Cases reported "Skin Neoplasms"

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1/72. Diagnostic relevance of chromosomal in-situ hybridization in Merkel cell carcinoma: targeted interphase cytogenetic tumour analyses.

    AIMS: To resolve the conflicting diagnoses of five pathologists (which included well-differentiated neuroendocrine carcinoma, malignant carcinoid, undifferentiated small-cell carcinoma, primitive neuroectodermal tumour, metastases of small-cell lung carcinoma (SCLC) and Merkel cell carcinoma (MCC)), and tumour-free lungs after necropsy, we investigated an alarmingly metastasizing MCC in a 32-year-old Caucasian man using chromosomal in-situ hybridization (CISH). Differences in incidence and course in males and females also prompted targeted analyses for chromosomes X and Y. The lesion was also analysed for p53 gene mutations. methods AND RESULTS: paraffin sections of the thorax, buccal lymph nodes and scalp tumours were stained with haematoxylin and eosin. immunohistochemistry was performed with antibodies against pancytokeratin, keratin 20, neuron-specific enolase (NSE), chromogranin, neurofilaments and vimentin, among others. Sections (5-6 microm) of the tumours were analysed with alpha-satellite probes for chromosomes 1, 6, 7, 11, 12, 17, 18, X and Y using CrSH; and exons 5-9 of the p53 gene were examined by polymerase chain reaction and single strand conformation polymorphism (PCR-SSCP) methods. Although positive for pancytokeratin, keratin 20, chromogranin, NSE, synaptophysin and vimentin, the similarity in antigen profiles expressed by SCLC and MCC prevented a definitive tumour diagnosis. Chromosomal in-situ hybridization, however, revealed trisomies 1 and 11, two frequent aberrations in MCC, and trisomy 18. Moreover, 71% of the tumour cells had two to three copies of X, whereas 98% of the cell nuclei in the hair follicles and normal epidermis (purported Merkel cell origins) displayed one x chromosome. No mutations were detected in the five exons of the p53 gene examined. CONCLUSIONS: Had CISH been performed earlier, treatment may have been tailored specifically to suit MCC, since MCC and SCLC have different therapeutic strategies. Finally, chromosome X may be of prognostic relevance in MCC, which apparently predominates in females and yet shows poorer prognosis in males, and hence be worthy of further investigation.
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2/72. Angiosarcoma of the scalp.

    An 82-year-old woman was seen at our dermatology Department for a plaque on the right parietal scalp that had recently increased in size, and bled. The lesion had been present for 3 months. The patient had a previous diagnosis of chronic bronchitis, noninsulin-dependent diabetes mellitus, and hypertension, but no previous history of cancer. physical examination revealed a 7 x 10 cm plaque, composed of a central necrotic and bleeding surface, surrounded by small purple-red satellite nodules. A biopsy showed an ill-defined infiltrative intradermal mass with a pattern of hypercellular sheets of large cells alternating with areas of dilated, irregular, blood-filled channels, dissecting the collagen bundles. The endothelial cells lining these channels were plump and pleomorphic, surrounded by other spindle-shaped cells with pleomorphic and atypical nuclei. The diagnosis of angiosarcoma was made, and the patient was sent to an oncology center for further evaluation and treatment, where a computed tomography head scan was taken revealing no erosion of the skull. The patient refused surgery, so radiotherapy was proposed. One month later, she developed lymph node enlargement of the left anterior cervical nodes. A needle aspiration biopsy was consistent with sarcoma. Two weeks later, she was started on palliative radiotherapy: a programmed dose of 4500 cGy was proposed of which she only received 3000 cGy because of treatment withdrawal and loss to follow-up. During this time, she showed partial initial response, but despite treatment the disease relentlessly progressed, with hemorrhage and severe pain being the most striking features.
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3/72. Common blue naevus with satellite lesions: possible perivascular dissemination resulting in a clinical resemblance to malignant melanoma.

    We report a case of common blue naevus with polymorphous guttate and linear satellite lesions, thereby mimicking peripherally spreading malignant melanoma. Histopathologic examination showed that the naevus cells are clustered around blood vessels in the primary as well as satellite lesions, suggestive of spreading of the naevus cells along the perivascular space. Such biological behaviour resulting in a clinical manifestation of a malignant melanoma-like lesion is a rarity in common blue naevus, a benign cutaneous disorder that is devoid of a malignant potential, and has not been described before.
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4/72. Analysis of tumor cell evolution in a melanoma: evidence of mutational and selective pressure for loss of p16ink4 and for microsatellite instability.

