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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although most examples of cutaneous malignant melanoma are easily recognized by their clinical appearances, in some cases this serious neoplasm may clinically simulate other less serious forms of skin cancer or benign processes. This study was undertaken to assess both the sensitivity of clinical diagnosis of cutaneous malignant melanoma and the efficacy of biopsies of clinically unsuspected melanomas in yielding specimens on which complete and accurate histologic assessments could be made. A retrospective analysis of 1784 cases of histologically proven melanomas diagnosed between 1985 and 1990 was performed in search of lesions not clinically suspected. Biopsy techniques used to sample these lesions were subjected to critique of their efficacy in yielding specimens that could be accurately diagnosed and completely assessed histologically. Of 1784 histologically proven primary cutaneous melanomas, 583 were not clinically suspected, yielding a sensitivity of 67%. Clinical diagnosis included nevi (33%), no diagnosis (17%), multiple diagnoses (13%), basal cell carcinoma (12%), keratosis (9%), and lentigo (9%) among others. The biopsy methods used to sample these lesions were shave (56%), excisional (24%), punch (11%), curettage (2%), and undetermined (6%). Eighty-six percent of shave biopsies could be accurately assessed while only 32% of punches and no curettages provided sufficient material for both definitive and complete evaluation of melanomas. Eighteen percent of specimens histologically reviewed were considered inadequate for complete evaluation. In 34%, the actual diagnosis of melanoma was uncertain because of inability to assess diagnostic features as a consequence of the biopsy technique. Melanoma may be unsuspected clinically in a significant number of cases and may be mistaken for less serious cutaneous neoplasms.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sensitivity of diagnosis of malignant melanoma: a clinicopathologic study with a critical assessment of biopsy techniques. 136 17

We investigated the skin-associated lymphoid tissue in arsenical skin cancers, including 14 Bowen's disease, 6 basal cell carcinoma and 6 squamous cell carcinoma patients from an endemic area by immunohistochemical and morphometric methods. There was a progressive decrease of Langerhans cells in the order of normal skin, normal appearing edge and arsenical cancers. A disruption of the uniform Langerhans cell dendrites was also noticed. The Langerhans cell density in arsenical tumors did not correlate with the peritumoral infiltrates. The prominent infiltrated cells in the peritumoral area had T cell markers. The number of peritumoral T lymphocytes in squamous cell carcinoma was significantly less than that of Bowen's disease and basal cell carcinoma. Peritumoral mononuclear infiltrates in Bowen's disease and squamous cell carcinoma showed a higher helper/suppressor T cell ratio than that in basal cell carcinoma. This may be accounted for by a selective increased recruitment of helper T cells to the tumor infiltrates in Bowen's disease and squamous cell carcinoma.
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PMID:Alterations of skin-associated lymphoid tissue in the carcinogenesis of arsenical skin cancer. 138 79

Amplification of the c-myc oncogene has been detected by Southern blotting in the DNA of radiation-induced skin cancers in the rat. In the current work the localization of oncogene amplification within specific cells in the different cancers and in multiple biopsies of the same cancer was studied by in situ hybridization. The amount of amplification was measured by counting grains on tissue sections hybridized in situ to biotin-labeled human c-myc third exon, rat v-H-ras, and rat v-Ki-ras probes. The in situ estimates of c-myc amplification were generally correlated with previous findings using the Southern blot method, but within each cancer only a fraction of cells exhibited amplification. Multiple biopsies of a squamous carcinoma showed amplification of v-H-ras and c-myc but not v-Ki-ras during tumor growth, but none of these oncogenes were amplified during tumor regression. The c-myc-positive cells were distributed uniformly within the cancers and exhibited a more uniform nuclear structure in comparison to the more vacuolated c-myc-negative cells. A high [3H]thymidine labeling index was found in irradiated epidermal cells on Day 7 after exposure, and yet no evidence of c-myc oncogene amplification was found in situ. No c-myc amplification was found in unirradiated normal epidermis or in irradiated epidermal cells in the vicinity of radiation-induced cancers. The data indicate that c-myc amplification is cell-specific within radiation-induced carcinomas and does not occur in epidermal cells proliferating in response to radiation exposure.
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PMID:Oncogene amplification detected by in situ hybridization in radiation-induced skin cancers in rats. 143 1

