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Biomedical subjects

M A Lutzner

Publications and source records attributed to M A Lutzner.

At least 19 recordsLinked to original sources
PubMed1985

Multiple cutaneous papillomas and carcinomas that develop spontaneously in a mouse mutant, the repeated epilation heterozygote Er/+.

After a chance observation that multiple cutaneous papillomas and squamous cell carcinomas occurred in 2 adult mice heterozygous for the repeated epilation gene Er, we surveyed a panel of 10 +/+ (wild type) and 30 Er/+ (heterozygous) mice from birth to over 2 years of age. Homozygous Er/Er mice could not be included since their defect is lethal at birth. Whereas no cutaneous tumors developed in the +/+ mice, 20 of the Er/+ mice, males and females, had developed 1-5 cutaneous papillomas and at least 1 cutaneous invasive squamous cell carcinoma by 2 years of age. No lesions were seen in mice younger than 6 months old. Although almost all Er/+ mice died with their tumor burden, no metastases have yet been proven histologically. The Er/+ mouse should serve as a useful model for the exploration of genetic factors in cutaneous squamous cell carcinomas in humans.

Alopecia↗
PubMed1985

[History of 2 cells in T cell lymphomas and leukemias: the cerebriform Lutzner cell in Sézary syndrome and the polylobulated or polypetaloid cell in acute T cell lymphoma/leukemia].

In normal blood, there appears to be two similar but different subsets of T-lymphocytes present: (1) the cerebriform or convoluted Sézary-syndrome Lutzner cell, which may give rise to cutaneous T-cell lymphoma; (2) the polypetaloid or lobated acute T-cell lymphoma/leukemia (ATLL) cell, which may give rise to ATLL. Both cell types can be differentiated by their characteristic nuclear shapes.

Acute Disease↗
PubMed1984

Clinical observations, virologic studies, and treatment trials in patients with epidermodysplasia verruciformis, a disease induced by specific human papillomaviruses.

We have studied 11 patients with the papillomavirus-induced disease epidermodysplasia verruciformis (EV). Clinical diagnostic features are widespread, long-lasting, pityriasis versicolor-like macules and flat, wart-like papules, both usually occurring in early childhood, with the subsequent development in the third decade of multiple skin cancers of the Bowenoid in situ and squamous cell types, primarily in sun-exposed skin. Virologic studies using the methods of immunofluorescence microscopy, restriction endonuclease analysis, and DNA blot hybridization have shown benign lesions to be associated with one or several types of the human papillomaviruses (HPVs) specifically associated with EV (at least 15 types recognized on the basis of sequence homology studies of molecularly cloned genomes). Skin cancers in these patients were associated with the genomes of either HPV-5, HPV-8 or HPV-14, suggesting that these three viruses are potentially oncogenic. A genetic factor appears to play a role in the pathogenesis of EV, since 5 of our patients were children of consanguineous parents and 2 had siblings also suffering with EV, suggesting a recessive inheritance pattern. Treatment of 4 EV patients with an oral retinoid resulted in partial temporary improvement of benign lesions, and the treatment of 2 patients with intralesional interferon injections into multiple Bowenoid cancers in situ has resulted in the disappearance of these lesions. Finally, EV serves as a model for studying the interplay of oncogenic viruses, genetic and immunologic factors, and sunlight in the production of skin cancer in humans.

Adult↗
PubMed1984

Molecular cloning and characterization of the genomes of nine newly recognized human papillomavirus types associated with epidermodysplasia verruciformis.

The genomes of 11 human papillomaviruses (HPVs) found in benign lesions of eight patients suffering from epidermodysplasia verruciformis were cloned in Escherichia coli after insertion into plasmid pBR322. The study of the sensitivity of the cloned HPV DNAs to 14 restriction endonucleases permitted the construction of physical maps. DNA-DNA hybridization experiments, performed under stringent conditions, showed that these viruses represent nine new types, HPVs 14 (with subtypes a and b), 15, 17 (with subtypes a and b), 19, 20, 21, 22, 23, and 24. These HPVs were divided into three groups based on an absent or very weak cross-hybridization among the genomes of the viruses belonging to different groups.

Chromosome Mapping↗
PubMed1984

Papillomaviruses and skin cancer in Africa.

