Biomedical subjects

Mahmoud R Hussein

Publications and source records attributed to Mahmoud R Hussein.

At least 37 records · Page 2Linked to original sources

PubMed2005

Analysis of the Bcl-2 and p53 protein expression in the lymphoproliferative lesions in the upper Egypt.

BACKGROUND: Lymphomagenesis involves poorly understood alterations in the proapoptotic and prosurvival molecules. In the Upper Egypt, the clinicopathologic and genetic characteristics (p53 and Bcl-2) of the lymphoproliferative lesions (reactive hyperplasia, RH; Non-Hodgkin's lymphoma, NHL and Hodgkin's disease, HD) is unknown. OBJECTIVES: To examine the lymphoproliferative lesions for: (1) their clinicopathologic features, (2) the p53, and Bcl-2 protein expression and (3) the correlation between the clinicopathologic features and the genetic alterations. METHODS: p53 and Bcl-2 protein expression was immunohistochemically evaluated in 68 lesions including 47 NHL, 10 HD, and 11 RH. The average weighted scores reflecting staining intensity and the percentage of positive cells were calculated. RESULTS: Clinically: 1) the mean age incidence gradually increased from HD to RH to NHL (16.1 +/- 5.9, 36.6 +/- 7.45 and 46.74 +/- 3.2, p = 0.001) and 2) NHL and RH showed slight female (1.1:1) and male (1.2:1) sex predilection, respectively. Also, HD has male (2.3:1) sex predilection. The bcl-2 average weighted scores showed gradual downregulation with the transition from low to intermediate to high grade NHL (9.50 +/- 1.12 > 6.67 +/- 0.70 > 6.28 +/- 0.83, p = 0.041). Alternatively, the p53 average weighted scores showed gradual upregulation with the transition from low to intermediate to high grade NHL (0.40 +/- 0.22 < 1.72 +/- 0.35 < 2.15 +/- 0.52, p = 0.023). There was a negative correlation between bcl-2 and p53 protein expression in NHL (r = -0.221, p = 0.165). In HD, Reed-Sternberg cells and their variants showed positive and negative reactivity for Bcl-2 and p53 protein expression, respectively. CONCLUSIONS: In the Upper Egypt: (1) lymphoproliferative lesions had some peculiar clinicopathologic features and (2) Bcl-2 and p53 proteins are altered in the lymphoproliferative lesions.

Down-Regulation↗

PubMed2005

Apoptosis in the ovary: molecular mechanisms.

Cell death was first described in rabbit ovaries (Graaffian follicles), the phenomenon being called 'chromatolysis' rather than apoptosis. In humans, the ovarian endowment of primordial follicles is established during fetal life. Apoptotic cell death depletes this endowment by at least two-thirds before birth, executed with the help of several players and pathways conserved from worms to humans. To date, apoptosis has been reported to be involved in oogenesis, folliculogenesis, oocyte loss/selection and atresia. Several pro-survival and pro-apoptotic molecules are involved in ovarian apoptosis with the delicate balance between them being the determinant for the final destiny of the follicular cells. This review critically analyses the current knowledge about the biological roles of these molecules and their relevance to the dynamics of follicle development. It also presents the existing literature and assesses the gaps in our knowledge.

Activins↗

PubMed2005

Alterations of p53 and Bcl-2 protein expression in the laryngeal intraepithelial neoplasia.

BACKGROUND: The squamous cell carcinoma of the larynx (SCC) is a common head and neck malignancy. I hypothesize that the development of laryngeal intraepithelial neoplasia (LIN) involves alterations of tumor suppressor genes (p53) and protooncogenes (Bcl-2). METHODS: To test this hypothesis, 40 vocal cord biopsy specimens were examined for p53 and Bcl-2 protein expression using immunoperoxidase staining methods and mouse monoclonal antibodies. RESULTS: The lesions appeared as localized , flat or papillary areas with white (leukoplakic) red (erythroplakic), or gray appearance. Histologically, the lesions entailed variable associations of mild (LIN I), moderate (LIN II), sever dysplasia (LIN III or in situ carcinoma) and superficially invasive SCC. As compared to the normal mucosa, the average weighted immunoreactivity scores for p53 and Bcl-2 proteins showed significant upregulation with the transitions from LIN I to LIN II to LIN III to superficially invasive SCC , respectively (0.0 +/- 0.0, 0.0 +/- 0.0, 1.8 +/- 0.8, 2.3 +/- 0.8, 5.8 +/- 3.2, p = 0.00 for p53 ) and (4.4 +/- 0.4, 4.0 +/- 0.8, 6.0 +/- 2.0, 9.6 +/- 1.6 and 10.7+/- 1.3, p = 0.00 for Bcl-2). There were insignificant positive correlation between p53 and both Bcl-2 (r = +0.8, p>0.13) protein expression. CONCLUSIONS: Alterations of the p53 and Bcl-2 proteins occur during the development of SCC.