The expression of gangliosides in non-malignant tissues (epidermis and pigmented nevus) and neoplastic lesions (melanoma, squamous cell carcinoma [SCC] and basal cell carcinoma [BCS]) of the human skin was analyzed immunohistochemically and biochemically to characterize the features associated with malignancy. Immunohistochemical staining with an anti-II3NeuAc-LacCer (GM3) monoclonal antibody (M2590 mAb) and an anti-II3(NeuAc)2-LacCer (GD3) mAb (R24) showed the expression of the gangliosides GM3 and GD3 to vary among the different tissues. M2590 clearly stained epidermal keratinocytes and the tumor cells of BCC and SCC, and strongly stained melanocytes and melanoma cells. In contrast, R24 did not stain epidermal keratinocytes and only faintly stained SCC cells, while it clearly stained BCC cells, and intensely stained melanocytes and melanoma cells. GM3 showed a similar level of staining among the tissue specimens, while the level of GD3 staining was quite variable among the tumor specimens. Biochemical analysis by thin-layer chromatography (TLC) with resorcinol staining and TLC immunostaining with either M2590 or R24 showed both GM3 and GD3 to be commonly expressed by both the normal and malignant skin tissues, including SCC. There was no close correlation between the intensity of immunohistochemical staining and the biochemically detected amounts of these gangliosides. This may have been partly due to the so-called cryptic expression of cell membrane gangliosides. Our results thus suggest that analysis of the tumor-associated expression of gangliosides requires several methods, since the sensitivity of the methods used may have a considerable effect on the diagnostic value of gangliosides as skin cancer markers.
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PMID:Common phenotypic expression of gangliosides GM3 and GD3 in normal human tissues and neoplastic skin lesions. 146 93

The epidemiology of gynecological and breast cancers are better known in France as a result of the mortality data provided by INSERM and the mortality data obtained from the French Tumor Register. Breast cancers are the most common form of cancer in women, accounting for about 30 p. cent of tumors (excluding skin cancers) followed by cancers of the uterine cervix, uterine body and the ovary. The change in incidence shows a definite reduction in the number of uterine cancers over the past 10 years, whereas the incidence of breast cancers is rising by 1 to 2 p. cent per year. Mortality due to breast cancer has risen steadily in France since 1950, particularly in higher age groups. At birth, the risk of developing a breast cancers is 7 p. cent, i.e. one woman in 14 will develop a breast cancer. The figures for cancers of the uterus and ovary are much lower. Survival curves for various types of cancer confirm the steady decline in survival for breast cancers, whereas for cancers of the cervix, uterine body and ovary, mortality rates stabilize after 5 years. The risk of a secondary cancer remains very high for breast tumors, and half the cases of a secondary tumor involve a contralateral breast tumor. In general, there is an increased risk of a secondary cancer after a primary gynecological tumor.
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PMID:[Descriptive epidemiology of gynecologic and breast cancers]. 148 74

Several genetic alterations that perturb normal cellular growth control mechanisms can cause cancers. These include point mutations, deletions, translocations, amplifications and gene rearrangements and occur primarily in two classes of interacting genes, oncogenes and tumor suppressor genes. While mutation or amplification of certain oncogenes can facilitate cell growth and tumor formation (Bishop, 1983, 1991; Hunter, 1991; Land, et al., 1983), loss or mutation of tumor suppressor genes, which normally inhibit these processes, can promote tumor formation (Knudson, 1985; Cavenee, et al., 1989; Marshall, 1991). Human skin tumors display multiple genetic alterations such as Ha-ras gene mutation and LOH, N-ras gene amplification, and mutations in p53 tumor suppressor gene. In most cases, the mutations in ras and p53 genes are localized to pyrimidine-rich sequences, particularly C-C sequences, which indicates that these sites are probably the targets for UV-induced DNA damage and subsequent mutation and transformation. Since UV radiation in sunlight is an environmental carcinogen it is important to understand the molecular mechanisms by which UV radiation induces human skin cancers. In addition, suitable animals models are available for comparative studies and risk assessment. By comparing the various genetic alterations detected in sunlight-induced human skin tumors with those present in UV-induced murine skin tumors, it may be possible to identify the carcinogen-related events that are involved in the multi-step process of carcinogenesis. Studies addressing these issues should provide further insights into the molecular mechanisms of UV carcinogenesis.
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PMID:Molecular alterations in human skin tumors. 152 30