Although it was suggested long ago that certain epithelial cancers preceded by papillomas might be caused by viruses, the first proof that papillomaviruses were associated with cancer dates from the work on rabbits in 1934 by Shope and Rose. In the 1970s, the introduction of the blot hybridization technique enabled Orth and his co-workers at the Institut Pasteur, Paris, to demonstrate the presence in man of the DNA of human papillomavirus type 5 (HPV-5) in cancers following Lutz-Lewandovsky epidermodysplasia verruciformis. Some years later, it was possible to demonstrate the presence of the same HPV-5 DNA in the skin cancer of an immunosuppressed recipient of a renal transplant. The number of potentially oncogenic papillomaviruses has recently been increased by the demonstration at the Institut Pasteur of the presence of the DNAs of HPV-8 and HPV-14 in the skin cancers of patients with epidermodysplasia verruciformis. In recent years, an association has been demonstrated between HPV-6, -10, -11, -16, and -18 with verrucous cancers of the skin and mucous membranes, Bowenoid papules, Bowenoid skin diseases and cervical cancer. Such cancers of the skin and mucous membranes are usually treated by surgery, but it has been shown that oral administration of retinoids (synthetic derivatives of vitamin A) or the use of leucocyte interferon intralesionally are effective in cancers in situ following epidermodysplasia verruciformis.

Africa↗
PubMed1978

Epidermodysplasia verruciformis. An autosomal recessive disease characterized by viral warts and skin cancer. A model for viral oncogenesis.

EV is an autosomal recessive disease which usually begins in infancy or childhood, with an average age of onset of 9. Flat warts are most common, but pityriasis-like warts occur in approximately 75% of patients. Warts are disseminated and chronic. Cancer may develop as early as age 13; the average age of onset is 31. About 1/3 rd. of patients develop cancer of the skin usually multiple and in light-exposed areas. It may take only two years from wart to cancer, or many more years. The cancer is carcinoma-in-situ of the Bowenoid type or squamous cell carcinoma. Two deaths have occured by local invasion and only one metastasis has been reported. One patient died of Burkitt's lymphoma and another was reported to have disseminated reticulosis. 8% of the patients are mentally retarded. Humoral immunity is normal; cell mediated immunity is depressed in most patients. The gene defect in EV has not yet been uncovered.

Adolescent↗
PubMed1976

Skin exfoliation and purulent conjunctivitis in a new mutant-the exfoliative mouse.

A spontaneous autosomal recessive mutation has been named the exfoliative mouse (genotype ex/ex). Exfoliative mice suffer a transient purulent conjunctivitis in their 3rd week and an exfoliative skin disease in their 4th week. Gram-negative bacilli are present in blood and cerebrospinal fluid during the conjunctivitis stage, and in skin during the exfoliative period. The mutant can be differentiated from the ichthyotic mouse mutant.

Animals↗
PubMed1976

The Sézary syndrome: a malignant proliferation of helper T cells.

The Sézary syndrome is a frequently lethal disease characterized by circulating malignant cells of thymus-derived (T)-cell origin. The capacity of circulating malignant lymphocytes from patients with this syndrome to synthesize immunoglobulins and to function as helper or suppressor cells regulating immunoglobulin synthesis by bone marrow-derived (B) lymphocytes was determined. Peripheral blood lymphocytes from normal individuals had geometric mean immunoglobulin synthetic rates of 4,910 ng for IgM, 1,270 ng for IgA, and 1,625 ng for IgG per 2 X 10(6) cells in culture with pokeweed mitogen for 7 days. Purified normal B cells had geometric mean synthetic rates of 198 ng for IgM, 145 ng for IgA, and 102 ng for IgG. Leukemic cells from patients with the Sézary syndrome produced essentially no immunoglobulins. Adding normal T cells to normal B cells restored their immunoglobin producing capacity. Leukemic cells from four of five patients tested had a similar capacity to help immunoglobulin synthesis by purified normal B cells. Additionally, Sézary cells from one patient studied induced a nearly 10-fold increase in IgA synthesis by lymphocytes from a child with ataxia telangiectasia and selective IgA deficiency. Furthermore, these Sézary cells induced more than a 500-fold increase in IgG and IgA synthesis by lymphocytes from a child with Nezelof's syndrome. When Sézary cells were added to normal unfractionated lymphocytes, they did not suppress immunoglobulin biosynthesis. In addition, unlike the situation observed when large numbers of normal T cells were added to purified B cells, there was no depression of immunoglobulin synthesis at very high malignant T-cell to B-cell ratios. These data support the view that Sézary T cells do not express suppressor cell activity. The results presented in this paper suggest that neoplastic lymphocytes from the majority of patients with the Sézary syndrome originate from a subset of T cells programmed exclusively for helper-like interactions with B cells in their production of immunoglobulin molecules.

Adult↗