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Biomedical subjects

H Bogaars

Publications and source records attributed to H Bogaars.

12 recordsLinked to original sources
PubMed1999

Systematized porokeratotic eccrine and hair follicle naevus: report of a case and review of the literature.

We report a unique case of a congenital keratinocytic naevus associated with severe alopecia, onychodysplasia and palmoplantar involvement in a 13-year-old girl. The lesions, consisting of scaly, spinous and verrucous papules and plaques, mainly followed Blaschko's lines and have remained unchanged since birth. The predominant histopathological picture was that of a column of parakeratosis overlying the eccrine ostia and hair follicles. This is the first case of a systematized keratinocytic naevus characterized by histopathology of eccrine and hair follicle porokeratosis and a widespread bilateral involvement. This may be a distinct entity to be included in the differential diagnosis of linear, hyperkeratotic dermatoses. We suggest its classification as systematized porokeratotic eccrine and hair follicle naevus.

Adolescent↗
PubMed1998

A new mouse model of experimental melanoma for vaccine and lymphokine therapy.

The annual incidence of malignant melanoma is estimated at 10-12 per 100,000 inhabitants in countries of central Europe and the United States, and alarmingly there has been a dramatic upward trend in that estimate. The B16 murine melanoma is a rapidly growing metastatic tumor of spontaneous origin, as are human malignant melanomas. Melanoma cells produce specific antigens which are uniquely different from normal cellular antigens, and the expression of such antigens is the cornerstone for preparation of anti-melanoma vaccines. One major problem in evaluating the effectiveness of vaccination and other biologic therapies is the variability of experimental tumor models. A new metastatic model of experimental melanoma which was developed in our laboratory imitates the major clinical stages of malignant metastatic melanoma: stage I, primary (local) tumor growth and bone marrow invasion; stage II, regional lymph node involvement; and stage III, metastasis to distant organs, such as the lungs. This model has been used successfully for screening vaccines constructed in our laboratory. Immunization with formalinized vaccines (of extracellular antigens, intact melanoma cells, or B700 antigen) or irradiated vaccines (of intact melanoma cells) partially inhibit primary melanoma tumor growth, reduce metastasis to regional lymph nodes and lungs, and significantly increase mean survival time. These anti-tumor effects were improved when polyvalent and monovalent vaccines were combined with IL-2 therapy. We also compared the immunogenic activity of vaccines made from B16 melanoma cells transfected with genes encoding murine IL-2 or GM-CSF, and effects on tumor bearing mice were compared with or without therapy using the corresponding lymphokines. In sum, comparison of antibody production, growth of primary melanoma tumors, number of surviving mice, mean survival time, and percent of mice with lung metastases, showed that the best course of immunotherapy involves vaccination of mice with irradiated B16 melanoma cells transfected to secrete GM-CSF, coupled with GM-CSF therapy.

Animals↗
PubMed1996

Immunization of mice with irradiated melanoma tumor cells transfected to secrete lymphokines and coupled with IL-2 or GM-CSF therapy.

We compared the immunogenic activity of irradiated vaccines prepared from B16 F10 melanoma cells with one made from B16 F10 melanoma cells transfected with genes encoding murine IL-2 or GM-CSF. Vaccines were studied in the conditions of treatment of C57BL/6 mice with or without the corresponding lymphokines. Control and prevaccinated mice were challenged with parental B16 F10 murine melanoma cells (5 x 10(5)) subcutaneously in the midtail to examine growth of the primary (local) tumor in the middle of the tall and metastases to the lungs. This experimental model is very close to the clinical stages of metastatic melanoma. The effectiveness of preimmunization of mice was determined by the levels of antibody production to a melanoma-associated antigen termed B700. The comparison of antibody production, growth of primary melanoma tumors, number of mice surviving at the end of the observation period, mean survival time and per cent mice with metastases in the lungs showed that the best course of immunotherapy was prevaccination of mice with a vaccine of irradiated B16 F10 melanoma cells transfected to secrete GM-CSF, coupled with GM-CSF therapy.

Animals↗
PubMed1995

Further characterization of a clinically relevant model of melanoma metastasis and an effective vaccine.

A major problem in evaluating the effectiveness of tumor cell vaccination and other biological therapies is the variability of experimental models. In this study we have further developed and characterized a model for metastatic melanoma that approximates the major clinical stages of metastatic dissemination: stage I--growth of the primary (local) tumor, stage II--dissemination to regional lymph nodes, and stage III--metastasis to distant organs (lungs). C57BL/6 mice were challenged subcutaneously with B16 F10 murine melanoma cells in the midtail, and within 3 weeks 100% of the mice had local tumors growing in their tails. By 5-7 weeks after challenge, most of the mice had developed metastases to the inguinal lymph nodes and subsequently had metastatic colonies in the lungs and in the bone marrow. Preimmunization of mice with a formalinized extracellular antigen vaccine, derived from B16 F10 melanoma cells, provided partial inhibition of the growth of the primary melanoma tumors, as well as reducing the number of metastases to the regional (inguinal) lymph nodes and lungs along with concomitantly increasing survival time. This model for melanoma metastasis provides a reasonable and reproducible test system for the study of anti-melanoma immunity and the different cellular and humoral mechanisms involved.

Animals↗
PubMed1994

Nude mouse model to study passive humoral immunotherapy directed against B16 F10 murine melanoma.