    Tumorigenesis and tumor progression can be considered an evolutionary process. In order to deduce information on the mutational and selective pressures during melanoma progression we performed microsatellite analysis at 42 autosomal and two X-linked loci in a microdissected primary melanoma and its nine metastases. Loss of heterozygosity at locus D9S259 was the only genetic change observed in all metastases. The pattern of loss of heterozygosity at loci D9S162 and D9S171 within the region of common loss on chromosome 9p21 which encompasses the tumor suppressor gene p16ink4 enabled the distinction of four genetically different tumor cell populations. Three cell lineages showed homozygous loss of the p16ink4 gene, which evolved independently in each tumor cell population within the primary tumor. Additional allele losses could be demonstrated at markers D14S53 and DXS998. The fourth lineage did not demonstrate loss of heterozygosity at loci D9S162 and D9S171 and contained the wild type p16ink4 gene but was characterized by abundant microsatellite instability. The evolutionary approach towards tumorigenesis and tumor progression used in this study thus confirms the role of p16ink4 inactivation for melanoma progression but not for melanoma initiation; it suggests the existence of additional putative tumor suppressor genes located on 9p as well as on the long arm of chromosome 14 and shows that microsatellite instability may represent an alternative pathway of tumor cell evolution in malignant melanoma.
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5/72. Molecular identification of metastatic cancer to the skin using laser capture microdissection: a case report.

    BACKGROUND: In the current study the authors report a 57-year-old woman with a scalp tumor and cervical lymphadenopathy who had a previously resected duodenal carcinoid. Histologic and immunophenotypic characteristics of the duodenal carcinoid differed from those of the scalp and cervical lymph node tumors, prompting the use of molecular methodologies to make the diagnosis. methods: paraffin embedded tissues from the duodenal carcinoid, scalp, and lymph node tumors were dissected using microscopic visualization and laser capture microdissection. DNA was extracted and polymerase chain reaction (PCR) was performed to evaluate loss of heterozygosity and microsatellite alterations using primers flanking 22 polymorphic microsatellite markers from 9 chromosomal regions, including genes associated with MEN-1 (11q), CDKN2 (9p), p53 (17p), and bronchial carcinoid (3p). Microdissected lymphocytes from the three tissues were used as source of constitutional DNA (controls). RESULTS: Fourteen of the 22 markers were informative (heterozygous in control lymphocytes). A marker on 3p12 showed loss of the same parental allele in the three tumors. A different marker on 3p14.2 showed an identical shifted band in the three tumors indicative of a common microsatellite alteration. CONCLUSIONS: The shared molecular abnormalities among the three tumors indicated a common clonal origin, leading to a diagnosis of primary duodenal carcinoid with clear cell metastases to the scalp and cervical lymph nodes. These findings led to radiation therapy and immunotherapy rather than chemotherapy. This case illustrates the novel application of laser capture microdissection combined with PCR-based analyses of genomic markers for the identification of the origin of metastatic disease.
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6/72. Blue nevus with satellitosis mimicking malignant melanoma.

    Blue nevus rarely develops a malignant melanoma. The loss of the regular border and the development of satellite lesions are ominous clinical indicators of the malignant change. A case is presented in which both of these clinical features--irregular border and satellite lesions--were present, but no malignant change was observed histopathologically. To our knowledge, such a single nodule with satellite lesions mimicking malignant melanoma has not been described previously.
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7/72. Eccrine sweat gland carcinoma: a case report and review of diagnosis and treatment.

    Carcinomas of the skin appendices are rare neoplasms but for prognostic reasons it is important to differentiate them from the indolent squamous and basal cell carcinomas, as their behavior is more aggressive. We report on a case of eccrine sweat gland carcinoma that displayed all the typical features of those neoplasms. The patient sought medical attention after a lesion in his foot, already present for four years, began to enlarge and developed satellite lesions. The pathological diagnosis was made only after the lesion was initially misdiagnosed as basal cell carcinoma of the skin. Multiple chemotherapeutic regimens and radiation therapy were administered with only temporary benefit. The patient developed distant metastatic disease but survived with metastases for three years. He died nine years after the initial lesion developed in his foot and five years after the diagnosis. The diagnosis of sweat gland carcinomas can be facilitated by histochemical stains. In contrast to squamous and basal cell carcinomas of the skin, these are generally positive for the carcinoembryonic antigen (CEA). Once metastatic, these neoplasms are only infrequently, and usually briefly, responsive to either chemotherapy or radiotherapy and new treatments are urgently needed. Early recognition of the entity may allow more timely treatment.
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8/72. Hereditary non-polyposis colorectal cancer associated with disseminated superficial porokeratosis. microsatellite instability in skin tumours.