Biomarkers, Tumor↗

PubMed2005

The relationships between p53 protein expression and the clinicopathological features in the uveal melanomas.

BACKGROUND: p53 alterations are common events in cancer and may have some prognostic ramifications. OBJECTIVES: To investigate the uveal melanoma for: (1) the p53 expression patterns, (2) the relationships among p53 expression and clinicopathological features of these lesions. MATERIALS AND METHODS: Using Immunoperoxidase-staining methods and mouse monoclonal antibodies, the expression of p53 protein in 60 uveal melanomas was examined. RESULTS: Based on p53 immunoreactivity, the lesions were divided into two groups: the first group included 9 tumors (15%) and had p53 protein overexpression. The second group included 51 (85%) tumors and was lacking p53 expression. p53 protein overexpression was significantly associated with extraocular extension and vascular invasion (p values, 0.01 and 0.04). No significant correlation was found between p53 protein expression and the clinicopathologic features of these lesions. CONCLUSIONS: p53 protein overexpression occurs in the uveal melanoma and may be associated with some unfavorable histological features (invasion).

Aged↗

PubMed2005

Microsatellite instability and alterations of mismatch repair protein expression in choroidal melanomas.

OBJECTIVES: To examine choroidal melanomas for genomic instability, manifested by microsatellite instability (MSI) and mismatch repair (MMR) protein alterations, and to determine the association of these alterations with selected clinicopathological features of the tumors. METHODS: Polymerase chain reaction-based microsatellite assays were applied to analyze 57 cases of choroidal melanomas using 11 microsatellite markers at 5 chromosomal regions: 1p, 2p, 4q, 9p, and 17p. Immunoperoxidase staining methods and mouse monoclonal antibodies were used to investigate the expression patterns of MMR proteins. RESULTS: Microsatellite instability was found at the 1p, 9p, and 17p regions in these lesions with an overall prevalence of 35% (20/57). The frequency of MSI ranged from 9% (1/11) to 27% (3/11), ie, low-level MSI (MSI-L). The instability was most commonly found at the 1p region (D1S2734, 55%; D1S2832, 40%; and D1S233, 20%). Two MSI banding patterns, band shifts and the appearance of additional bands, were found in 10% and 90% of the unstable lesions, respectively. The average percentages of hMLH1 and hMSH2 positively stained cells were insignificantly reduced in the unstable lesions (81.7 +/- 9.3 and 76.7 +/- 16.7) as compared with the stable lesions (84.1 +/- 15.5 and 78.6 +/- 19.6; P = .62 and 0.74 for hMLH1 and hMSH2, respectively). There was no significant difference in survival between the 2 groups; however, relative to the stable subset, the unstable tumors showed a trend (P<.10) toward occurring at a younger age and having tumor cells in vascular lakes. CONCLUSIONS: The presence of MSI-L in some choroidal melanomas defines a novel genetic subset of these tumors and suggests that MSI (genomic instability) may play a role in their molecular pathogenesis. Elucidation of the underlying mechanisms for MSI will require further investigation. CLINICAL RELEVANCE: Detection of the MSI-L pattern might prove to be useful as an adjunct to the conventional diagnosis of choroidal melanomas. Larger series are needed to determine whether any of the correlative trends noted in this study will achieve statistical significance. To the best of our knowledge, this study is the first to define both the MSI and MMR protein expression features of choroidal melanomas.

Base Pair Mismatch↗

PubMed2005

Rhinosporidiosis in Egypt: a case report and review of literature.

