Viral “Tumorigenesis” in man: Cell markers in <i>condylomata acuminata</i>

Friedman, Jan M.; Fialkow, Philip J.

doi:10.1002/ijc.2910170109

Cited by 34 publications

(7 citation statements)

References 10 publications

(5 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Strong as this evidence is, it must be remembered that it is not universal. Some tumors, such as 'venereal' warts in man (90) and fibrosarcoma induced by relatively high doses (91) of methylcholanthrene in mice have been shown to arise from more than one clone (92). Furthermore, some human cancers are characterized by numerous loci of neoplastic change.…”

Section: Origin Of Tumor Heterogeneitymentioning

confidence: 99%

Tumor heterogeneity: biological implications and therapeutic consequences

1983

View full text Add to dashboard Cite

It is now appreciated that cancers can be composed of multiple clonal s~bpopulations of cancer cells which differ among themselves in many properties, including karyotype, growth rate, ability to metastasize, immunological characteristics, production and expression of markers, and sensitivity to therapeutic modalities. Such tumor heterogeneity has been demonstrated in a wide variety of animal tumors of differing etiology, tissue and cellular origin, and species. It has been shown in autochthonous, as well as transplanted, tumors. Similar results have been reported for human cancers, although much of the evidence that heterogeneity of human cancers, also reflects, at least in part, the existence of clonal subpopulations, is still indirect. Heterogeneity is not a unique property of malignancy. Preneoplastic tumors, as well as normal tissues, are also composed of cellular subpopulations.Proposed mechanisms for the origin of tumor heterogeneity include coalescence of multiple loci of cancer clones and the generation of diverse subpopulations from a single clone. This latter process could be due to genetic errors arising from classical genetic mechanisms or to the production of cellular variants as in normal tissue differentiation. Indeed, certain tumor subpopulations have been shown to produce variants at high frequency. In some cases this frequency can be modified by environmental circumstances. Nontumor cells may also contribute to production of cancer cell variants, perhaps, in the case of infiltrating phagocytic cells, by producing mutagens or by somatic hybridization with cancer cells. Production of tumor cell variants is a dynamic process which can occur at any time.Although tumors are mixed populations of cells, knowledge of the characteristics of individual components is not sufficient to predict the behavior of the whole. Individual cancer subpopulations can interact to affect each other's growth, immunogenicity, ability to metastasize, sensitivity to drugs, and clonal stability. The existence of multiple, interactive subpopulations provides a basis for the well-known phenomenon of 'tumor progression' in which tumors undergo qualitative changes in characteristics over the course of time. Selection of subpopulations better able to survive changing environmental circumstances allows for such changes as autonomy in regard to endogenous growth regulation, more "malignant' behavior, and loss of response to therapy. Tumor subpopulation interactions may play a regulatory role in this process.Tumor heterogeneity has obvious consequences to the design of effective therapy. It provides one rationale for combination therapies and suggests that initial treatment should be early and comprehensive. The continuing emergence of new clones suggests that treatment which is unsuccessful at one point might be effective later. Assays to predict effective therapy for individual patients need to address the multiplicity of tumor subpopulations and the ability of these subpopulations to influence each other. Subpopulation interacti...

show abstract

Section: Origin Of Tumor Heterogeneitymentioning

confidence: 99%

Tumor heterogeneity: biological implications and therapeutic consequences

1983

View full text Add to dashboard Cite

show abstract

“…Human papilloma viruses (HPVs) cause a broad spectrum of disease, the most prevalent being the ordinary wart (1,2). However, infections of genital and oral epithelia by HPVs cause epithelial lesions ranging from benign condylomata associated with types 6 and 11 to intraepithelial dysplasias associated with types 16, 18 and other closely related types.…”

Section: Introductionmentioning

confidence: 99%

“…Crystallographic parameters 1 Mathew's number. 2 Resolution cut-off where <I> > 3σ. 3 R sym = ΣjI -<I>j/ΣI.…”

mentioning

confidence: 99%

X-ray crystal structures of half the human papilloma virus E2 binding site: d(GACCGCGGTC)

Finley

Luo

1998

Nucleic Acids Research

View full text Add to dashboard Cite

The X-ray crystal structure of the DNA decamer d(GACCGCGGTC), containing half the human papilloma virus E2 binding site, has been solved from two crystals grown at different ionic conditions (50 mM MgCl2and 50 mM spermine or 1.56 mM MgCl2and 1.56 mM spermine). Despite the variation in salt concentration, the two DNA structures are in a very similar, A-type DNA conformation, with helical axes curving towards the major groove. Although the salt concentrations do not effect the helical parameters or hydration to a large degree, there is a change in the overall helical curvature; 18 degrees and 31 degrees for the low and high salt structures, respectively. This curvature appears to be sequence specific and biologically relevant when compared with similar DNA structures, including the E2 binding site of a protein-DNA complex.

show abstract

“…Individual Burkitt tumors have clonal origin (Fialkow et al 1973) and if immunological surveillance is, in fact, important in controlling the disease's development, one might expect that all tumors in the same patient would be the progeny of a single malignant clone which has escaped the surveillance system ( Figure 2). Two tumors were studied from each of 11 patients with Burkitt lymphoma using the G-6-PD system and in each case both tumors were of the same single G-6-PD type (Fialkow et al 1973, Fialkow 1975. The probability that this occurred by chance alone is less than 0.1 %.…”

Section: Introductionmentioning

confidence: 99%