    A 73-year-old man presented with typical lesions of disseminated superficial porokeratosis (DSP) and multiple seborrhoeic keratoses on his face, trunk and extremities, and later developed a keratoacanthoma on his lip. He belonged to a cancer-prone pedigree susceptible to colonic, uterine and other internal cancers, and had a personal history of early gastric cancer and advanced adenocarcinoma of the descending colon without adenomatous polyps at age 59 years. polymerase chain reaction amplification of skin samples for seven separate microsatellite polymorphisms revealed microsatellite instability (MSI) at multiple loci in five of six seborrhoeic keratoses and the keratoacanthoma, strongly suggesting underlying defects in dna mismatch repair. Although no germline mutations in two mismatch repair genes hMSH2 and hMLH1 were found, our patient was recognized as having hereditary non-polyposis colorectal cancer (HNPCC) based on the family history and the findings of the microsatellite analysis of skin tumours. This confirmed the usefulness of detection of MSI in prevalent and readily accessible skin lesions, including non-sebaceous non-dysplastic tumours such as seborrhoeic keratosis in the screening of HNPCC families. Although DSP may also be inherited as an autosomal dominant condition, this particular skin disease appeared to be sporadic in our patient and, to our knowledge, no association of DSP or other forms of porokeratosis with HNPCC has previously been reported. In contrast to the seborrhoeic keratoses and keratoacanthoma, no MSI was observed in two samples from DSP lesional epidermis examined.
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keywords = satellite
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9/72. Animal type melanoma: a report of a case with balloon-cell change and sentinel lymph node metastasis.

    Animal type melanoma is a rare histopathologic variant of melanoma characterized by sheets and nodules of heavily pigmented epithelioid melanocytes that involve the entire thickness of the dermis. This human neoplasm mimics melanocytic neoplasms seen in gray horses and laboratory animals; thus, is termed animal type melanoma. It is quite rare and, with only a few reported cases, its biological behavior is not well understood. We report an example of animal type melanoma on the back of a 27-year-old man. The lesion showed areas of melanoma in situ, which ruled out the possibility of metastatic melanoma. Features of regression were also seen at dermo-epidermal junction and papillary dermis. In some areas, neoplastic melanocytes exhibited a balloon-cell appearance; in others the neoplasm was composed of sheets and fascicles of heavily pigmented epithelioid melanocytes that permeated the entire dermis and extended into the dermal-subcutaneous interface, mimicking a cellular blue nevus. Epithelioid melanocytes in deeper areas showed abundant, heavily pigmented cytoplasm and pleomorphic nuclei with prominent eosinophilic nucleoli and some mitotic figures. The neoplastic cells did not show evidence of maturation in deeper areas of the lesion. In some sections, a nodule of heavily pigmented epithelioid melanocytes was seen far from the main bulk of the lesion, at the dermal-subcutaneous interface, raising the possibility of a satellite lesion. A lymphoscintigraphy showed a sentinel lymph node in the right axilla and a subsequent axillary lymphadenectomy demonstrated that the architecture of the sentinel lymph node was effaced by metastatic melanoma. The patient received adjuvant chemotherapy with inteferon alfa-2b and four months after this treatment the patient is alive and well, without evidence of recurrences or additional metastases.
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10/72. A stop codon in xeroderma pigmentosum group C families in turkey and italy: molecular genetic evidence for a common ancestor.

    xeroderma pigmentosum family G from Van, turkey had two severely affected children: a son with multiple skin cancers who died at age 10 (XP67TMA), and an 8 y old daughter who began developing skin cancer before 3 y of age (XP68TMA). XP67TMA and XP68TMA cells were hypersensitive to killing by ultraviolet and the post-ultraviolet dna repair level was 12-16% of normal. Host cell reactivation of an ultraviolet-treated reporter plasmid cotransfected with a vector expressing wild-type XPC cDNA assigned XP67TMA to xeroderma pigmentosum complementation group C. The XPC mRNA level was markedly reduced. Sequencing of the 3.5 kb XPC cDNA from XP67TMA showed a C-T mutation in XPC exon 8 at base pair 1840. This mutation converts the CGA codon of arginine at amino acid 579 to a UGA stop codon resulting in marked truncation of the 940 amino acid xeroderma pigmentosum C protein. Restriction fragment length polymorphism analysis of XPC exon 8 DNA in XP67TMA and XP68TMA showed that both affected children had a homozygous mutation and that both parents had heterozygous normal and mutated sequences at the same position consistent with a history of consanguinity in the family. The mutated allele also contained two XPC single nucleotide polymorphisms. The same mutated XPC allele was reported in an Italian family. Studies of 19 microsatellite markers flanking the XPC gene on chromosome 3 suggest that the XPC allele passed between italy and turkey approximately 300-500 y ago. This XPC allele containing a nonsense mutation is associated with severe clinical disease with multiple skin cancers and early death.
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