Rhinosporidiosis is an infection caused by Rhinosporidium seeberi that frequently presents as a polypoidal nasal lesions. Here, we report the first indigenous case of tumoral rhinosporidiosis in Egypt. In this case, a 25-year-old male patient from a rural background of Assuit City presented with epistaxis and a nasal polyp. The patient had not traveled abroad. The diagnosis was established on the morphological basis by the identification of 5- to 10-microm endospores and 50- to 1000-microm sporangia. The clinicopathological and immunologic features were discussed and the literature was reviewed. To the best of our knowledge this is the first case of this disease to be reported in Egypt in the human literature.

Adult↗

PubMed2005

Phenotypic characterization of the immune and mast cell infiltrates in the human testis shows normal and abnormal spermatogenesis.

OBJECTIVE: To assess the types, distributions, and numbers of immune cell infiltrates in the testes of men with azoospermia. DESIGN: Prospective study. SETTING: University research and clinical institutes. PATIENT(S): Thirty-one men with azoospermia showing normal spermatogenesis (n = 10), germ cell maturation arrest (GA, n = 12), and Sertoli cell-only syndrome (SCO, n = 9). INTERVENTION(S): Testicular tissue biopsies. Sections were stained with routine (hematoxyline and eosin), special (Masson Trichrome, Gordon, Periodic Acid Schiff, Aldehyde Fuchsin, and Orcein stains), and immunoperoxidase stains (using monoclonal antibodies for B and T cells and CD68 macrophages). MAIN OUTCOME MEASURE(S): Serum levels of T, FSH, and LH in addition to histopathological analysis. RESULT(S): Hormonal profiles were unremarkable in all patients. Marked deposition of the reticular and collagen fibers was seen more in abnormal than normal spermatogenesis. The immune (B and T lymphocytes and CD68 macrophages) and mast cells were found in the interstitium, tubular walls, and lumens of all the testes analyzed. The differential counts of these cells (B and T lymphocytes, CD68 macrophages, and mast cells, respectively) were higher in SCO (1.66 +/- 0.46, 9.14 +/- 1.30, 2.26 +/- 1.68, 3.35 +/- 0.23) and GA (2.03 +/- 0.48, 4.70 +/- 1.00, 2.61 +/- 0.70, and 4.18 +/- 0.13) when compared with those in normal spermatogenesis (1.22 +/- 0.19, 5.41 +/- 0.58, 1.55 +/- 0.33, and 2.26 +/- 0.13). Increased cellular counts were not statistically significant for T and B cells and macrophages. However, these differences were statistically significant for mast cells. CONCLUSION(S): Abnormal spermatogenesis is associated with increased numbers of the immune and mast cells. Our findings may reflect an exaggerated immune response in these cases.

Adult↗

PubMed2005

Ultraviolet radiation and skin cancer: molecular mechanisms.

Every living organism on the surface of the earth is exposed to the ultraviolet (UV) fraction of the sunlight. This electromagnetic energy has both life-giving and life-endangering effects. UV radiation can damage DNA and thus mutagenize several genes involved in the development of the skin cancer. The presence of typical signature of UV-induced mutations on these genes indicates that the ultraviolet-B part of sunlight is responsible for the evolution of cutaneous carcinogenesis. During this process, variable alterations of the oncogenic, tumor-suppressive, and cell-cycle control signaling pathways occur. These pathways include (a) mutated PTCH (in the mitogenic Sonic Hedgehog pathway) and mutated p53 tumor-suppressor gene in basal cell carcinomas, (b) an activated mitogenic ras pathway and mutated p53 in squamous cell carcinomas, and (c) an activated ras pathway, inactive p16, and p53 tumor suppressors in melanomas. This review presents background information about the skin optics, UV radiation, and molecular events involved in photocarcinogenesis.

Basal Cell Carcinoma↗

PubMed2005

Transforming growth factor-beta and malignant melanoma: molecular mechanisms.