A model to study passive humoral immunotherapy of experimental melanoma was generated by subcutaneous injection of B16 F10 murine melanoma cells in the midtail of BALB/C nude (nu/nu) mice. Mice were challenged with melanoma cells pretreated: (1) with complete culture medium, (2) with 10% adjuvant control serum, (3) with 10% anti-fECA (formalinized extracellular antigens) immune serum, or (4) with a monoclonal antibody (mAB H2-3-3) specific for the B700 melanoma-associated antigen. All control mice challenged with melanoma cells pretreated either with culture medium or with medium containing adjuvant control serum (Groups I and II) died during the observation period of 84 days. At day 84, 60% of the mice challenged with melanoma cells pretreated with anti-fECA immune serum (Group III) survived, as did 100% of the mice challenged with cells pretreated with mAb H2-3-3 (Group IV). Injection of melanoma cells pretreated with mAb H2-3-3 was associated with the greatest reduction of subsequent local tumor growth and the lowest number of metastatic lung tumors. The inhibitory effects of immune sera in vivo also correlated with in vitro effects of anti-fECA immune serum and mAb H2-3-3, determined on B16 F10 melanoma target cells using assays for DNA synthesis and antibody dependent cellular cytotoxicity (ADCC). In sum, this nude mouse model for the study of passive humoral immunotherapy of experimental melanoma was utilized to demonstrate significant protective effects against B16 F10 melanoma cell challenge by treatment with anti-fECA immune sera or a melanoma-specific monoclonal antibody.

Animals↗
PubMed1993

Preimmunization of mice with formalinized extracellular antigens of melanoma in combination with IL-2 and surgical resection increased survival and tumor control in metastatic melanoma model.

Recently we found that immunization with formalized extracellular antigens (FECAs) could induce the production of specific antimelanoma antibodies and increase the defense mechanisms of antimelanoma cellular and humoral immunity. In experiments we used pathogen-free female mice C57BL/6 18-20 g. We injected FECA (0.02 mg of protein/per S.C.--subcutaneous injection) for 1 month, once per week. Concurrently we injected S.C. human recombinant IL-2: 100 U/g of weight (2,000 U/per mouse). Interleukin-2 (IL-2) was injected for 1 month, 5 days/week. On days 7, 14, 21, and 28 we took retroorbital blood from mice for the study of anti-FECA and anti-IL-2 antibody production with ELISA. Control and experimental mice were then given a subcutaneous injection with 0.5 x 10(6) cells B16-F10 melanoma in 25 microliters into the middle of the tail. By 18 days 100% developed local melanoma tumors. We resected tails of all control and experimental animals 5 mm distal the base of the tail under metaphan anesthesia. The production of antibodies to FECA and IL-2 started after the 21st day and was higher in the group of mice immunized with FECA and with IL-2 than in control animals. Combining preimmunization with FECA and IL-2 and resection of local melanoma tumors decreased the mortality and the number of mice with local recurrence and metastatic melanoma tumors to the lungs.

Animals↗
PubMed1983

Moist wound healing under a vapor permeable membrane.

Ten ambulatory patients with unilateral and eight with bilateral ulcers of various etiologies were studied to determine the effects of keeping a wound bed moist under a water vapor and oxygen permeable membrane (VPM). In the bilateral group, VPM healing was compared with a debriding enzyme ointment and 10% benzoyl peroxide in the same patient. The faster healing rate with VPM was compared to the healing rate with control substances by the paired t test, with significance at less than 0.05 level. In the unilateral group two patients with ulcers to bone or joint capsule and one patient who had failed grafting healed without surgery. Two patients failed to heal with the VPM. All healing occurred in the face of gross bacterial contamination. Three patients treated with VPM developed cellulitis. Wound healing under a vapor permeable membrane occurs with an increase of the average healing rate by a factor of 2.6 when compared to control substances in ambulatory patients.

Benzoyl Peroxide↗
PubMed1983

Treatment of bullous mastocytosis with disodium cromoglycate.

We describe two children with bullous mast cell disease. Both had been unresponsive to conventional therapy. Oral disodium cromoglycate in doses ranging from 60 to 200 mg per day produced dramatic improvement of the disease. Over the year of the study, no untoward reactions have been noted.

Administration, Oral↗
PubMed1983

Becker's melanosis: associated abnormalities.

Becker's melanosis is a distinct clinical entity. We report herein two cases with extensive lesions accompanied by subjacent and distant soft tissue and bony abnormalities. Review of the world's literature reveals several additional cases of structural abnormalities associated with Becker's melanosis. Rather than just a dermatologic curiosity, Becker's melanosis may be a marker for underlying structural anomalies.

Acanthosis Nigricans↗
PubMed1982

The surgical management of "in situ" melanoma.

The concept of melanoma "in situ" is discussed pointing out that these lesions have the potential to become invasive tumors if not adequately treated. If such a pathologic diagnosis is made, each margin of the specimen should be carefully checked for the presence of atypical melanocytes. In our experience, with excision margins of 0.5-1 cm, local recurrence has not been a problem.

Aged↗
PubMed1978

Rhinophycomycosis entomophthorae.

Rhinophycomycosis entomophthorae is a variant type of subcutaneous phycomycosis of the face that is caused by Entomophthora coronata. The case we describe was the first patient reported in the world literature, to our knowledge. His infection reappeared after an extended dormant period. Although his condition exhibited an early partial response to surgical and medical management, the condition became refractory to treatment.

Adult↗