinoma 755, glioma 26, and Brown-Pearce carcinoma (327), U210 leukemias (328), Ehrlich ascites tumors (329), mouse viruses (330), bacterial viruses (331), bacteria and fungi (332), L. caseii (333), bacterial mutagenicity (334), aggregation of Dictostelium discoideum (335), develop ing frog embryo (336), developing chick embryo (337) , growth and mOf phogenesis of Drosophila (338), p32 incorporation into nucleic acids in vivo (339), incorporation of glycine-2-C14 into Ehrlich ascites tumor cell purines and proteins in vitro(340), and the incorporation of p32 and formate into the nucleic acids of slices of Flexner-Jobling carcinoma and rat spleen(341). The test systems used were : Sarcoma 180 (323), a spectrum of rat and mouse tumors (324), mammary adenocarcinoma RC (325), transplants of spontaneous mammary adenocarcinomas (326), mam mary adenocarcinoma 755, glioma 26, and Brown-Pearce carcinoma (327), U210 leukemias (328), Ehrlich ascites tumors (329), mouse viruses (330), bacterial viruses (331), bacteria and fungi (332), L. caseii (333), bacterial mutagenicity (334), aggregation of Dictostelium discoideum (335), develop ing frog embryo (336), developing chick embryo (337) , growth and mOf phogenesis of Drosophila (338), p32 incorporation into nucleic acids in vivo (339), incorporation of glycine-2-C14 into Ehrlich ascites tumor cell purines and proteins in vitro(340), and the incorporation of p32 and formate into the nucleic acids of slices of Flexner-Jobling carcinoma and rat spleen(341).…”

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confidence: 99%

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Biochemistry of Cancer

Heidelberger¹

1956

Annu. Rev. Biochem.

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During the past year researches on the biochemistry of cancer have con tinued at an increasJng pace, which places the reviewer at a correspondingly increased disadvantage. In treading a tortuous path between the opposing goals of all-inclusiveness and critical evaluation, the reviewer finds himself entangled in a maze of almost inexhaustive literature (over 1200 references were considered), which taxes to the utmost his resources of judgment and common sense. A brilliant precedent has been set by Haddow (1), whose re view on the same subject in last year's volume shows an impressive grasp of the fields of oncology, biology, physics, and chemistry and which is writ ten in a characteristically lucid and elegant style.Because of the stringent limitations of space, it has been necessary to curtail subject matter strictly to studies concerned directly with cancer. The following topics, many with enough material to justify separate re views, have been arbitrarily excluded: effects of tumors on serum and urinary enzyme levels, diagnostic tests, clinical evaluation, the mechanisms of radiation effects, histochemistry, morphology, chemical syntheses and isola tions, genetics, biology of transplantation, steroid metabolism, oncolytic viruses, plant and reptilian tumors, and cytogenetics. Lest the reader feel that this review is all-exclusive it should now be mentioned that carcino genesis, tumor biochemistry and immunology, and chemotherapy will be dealt with in that order.An attempt has been made to cover the literature through September, 1955, and there has been little duplication of references cited by Haddow (1). CARCINOGENESISDuring the past year there has been an increased acceptance of the concept of protein deletion as playing a key role in the initiation of chemical carcinogenesis. The pioneer demonstration by the Millers in 1947 (2) that, following feeding of DAB, bound dye was found in the liver proteins, was followed by the development of an impressive correlation between protein binding and the carcinogenic process (3). Miller demonstrated (4) that fol lowing application of BP to the skin of mice, fluorescence was liberated by 1 The following abbreviations are used in this chapter: AAF for 2-acetylamino fluorene; ACTH for adrenocorticotrophic hormone; ADP for adenosinediphosphate; ATP for adenosinetriphosphate; BA for l,2-benzanthracene; BP for benzpyrene; DAB for p-dimethylaminoazobenzene; DBA for dibenzanthracene; DMBA for 9,10dimethyl-l,2-benzanthracene; DNA for deoxyribonucleic acid; DPN for diphos phopyridine nucleotide ; DPNH for diphosphopyridine nucleotide (reduced form) ; MeA for methyIcholanthrene; RNA for ribonucleic acid; TEM for triethvlene melamine.Annu. Rev. Biochem. 1956.25:573-612. Downloaded from www.annualreviews.org Access provided by University of Western Ontario on 02/07/15. For personal use only. Quick links to online content Further ANNUAL REVIEWS Annu. Rev. Biochem. 1956.25:573-612. Downloaded from www.annualreviews.org Access provided by University of Western Ontario on 02/07/15. For ...

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Section: Chemotherapymentioning

confidence: 87%

Section: Chemotherapymentioning

confidence: 99%

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confidence: 99%

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Biochemistry of Cancer

Heidelberger¹

1956

Annu. Rev. Biochem.

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“…In work with cell-free preparations, Salser et al (172) found that conversion of IMP to adenylosuccinic acid, and thus AMP, in Streptococcus tfaecalis preparations and of IMP to XMP, and thus GMP, in pigeon liver !extracts were both inhibited by mercaptopurine ribotide; conditions and <accuracy of the assays did not, however, permit quantitative comparisons 'of the two sites of inhibition. However, no preferential effects on DNA synthesis w&e apparent in isotope incorporation experiments (194) . Mercaptoadenylosuccinate was itself cleaved by the enzyme to mercaptopurine ribotide (191), but its effect was greater than could be accounted for by this conversion and, hence, was ap parently independent (193) .…”

Section: Anticancer Agentsmentioning

confidence: 96%

Biochemistry of Cancer

Anderson¹,

Law²

1960

Annu. Rev. Biochem.

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“…Even though much of the specialized metabolic equipment of a cell may have been deleted along with that lost in the deletion which was carcinogenic, the fragments of this equipment left can lead to greatly varied responses to drugs used for chemotherapy. The result, as this author 15 pointed out earlier, is that chemotherapy must be able to treat cancer as a large group of diseases. Any one drug treatment will probably affect only a small percentage of a spectrum of clinical cancers.…”

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confidence: 87%

Part V. Use of combinations of antimetabolites for chemotherapy of cancer

LePage

1961

Clin Pharma and Therapeutics

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It is possible to view the approach to a chemotherapy of cancer more rationally if it is given a frame derived from a recent concept of how cancer arises and progresses. This concept will be referred to as the "deletion concept." The experimental evidence for this concept is available mainly from studies on chemical carcinogenesis and has been discussed elsewhere. 16, 20-22 By this concept, a cancer cell arises when a normal call is subject to deletions that are not lethal, but leave it without the components responsive to normal growth controls. What specific deletions are necessary to achieve this result are as yet unknown. It may be that the same net result can be reached by any of several different deletions. Potter21 has suggested one plausible way in which this could occur and cites several examples. When cells have alternate metabolic pathways such that a substrate can be either catabolized for energy or used to synthesize new material for cell growth, the deletion of the catabolic pathway could lead to uncontrolled growth. One example cited is that of uracil, which can be used by liver cells to synthesize uracil nucleotide

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Studies of Nucleic Acid Synthesis in Ascites Tumor Cells

Cited by 3 publications

References 1 publication

Biochemistry of Cancer

Biochemistry of Cancer

Biochemistry of Cancer

Part V. Use of combinations of antimetabolites for chemotherapy of cancer

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