Transforming growth factor family members (TGF-beta) are secretory polypeptides that have dual tumor-suppressor and oncogenic effects. They signal through kinase receptor complexes on the cell surface, which phosphorylate cytoplasmic mediators (SMADs). Upon phosphorylation, SMADs march to the nucleus and interact with coactivators or corepressors to mediate the transcriptional regulation of several genes resulting in diverse effects. In tumorigenesis, malignant cells escape from the tumor-suppressive effects of TGF-beta by mutational inactivation or dysregulated expression of the molecular components in TGF-beta signaling pathway. Although melanoma cells are resistant to the tumor-suppressive effects of TGF-beta, there are no detectable defects at the receptor/SMAD level. Therefore, in these lesions, it is possible that TGF-beta effects occur independently of TGF-beta receptor/SMAD pathway. This review seeks to examine the present knowledge about TGF-beta receptor/SMAD signaling pathway and its related genes (SMADs, SKI, Filamin, endoglin, Follistatin, and other molecules) in melanomas.

Animals↗

PubMed2005

Ultrastructural evaluation of the radioprotective effects of melatonin against X-ray-induced skin damage in Albino rats.

Our knowledge about the radioprotective effects of melatonin against X-ray-induced skin damage is still lacking. To examine these effects, an animal model of 60 Albino rats was used. The animals were divided into five groups: Group 1, nonirradiated; Group 2, X-ray irradiated (XRI, 8 Gy); Group 3, XRI pretreated with solvent (ethanol and phosphate-buffered saline); Group 4, nonirradiated group treated with melatonin; and Group 5, XRI pretreated with melatonin. The skin was evaluated for ultrastructural changes using transmission electron microscopy (TEM). When compared to the nonirradiated skin (Groups 1 and 4), XRI skin (Groups 2 and 3) showed features of both cell injury and increased metabolic activity. The former included changes such as condensation of the nuclei, vacuolization of the cytoplasm, dilatation of the rough endoplasmic reticulum, swelling of the mitochondria with cristolysis, destruction of the ribosomes and intermediate filaments, fragmentation of the keratohyaline granules and loss of the irregularity of the basal cell borders. The central cells of the sebaceous gland alveoli had larger irregular nuclei and few lipid droplets in their cytoplasm. The hair follicle cells had heterochromatic nuclei and less electron dense cytoplasm containing few complements of the organelles. The features of increased metabolic activity included increased euchromatin, irregularity of the nuclear membrane and increased branching of the melanocytes. Also, an increased number of the Birbeck granules were seen in the Langerhans cells. When compared to the irradiated skin (Groups 2 and 3), these changes were mild or absent in the skin of XRI animals pretreated with melatonin (Group 5). The ability of melatonin to minimize the injurious effects of XRI suggests a radioprotective role. The clinical ramifications of these observations warrant further studies.

Albinism↗

PubMed2005

Enhancement of the repair of meniscal wounds in the red-white zone (middle third) by the injection of bone marrow cells in canine animal model.

Bone marrow stem cells (BMSCs) can differentiate into several cells that participate in the healing of meniscal wounds. To test this hypothesis, we examined the effects of injected BMSCs on the healing of meniscal wounds. Autologous BMSCs from eight adult dogs were injected into meniscal wounds (knee joints). After 12 weeks, the healing process was clinically and immunomorphologically evaluated using: (i) histochemical stains (haematoxylin and eosin, Masson trichrome and periodic acid-Schiff) and (ii) immunoperoxidase staining methods (CD3, CD79a, CD68, CD31 and alpha smooth-muscle actin for T, B lymphocytes, macrophages, endothelial cells and smooth-muscle lineage). Complete (six vs. three), partial (one vs. one) and no healing (one vs. four animals) of the meniscal wounds were observed in the injected and noninjected menisci. As compared with the noninjected menisci, examination of the tissues from the injected ones revealed: (i) marked angiogenesis (microvessel density: 3.22 +/- 0.66 vs. 6.50 +/- 2.10); (ii) chondrogenesis; (iii) prominent immune cell infiltrate (4.07 +/- 0.78 vs. 9.56 +/- 1.69, 8.33 +/- 0.77 vs. 3.67 +/- 1.00 and 4.38 +/- 0.62 vs. 11.1 +/- 1.43 for the total numbers of immune cells, lymphocytes and macrophages, respectively); and (iv) proliferation of the fibroblasts with marked deposition of collagen fibres (2.0 +/- 0.84 vs. 2.66 +/- 0.48). These values were statistically significantly higher for the injected menisci as compared with the noninjected ones (P >/= 0.05). Autologous BMSCs can improve meniscal wound healing. Whether this improvement occurs through BMSC differentiation into cells operational in the repair process, the release of certain mediator or other unknown mechanisms mandates further investigations.

