Bivariate flow cytometric analysis of DNA content versus immunopositivity for ribonucleotide reductase M1 subunit in the cell cycle

Mangiarotti, Rosanna; Bottone, Maria Grazia; Danova, Marco; Pellicciari, C.

doi:10.1002/(sici)1097-0320(19980601)32:2<78::aid-cyto2>3.0.co;2-a

Cited by 6 publications

(7 citation statements)

References 16 publications

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“…Our results (and conclusions) deviate to some extent from those of the latter study, probably because a different indicator of proliferative capacity was used; that reality underscores that each monoclonal antibody used in PI studies (e.g., antiproliferating cell nuclear antigen, MIB-1, Ki-S5) shows its own distinctive "profile" in paraffin sections of various neoplastic tissues, and those reagents therefore cannot be compared with one another directly (27,28). In the Rudolph et al (12) study, a mean PI of 6.38% was seen in 57 in situ melanomas, and that was significantly different from the Ki-S5 index in benign nevi.…”

Section: Discussioncontrasting

confidence: 80%

Concurrent Ki-67 and p53 Immunolabeling in Cutaneous Melanocytic Neoplasms: An Adjunct for Recognition of the Vertical Growth Phase in Malignant Melanomas?

et al. 2000

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In attempts to extend morphologic observations in the prediction of biologic behavior, several adjunctive techniques have been applied to cutaneous melanocytic lesions of all types. These procedures have included nuclear morphometry (1); immunostaining for p53 proteins (2-4), the INK4A/CDKN2 tumor suppressor gene product (5), proliferating cell nuclear antigen (6 -8), or the Ki-67 nuclear protein (9 -13); and histochemical analysis of nucleolar organizer regions (14).A particularly challenging facet of dermatopathology concerns the more narrow setting of melanocytic malignancy. In that context, it is important to identify the growth phases (radial or vertical) of melanomas, in recognition of the prognostic importance attached to them (15). Our laboratory has

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Section: Discussioncontrasting

confidence: 80%

Concurrent Ki-67 and p53 Immunolabeling in Cutaneous Melanocytic Neoplasms: An Adjunct for Recognition of the Vertical Growth Phase in Malignant Melanomas?

et al. 2000

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“…This protein is a large subunit of the enzyme catalyzing the rate-limiting step in DNA synthesis, the conversion of ribonucleotides to deoxyribonucleotides. Due to its persistence through the cell cycle in rapidly cycling cells and relatively long halflife, ribonucleoside diphosphate reductase M1 protein is considered a suitable marker for cellular proliferation (13). Decreased expression of this protein in treated HCT 116 cells conforms to their observed diminished proliferative capacities.…”

Section: Discussionmentioning

confidence: 99%

Differential antiproliferative mechanisms of novel derivative of benzimidazo[1,2-α]quinoline in colon cancer cells depending on their p53 status

Sedić¹,

Poznic²,

Gehrig³

et al. 2008

Molecular Cancer Therapeutics

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In the present article, we describe a mechanistic study of a novel derivative of N-amidino-substituted benzimidazo [1,2-A]quinoline in two human colorectal cancer cell lines differing in p53 gene status. We used a proteomic approach based on two-dimensional gel electrophoresis coupled with mass spectrometry to complement the results obtained by common molecular biology methods for analyzing cell proliferation, cell cycle, and apoptosis.

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“…In both normal and malignant cells, levels of RR were found to correlate with markers of proliferation such as Ki-67 and proliferating cell nuclear Ag. 41 In cervical carcinoma cells, for example, the cytoplasmic levels of the R2 catalytic subunit of RR increased 17-fold as cells entered S phase compared with quiescent cells in G 2 -M phase. 42 However, in sharp contrast to normal cells, malignant cells were shown to express high levels of RR in vivo and in vitro even in a quiescent state, possibly as a result of being arrested in G 1 phase, where RR is expressed.…”

