Immunohistological detection of proliferating cells in normal and psoriatic epidermis using Ki-67 monoclonal antibody

Ando, Masaaki; Kawashima, T.; Kobayashi, Hitoshi; Ohkawara, Akira

doi:10.1016/0923-1811(90)90014-5

Cited by 37 publications

(25 citation statements)

References 10 publications

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“…Gastric cancer may arise in association with other types of proliferative lesions (4,23). Psoriasis is an inflammatory and epidermal hyperproliferative disease of the skin (32). Ki-67 immunoreactivity, BrdU exposure in vitro, and immunohistochemistry were used to evaluate rates of cell proliferation in epidermis of normal and psoriatic subjects.…”

Section: Ratsmentioning

confidence: 99%

“…Ki-67 immunoreactivity, BrdU exposure in vitro, and immunohistochemistry were used to evaluate rates of cell proliferation in epidermis of normal and psoriatic subjects. Patients with psoriasis had greatly increased numbers of labeled cells in the basal layer (some of which are probably stem cells) and other layers of the epidermis (32). Yet, epidemiological studies have not found an increased risk for skin tumors in these patients (33).…”

Section: Ratsmentioning

confidence: 99%

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Cell proliferation not associated with carcinogenesis in rodents and humans.

Ward

Uno

Kurata

et al. 1993

Environ Health Perspect

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Cell proliferation has often been found to be associated with carcinogenesis in rodents and humans at different stages of the multistage carcinogenesis process. The multistage process includes initiation, promotion, and progression phases. At each phase, increasing the normal level of cell turnover of target cells may enhance carcinogenesis. However, we present evidence that normal levels of cell turnover, or increasing the rate of cell turnover at these different stages, do not necessarily lead to enhanced carcinogenesis. In normal tissues, the length of the cell cycle depends on the age of the host and varies from tissue to tissue. Tissues with normal short cell cycles, such as intestine and bone marrow, do not show a high rate of spontaneous tumors in most species. Cells with higher turnover should be more susceptible to carcinogens at the initiation stage of carcinogenesis if cell proliferation per se causes cancer and if these cells or their progeny survive. Cancer in humans is more often associated with specific etiological factors rather than with the natural proliferative rate of specific tissues. For many tissues of humans and rodents, age-related diseases develop in a progressive, irreversible manner. Often, naturally occurring chronic degenerative and inflammatory changes in a tissue (e.g., kidney, liver, heart, reproductive tract) lead to chronic regeneration of the damaged tissue. Yet, cancer is rarely found in these tissues. In rodent carcinogenesis experiments, chronic toxic lesions, accompanied by increases in normal levels of cell turnover, have sometimes been observed in target organs of nongenotoxic carcinogens. More often, however, organ-specific nongenotoxic toxins are not carcinogens. These toxins include compounds toxic for the liver, kidney, and nasal cavity. In 19 inhalation bioassays conducted by the National Toxicology Program, 5/5 nasal carcinogens and 12/14 nasal noncarcinogens caused nasal lesions usually associated with chronic cell proliferation. Although cell proliferation may contribute to multistage carcinogenesis, cell proliferation is not necessarily a tumor promoter or cocarcinogen.

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Section: Ratsmentioning

confidence: 99%

Section: Ratsmentioning

confidence: 99%

Cell proliferation not associated with carcinogenesis in rodents and humans.

Ward

Uno

Kurata

et al. 1993

Environ Health Perspect

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“…20 Nevertheless, the overall findings and immunostaining pattern mirrored that of conventional psoriasis. 9–11,21 …”

Section: Discussionmentioning

confidence: 99%

“…Additionally, tissue samples from the 4 cases were stained for Keratin 16 and Ki-67 antigen as markers of keratinocyte hyperproliferation and compared with findings in conventional psoriasis lesions. 9–11 …”

Section: Methodsmentioning

confidence: 99%

Psoriasiform eruptions during Kawasaki disease (KD): A distinct phenotype

Haddock

Calame

Shimizu

et al. 2016

Journal of the American Academy of Dermatology

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Background A psoriasis-like eruption develops in a subset of patients with Kawasaki disease (KD). Objective To systematically compare KD-associated psoriasiform eruptions with classic psoriasis and the outcomes of KD in children with and without this rash. Methods This was a retrospective study of 11 KD cases with a psoriasiform eruption matched 1:2 by age, gender, and ethnicity with psoriasis-only and KD-only controls. Genotyping was performed in 10 cases for a deletion of two late cornified envelope (LCE) genes, LCE3C_LCE3B-del, associated with increased risk for pediatric-onset psoriasis. Results Similar to classic psoriasis, KD-associated eruptions were characterized clinically by well-demarcated, scaly pink plaques and histopathologically by intraepidermal neutrophils, suprabasilar keratin 16 expression, and increased Ki-67 expression. They showed less frequent diaper area involvement, more crust and serous exudate, and an enduring remission (91% vs. 23% with confirmed resolution; p < 0.001). Frequency of LCE3C_LCE3B-del and major KD outcomes were similar between cases and controls. Limitations The study was limited by the small number of cases, treatment variation, and availability of skin biopsy specimens. Conclusions Although the overall clinical and histopathologic findings were similar to conventional psoriasis, this appears to be a distinct phenotype with significantly greater propensity for remission. No adverse effect on KD outcomes was noted.

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“…In con trast, the antibody K.i-67 is a well-established marker for evaluating the number of proliferating cells. Furthermore, this antibody allows a quick and easy evaluation of the growth fraction of normal [13] and neoplastic cell popula tions [6]. A relative disadvantage at the beginning was that the antibody was exclusively applicable on frozen tis sue sections.…”

Section: Discussionmentioning

confidence: 99%

Identification of Proliferating Keratinocytes in Middle Ear Cholesteatoma Using the Monoclonal Antibody Ki-67

Bujía

Holly²,

Sudhoff³

et al. 1996

ORL

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Cholesteatoma epithelium is characterized by a keratinocyte dysregulation with aggressive growth subsequently destroying the middle ear mucosa. The monoclonal antibody Ki-67 recognizes a nuclear antigen expressed by cells in the G₁, S, and G₂/M phases being used to determine the growing cell fraction in tissue samples. Cryostat sections of skin and cholesteatoma biopsies were examined immunohistochemically for reactivity with Ki-67 using the alkaline phosphatase-anti-alkaline phosphatase method. Nuclear staining was seen in a small number of keratinocytes located in the basal cell layer of normal auditory meatal skin. In contrast, numerous cells of the basal and suprabasal layers in cholesteatoma were found to react with Ki-67. A cytoplasmic staining was also observed in both skin and cholesteatoma. In cholesteatoma, the cytoplasmic staining was stronger. These results clearly show that cholesteatoma epithelium proliferates at a higher rate than normal epidermis, confirming the hyperproliferative behavior of cholesteatoma.

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Immunohistological detection of proliferating cells in normal and psoriatic epidermis using Ki-67 monoclonal antibody

Cited by 37 publications

References 10 publications

Cell proliferation not associated with carcinogenesis in rodents and humans.

Cell proliferation not associated with carcinogenesis in rodents and humans.

Psoriasiform eruptions during Kawasaki disease (KD): A distinct phenotype

Identification of Proliferating Keratinocytes in Middle Ear Cholesteatoma Using the Monoclonal Antibody Ki-67

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