Animals↗

PubMed2005

The biochemical and morphological alterations following administration of melatonin, retinoic acid and Nigella sativa in mammary carcinoma: an animal model.

Worldwide, breast cancer is the second leading cause of cancer death among women and the third most common cancer. Although our understanding of the molecular basis of this fatal disease has improved, this malignancy remains elusive. Melatonin (Mel), retinoic acid (RA) and Nigella sativa (NS) are substances with anticancer effects. To date, our understanding of the mechanisms of therapeutic effects of these products in mammary cancer is still marginal. To look at the preventive and therapeutic values of these products, we carried out this investigation. An animal model formed of 80 rats was established. The animals were divided into eight groups of 10 animals each: (a) control group injected with the same vehicle used for treatments in the relevant dosages and routes; (b) carcinogen group injected with the known carcinogenic substance 7,12-di-methylbenz(a)anthracene (DMBA) that induces mammary carcinoma; (c) three prophylactic (Pro) groups (Mel-Pro, RA-Pro and NS-Pro) injected with test substances (Mel, RA and NS, respectively) 14 days before the intake of the carcinogenic substance DMBA and then continued until the end of the experiments; and (d) three treated (Tr) groups (Mel-Tr, RA-Tr and NS-Tr) injected with the vehicles after the intake of DMBA. In both the Pro and Tr groups, the drugs were daily administered for 3 months. The animals were killed, and their serum and tissues were evaluated for (a) markers of tumorigenicity [serum levels of total sialic acid (TSA) and lipid-bound sialic acid (LSA)], (b) markers of endocrine derangement (serum prolactin, estradiol and progesterone levels), (c) apoptotic changes [serum tumour necrosis factor (TNF)-alpha, tissue caspase-3 activity, percentage of DNA fragmentation and ultrastructural features of apoptosis] and (d) markers of oxidative stress (tissue levels of lipid peroxides and nitric oxide). Carcinoma was absent both in the control and in the NS-Pro groups. Mammary carcinoma occurred in DMBA and other Pro and Tr groups. The frequency of mammary carcinoma was high in the carcinogen DMBA group (60%), followed by the Tr (56%) and finally the Pro groups (33%). These tumours included papillary, comedo and cribriform carcinomas. As compared with the control group, the development of carcinoma in the carcinogen DMBA group was associated with increased levels of (a) markers of tumorigenicity (77.0 +/- 3.3 vs. 209.0 +/- 5.6 and P < 0.05 for TSA; 28.7 +/- 1.7 vs. 41.8 +/- 1.2 and P < 0.01 for LSA), (b) markers of endocrine derangement (2.5 +/- 0.1 vs. 3.6 +/- 0.3 and P < 0.05 for prolactin; 39.6 +/- 1.3 vs. 24.8 +/- 2.1 and P < 0.01 for progesterone and 31.0 +/- 0.7 vs. 51.1 +/- 3.4 and P < 0.01 for estradiol) and (c) markers of oxidative stress (2.3 +/- 0.2 vs. 5.2 +/- 0.7 and P < 0.01 for lipid peroxides and 4.4 +/- 0.2 vs. 7.6 +/- 0.8 and P < 0.01 for nitric oxide). Also, it was associated with decreased levels of markers of apoptotic activity (20.8 +/- 1.1 vs. 13.4 +/- 0.7 and P < 0.01 for caspase-3; 29.0 +/- 1.7 vs. 20.9 +/- 1.3 and P < 0.05 for percentage of DNA fragmentation; and 9.4 +/- 0.8 vs. 52.1 +/- 3.3 and P < 0.01 for TNF-alpha). When compared with the carcinogen DMBA group, the development of carcinoma in the Pro and Tr groups was associated with decreased levels of (a) markers of tumorigenicity, (b) markers of endocrine derangement and (c) markers of oxidative stress. Alternatively, carcinogenicity was associated with statistically significant (P < 0.01) increased levels of markers of apoptotic activity. To conclude, the administration of Mel, RA and NS reduced the carcinogenic effects of DMBA, suggesting a protective role. The possible underlying mechanisms of these effects await further investigations.