Section: Discussionmentioning

confidence: 99%

Multi-attenuated herpes simplex virus-1 mutant G207 exerts cytotoxicity against epithelial ovarian cancer but not normal mesothelium and is suitable for intraperitoneal oncolytic therapy

et al. 2000

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Recombinant strains of herpes simplex virus-1 (HSV-1) harboring mutations in the infected cell product (ICP)34.5 region lose their neurovirulence and replicate more efficiently in dividing tumor cells than stationary cells, becoming replication-selective oncolytic agents. Additional mutation of the ICP6 gene, which encodes ribonucleotide reductase, further impairs the ability of HSV-1 mutants to replicate in normal cells, enhancing tumor selectivity. The present study investigated the effect of HSV-G207, a recombinant HSV-1 lacking ICP34.5 and ICP6, against epithelial ovarian cancer (EOC) in vitro and in vivo in a mouse xenograft model. To assess the selectivity of multimutated HSV-G207 against malignant cells, HSV-G207 and wild-type HSV-F were comparatively tested against normal human peritoneal mesothelial cells and EOC cells in vitro. HSV-G207 infected both EOC cells and mesothelial cells; however, unlike EOC cells, mesothelial cells provided a poor substrate for replication of HSV-G207. In contrast to wild-type HSV-F, HSV-G207 exerted a potent oncolytic effect on EOC cells but spared normal mesothelial cells in vitro. Primary EOC cells were more sensitive to the virus than established EOC cell lines. A single intraperitoneal injection of HSV-G207 resulted in a significant reduction in tumor volume and tumor spread in vivo. HSV-G207 was shown to penetrate deeply within tumor nodules and caused no apparent intraperitoneal toxicity. Oncolytic therapy with multimutated replication-restricted HSV may offer a novel approach in the treatment of EOC. Cancer Gene Therapy (2000) 7, 275-283 Key words: Viral oncolytic therapy; herpes simplex virus; ovarian cancer; intraperitoneal therapy.V iral-based oncolytic therapy has gained renewed interest due to recent advances in molecular virology allowing for manipulation of the viral particles and enhancement of their tumor specificity. 1,2 Replicationselective herpes simplex virus-1 (HSV-1) mutants have been engineered by deletions of both copies of the RL1 gene. 3 Its product, infected cell product (ICP)34.5 protein, plays a major role in neurovirulence 4 and in prevention of the premature shutoff of protein synthesis in infected cells. 5 ICP34.5-null HSV-1 mutants such as HSV-1716 and HSV-R3616 have been shown to replicate preferentially in tumor cells, causing a direct oncolytic effect. 2,6 HSV-G207 was further attenuated by inserting the Escherichia coli lacZ gene into the HSV ICP6 gene, which encodes ribonucleotide reductase (RR), on the ICP34.5 Ϫ backbone of HSV-R3616. 7 HSV-G207 was shown to be hypersensitive to the antiherpetic drug ganciclovir 7 and to display no detectable neurovirulence. 7,8 Replication-selective HSV-1 mutants have been demonstrated to be efficacious antitumor agents in experimental models of various central nervous system (CNS) tumors. 3,4,8 -17 Based on promising preclinical results in experimental CNS tumors, dose escalation phase I clinical trials have begun using stereotactic application of HSV-G207 and HSV-1716 for the treatment of malignan...

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Bivariate flow cytometric analysis of DNA content versus immunopositivity for ribonucleotide reductase M1 subunit in the cell cycle

Cited by 6 publications

References 16 publications

Concurrent Ki-67 and p53 Immunolabeling in Cutaneous Melanocytic Neoplasms: An Adjunct for Recognition of the Vertical Growth Phase in Malignant Melanomas?

Concurrent Ki-67 and p53 Immunolabeling in Cutaneous Melanocytic Neoplasms: An Adjunct for Recognition of the Vertical Growth Phase in Malignant Melanomas?

Differential antiproliferative mechanisms of novel derivative of benzimidazo[1,2-α]quinoline in colon cancer cells depending on their p53 status

Multi-attenuated herpes simplex virus-1 mutant G207 exerts cytotoxicity against epithelial ovarian cancer but not normal mesothelium and is suitable for intraperitoneal oncolytic therapy

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