Over 500,000 nonmelanoma skin cancers are diagnosed and treated in this country each year. All treatment modalities quote a 90% or greater cure rate. Even with high cure rates, thousands of patients will require secondary treatment. Some nonmelanoma skin cancers are very aggressive and may not be resectable following single treatment failure. Recurrent tumors in critical anatomic locations require a multidisciplined approach. Combined tumor board evaluation and management are advocated.
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PMID:Unresectable primary facial cutaneous carcinoma. 153 49

Since tumors of the globe and ocular adnexa, other than skin cancers of the eyelid, are uncommon, most oncologic specialists have little opportunity to become experienced in the management of eye tumors. In general, a malignancy that does not penetrate a bony orbital wall can be resected with an adequate margin by inclusion of the adjacent wall and periorbita. The decision to save or sacrifice a globe when a malignancy penetrates the bone but not the periorbita should be based on such factors as the tumor histology, contralateral vision, the probability of permanent diplopia, and the need for irradiation in doses that would destroy vision. Because of the complications involved with irradiation of orbital tumors, surgical resection has been the treatment of choice. In addition, orbital exenteration presents a unique challenge to the maxillofacial prosthodontist. Prosthetic restoration of the orbit is often complicated by the extent of resection, tissue response, and method of retention.
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PMID:Surgical and prosthetic considerations in the management of orbital tumors. 154 92

The mortality rate of nonmelanoma skin cancer is higher than generally considered. An actual nonmelanoma skin cancer is a risk factor not only for other skin cancers but also for cancers in other organs. The recurrence rate can, according to the method of calculation, yield surprisingly diverging results. Statistical mapping of subclinical tumor growth in basal cell carcinoma supplies the margins for tumor-free excision. An even better but more expensive tool for therapy planning is tumor imaging with magnetic resonance imaging. Psoralen plus ultraviolet light of the A wavelength-treated patients run a dose-dependent risk of developing squamous cell carcinoma of the skin but also cancers in other organs. Human papilloma virus-16 seems not to be associated with squamous cell carcinoma of the skin except for the anogenital region and possibly the finger. The finding of retroviruslike particles in endemic non-acquired immunodeficiency syndrome Kaposi's sarcoma strongly suggests that a virus other than human immunodeficiency virus may play a role in the pathogenesis of this disease.
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PMID:Basal cell and squamous cell carcinoma and Kaposi's sarcoma. 159 11

UV radiation is a potent DNA-damaging agent and a known inducer of skin cancer in experimental animals. To elucidate the role of oncogenes in UV carcinogenesis, we analyzed UV-induced murine skin tumors for mutations in codon 12, 13, or 61 of Ha-ras, Ki-ras, and N-ras oncogenes by amplification of genomic tumor DNAs by the polymerase chain reaction followed by dot-blot hybridization to synthetic oligonucleotide probes designed to detect single base-pair mutations. In addition to UV-induced C3H mouse skin tumors, we also analyzed skin tumors induced in the same strain of mice by other carcinogenic agents such as 8-methoxypsoralen + UVA, angelicin + UVA, dimethylbenz-[a]anthracene + UV + croton oil, and 4-nitroquinoline-1-oxide. We found that 4 of 20 UV-induced skin tumors contained either C----A or A----G base substitutions at N-ras codon 61. In addition, 2 of 5 melanomas possessed a G----A transition in N-ras codon 13 and an A----T transversion in N-ras codon 61, respectively. Interestingly, none of the 8-methoxypsoralen + UVA- or angelicin + UVA-induced tumors we analyzed contained mutations in any of the ras genes. However, 1 of 4 4-nitroquinoline-1-oxide-induced tumors exhibited a G----T transversion at Ki-ras codon 12, a potential site for formation of a 4-nitroquinoline-1-oxide adduct with a guanine residue. We also found that 2 nonmelanoma tumors induced by dimethylbenz[a]anthracene + UV + croton oil contained an A----T transversion at Ha-ras codon 61 position 2, which is characteristic of most dimethylbenz[a]anthracene-induced tumors. These results suggest that UV-induced C3H mouse tumors display mutations preferentially in the N-ras oncogene. Since most N-ras mutations in UV-induced tumors occurred opposite dipyrimidine sequences (T-T or C-C), one can infer that these sites are the targets for UV-induced mutation and transformation.
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PMID:N-ras mutation in ultraviolet radiation-induced murine skin cancers. 161 70


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