Animals↗

PubMed2005

Analysis of the mononuclear inflammatory cell infiltrate in the non-tumorigenic, pre-tumorigenic and tumorigenic keratinocytic hyperproliferative lesions of the skin.

BACKGROUND: The keratinocytic hyperproliferative lesions include non-tumorigenic, pre-tumorigenic (actinic keratoses, AK), and tumorigenic (squamous cell carcinomas, SCC) conditions. Although mononuclear inflammatory cell infiltrate (MICs) is a constant feature in these lesions, their immunophenotypic characterization is still incomplete. We hypothesized that the development of non-tumorigenic, pre-tumorigenic, and tumorigenic keratinocytic hyperproliferative lesions is associated with alterations in the mononuclear inflammatory cell infiltrate in response to altered antigenicity of the lesional cells. This study tries to test this hypothesis and to characterize MICs in these lesions. METHODS: Fifty lesions (non-tumorigenic lesions, 29; AK, 9 and SCC, 12) were examined using immunoperoxidase staining methods and antibodies targeting histiocytes (CD68), T cells (CD3), B cells (CD20), and T cells with cytotoxic potential (TIA-1). RESULTS: As compared to the normal skin, the development of the keratinocytic hyperproliferative lesions (normal skin; non-tumorigenic; AK and SCC) was associated with a statistically significant increase (p = <0.05) in: (1) CD20+ B lymphocytes (0.0 +/- 0.0 vs. 3.1 +/- 0.5 vs. 7.5 +/- 0.3 vs. 14.5 +/- 5.5); (2) CD68 histiocytes (4.0 +/- 1.0 vs. 26.5 +/- 3.9 vs. 23 +/- 1.9 vs. 41.3 +/- 6.8); (3) CD3+ T lymphocytes (3.0 +/- 1.1 vs. 58.3 +/- 10.3 vs. 54.5 +/- 0.2 vs. 41.0 +/- 16.0); and (4) TIA-1+ cytotoxic T cells (1.8 +/- 0.4 vs. 2.9 +/- 0.7 vs. 9.6 +/- 1.1 vs. 13.7 +/- 5.2). CONCLUSIONS: The increase in the number of infiltrating mononuclear cells in all pathologic lesions compared to normal skin may reflect increased antigenicity of the lesional cells. Both humoral and cell mediated immunity are involved in these lesions.

Antigens, CD↗

PubMed2005

Role of fine needle aspirate mapping and touch imprint preparations in the evaluation of azoospermia.

OBJECTIVE: To assess the utility of fine needle aspiration cytology (FNAC) and touch imprint cytology (TIC) in the evaluation of azoospermia. STUDY DESIGN: FNAC, TIC and open testicular biopsy (OTB) were used to evaluate 31 azoospermic men. RESULTS: OTB revealed normal spermatogenesis (10), spermatogenic arrest (12), Sertoli cell only syndrome (SCO) (7) and unsatisfactory cases (2). Cytologic examinations (TIC vs. FNAC) revealed normal spermatogenesis (11 vs. 9), spermatogenic arrest (13 vs. 7), SCO (2 vs. 1) and unsatisfactory cases (5 vs. 5). Sensitivity and specificity of TIC and FNAC were 98% vs. 83% and 100% vs. 93%, respectively. CONCLUSION: Testicular FNAC is a reliable and simple method for the evaluation of azoospermia.

Adult↗

PubMed2005

Quantitative comparison of infected Schistosomiasis mansoni and Haematobium: animal model analysis of the granuloma cell population.

To evaluate the hypothesis that the granuloma cell population in S. haematobium is different from that of S. mansoni infections, a hamaster animal model was established. Infection of hamesters was induced by abdominal skin exposure of male golden hamsters with 300 cercariae. S. haematobium granuloma cell population in the small intestine, urinary bladder, liver and spleen and those of S. mansoni granuloma in the small intestine and liver of infected hamsters were histologically examined between 6 and 12 weeks post-exposure. In both species, the granuloma cell population was fomed of lymphocytes (47%), histiocytes (28%), eosinophils (16%) and polymorphs (8%). As compared to granuloma cell population in S. haematobium; S. mansoni granulomas had: (a) higher population of eosinophils (28% vs. 11%), (b) lower population of polymorphs (4% vs. 10%) and histiocytes (22% vs. 31%) and (c) similar population of lymphocytes (46% vs.47%). The mean diameter of liver granuloma was higher in S. mansoni (175.8 +/- 12.34) than for S. haematobium (125.4 +/- 16.12). As compared to S. haematobium, the numbers of isolated male, female and total worms were significantly higher in S. mansoni (24.5 +/- 2.7 vs. 7.3 +/- 2.3; 6.3 +/- 0.8 vs. 2.2 +/- 0.5; 80 +/- 2.2 vs. 56.3 +/- 3.8, p < .0.05). The heterogeneity of cell population in granuloma suggests the involvement of different immune mechanisms in their development. The cells achieving numerical dominance in the granulomas were in the following order: lymphoyctes > monocytes > eosinophils > polymorphs. The differrence in the granuloma cell population between S. haematobium and S. mansoni may reflect different tissue reactions to the deposited ova.

Animals↗

PubMed2004

Alterations of p53, Bcl-2, and hMSH2 protein expression in the normal breast, benign proliferative breast disease, in situ and infiltrating ductal breast carcinomas in the upper Egypt.

BACKGROUND: Tumorigenesis involves alterations in the tumor suppressor genes (p53), protooncogenes (Bcl-2) and housekeeping genes [human MutS homologue-2 (hMSH2)]. We hypothesized that mammary carcinogenesis involves interactions among p53, Bcl-2 and hMSh2 proteins. In the Upper Egypt, the clinicopathologic features and genetic changes during mammary carcinogenesis are unknown. METHODS: To test our hypothesis and to examine these issues, 53 mastectomy specimens, each entailing normal breast, benign proliferative breast disease (BPBD), duct carcinoma in situ (DCIS) and infiltrating ductal carcinoma (IDC) were immunostained for p53, Bcl-2 and hMSH2 protein expression. RESULTS: The average age incidence of ductal carcinomas was 43.2 +/- 7.06 years. The tumors were common in the left than right side (1.2:1, respectively, p > 0.05). Infiltrating ductal carcinoma of non-specific type was the most common histologic type. Examination of the average weighted scores in the normal breast, BPBD, DCIS and IDC, respectively, showed: (1) significant upregulation of p53 proteins (0.00 +/- 0.00, 0.00 +/- 0.00, 6.25 +/- 2.42, 6.62 +/- 2.15, p = 0.001), (2) insignificant downregulation of Bcl-2 (6.67 +/- 1.33, 5.17 +/- 2.20, 4.79 +/- 2.27 and 4.42 +/- 2.83, p = 0.37), and (3) significant downregulation of hMSH2 (11.3 +/- 0.75, 10.70 +/- 1.27, 7.11 +/- 1.50 and 7.0 +/- 1.33, p = 0.0006). There were insignificant negative correlations between p53 and both Bcl-2 (r = -0.20, p > 0.05) and hMSH2 (r = -0.15, p > 0.05) protein expression. CONCLUSIONS: In the Upper Egypt: (1) breast cancer had similar clinicopathologic features to those in the high risk regions, and (2) alterations of the p53, Bcl-2 and hMSH2 proteins occur during mammary carcinogenesis.

Adult↗

PubMed2004

Analysis of p53 and bcl-2 protein expression in the non-tumorigenic, pretumorigenic, and tumorigenic keratinocytic hyperproliferative lesions.

BACKGROUND: The hyperproliferative keratinocytic lesions encompass a wide range of non-tumorigenic, pretumorigenic, and tumorigenic conditions. The aim of this work was to examine the expression patterns of apoptosis-linked molecules (bcl-2 and p53) in these lesions. METHODS: Immunoperoxidase staining methods were applied to analyze p53 and bcl-2 protein expression in a total of 66 cases, including 12 squamous cell carcinomas (both in situ and invasive SCC), 11 actinic keratoses (AK), 13 psoriasis vulgaris (PV), eight verruca vulgaris (VV), six chronic dermatitis (CD), five seborrheic keratosis (SK), four lichen planus (LP), three epidermodysplasia verruciformis (EDV), two condyloma acuminata (CA), two lichen simplex chronicus (LSC), and 10 specimens from normal skin. RESULTS: As compared to normal skin (0.70 +/- 0.26), the bcl-2 average weighted scores in the non-tumorigenic (0.76 +/- 0.16), pretumorigenic (1.45 +/- 0.28), and tumorigenic lesions (2.83 +/- 0.50 and 2.92 +/- 0.50 for in situ and invasive SCC, respectively) showed significant up-regulation (p = 0.001). In the non-tumorigenic lesions, the bcl-2 expression values decreased in the following order: SK > EDV > CD > LP > CA > PV > VV (1.40 +/- 0.24 > 1.33 +/- 0.67 > 0.83 +/- 0.40 > 0.67 +/- 0.21 > 0.50 +/- 0.20 > 0.46 +/- 0.22 > 0.13 +/- 0.01, respectively). As compared to normal skin (1.10 +/- 0.23), the p53 average weighted scores in the non-tumorigenic (1.86 +/- 0.18), pretumorigenic (3.64 +/- 0.53), and tumorigenic lesions (5.00 +/- 1.00 and 5.08 +/- 0.86 for in situ and invasive SCC, respectively) showed significant up-regulation (p = 0.021). In the non-tumorigenic lesions, p53 average weighted scores decreased in the following order: SK > PV > CA > LP > CD > VV > EDV (3.20 +/- 0.49 > 2.38 +/- 0.27 > 2.0 +/- 0.0 > 1.83 +/- 0.48 > 1.0 +/- 0.37 > 1.0 +/- 0.33 > 1.0 +/- 0.0, respectively). There was a positive correlation between bcl-2 and p53 protein expression in normal skin (r = 0.966, p = 0.0001), non-tumorigenic (r = 0.775, p = 0.0001), pretumorigenic (r = 0.830, p = 0.001), and tumorigenic lesions (r = 0.757, p = 0.003). CONCLUSIONS: Bcl-2 and p53 proteins are altered in the keratinocytic hyperproliferative lesions. Determination of whether these alterations reflect underlying gene mutations will require further investigations.

Adult↗

PubMed2004

Alterations of p53, Bcl-2, and hMSH2 protein expression in the cirrhotic, macroregenerative, dysplastic nodules and hepatocellular carcinomas in Upper Egypt.

BACKGROUND: Hepatocarcinogenesis involves alterations in p53, Bcl-2 and human Mut S homologue-2 (hMSH2) genes. In Upper Egypt, the clinicopathologic and genetic changes during hepatocarcinogensis (cirrhotic nodules (CN); macroregenerative nodules (MRN) and dysplastic nodules (DN) are unknown. METHODS: To examine these issues, 48 hepatic resection specimens entailing 25 CN, 16 MRN, 23 DN and 48 hepatocellular carcinoma (HCC) were immunohistochemically evaluated for p53, Bcl-2 and hMSH2 protein expression. RESULTS: HCC was common in males than in females (2.6:1, P<0.05) and with hepatitis C virus than hepatitis B virus infection (77.1% vs. 18.7%, P=0.001). p53 expression was found in DN (3/23) and HCC (12/48). Its average weighted scores were high in DN/HCC as compared with CN (1.60+/-0.40 and 7.20+/-1.20, P=0.0001). Bcl-2 expression was seen in CN, MRN, DN and HCC (7/48). Its average weighted scores were high in DN (7.60+/-1.60), HCC (6.86+/-0.85) as compared with CN (6.14+/-0.42) and MRN (6.50+/-0.50, P=0.22). hMSH2 average weighted scores were reduced in HCC (7.94+/-1.06) as compared with CN (8.47+/-0.52), MRN (8.00+/-1.00) and DN (8.20+/-0.80, P>0.05). CONCLUSION: In Upper Egypt: (1) HCC had similar clinicopathologic features to those in the high-risk regions, and (2) alterations of the p53, Bcl-2 and hMSH2 proteins occur during hepatocarcinogensis.

Adult↗