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Query: UMLS:C0025202 (melanoma)
 69,561 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lichenoid tissue reactions can occur in malignant melanoma and may cause partial regression of the lesion. We studied a series of melanomas to determine how frequently lichenoid tissue reaction obscures the diagnosis of malignant melanoma. We retrospectively reviewed 342 cases of invasive malignant melanoma and melanoma in situ from the head, neck, chest, and back. Of the 342 cases, 23 (6.7%) had a lichenoid tissue reaction obscuring a portion of the lesion. In 6 cases (1.8%), the lichenoid tissue reaction replaced a major portion of the lesion. Knowledge of this phenomenon can prevent misdiagnosis.
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PMID:Lichenoid tissue reaction in malignant melanoma: a potential diagnostic pitfall. 1209 Apr 26

A 63-year-old patient with a malignant melanoma of the uterine cervix is described. Subtle epitheliotropism of the neoplastic cells within the endocervical columnar epithelium suggested melanoma in situ and the possibility of a primary uterine cervical melanoma, despite a negative anti-S-100 protein immunohistochemical stain. An exhaustive clinical workup, and ultimately, complete autopsy failed to reveal any other primary tumor site, and the diagnosis of melanoma was confirmed by histology and immunohistochemistry on the hysterectomy specimen. A world literature review revealed 54 previously reported cases of uterine cervical melanoma of which 43 had been reported as primary uterine cervical melanoma. A true intraepithelial melanocytic component was found in only 14 of those cases, however, and none of those reports illustrated this with the clarity with which it was seen in the endocervical glandular and surface columnar epithelium of the present case. Primary uterine cervical melanoma is usually discovered at an advanced stage and is no longer amenable to curative therapy. Even when this tumor is discovered early, however, the diagnosis may be unnecessarily delayed if the often subtle interaction of the neoplastic cells with the benign cervical squamous or glandular epithelium is not appreciated, or if the possibility of malignant melanoma is not entertained based on other histologic or immunohistologic characteristics of the tumor cells.
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PMID:Primary malignant melanoma of the uterine cervix: case report with world literature review. 1209 May 96

The incidence of cutaneous malignant melanoma has been increasing in Sweden for several decades. In the Stockholm-Gotland area educational activities for healthcare professionals were started in the late 1970s and public primary and secondary prevention campaigns were initiated in the mid-1980s. Melanoma incidence trends have been studied in Sweden, with special reference to trends in the Stockholm-Gotland area where these prevention campaigns were first started. During 1976-1994 the average annual increase of age-standardized incidence in the Stockholm-Gotland area was about 5%, the increase being associated mainly with thin tumors and melanoma in situ. During the 1990s, the incidence among males leveled off. In contrast, no such shift in trend was observed among females, or among males or females residing outside the Stockholm-Gotland area. The campaigns may have contributed to a trend towards earlier diagnosis but there is still no clear effect of the primary prevention efforts.
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PMID:Trends in incidence of cutaneous malignant melanoma in a Swedish population 1976-1994. 1210 57

The incidence of skin cancer, and particularly of cutaneous melanoma, has increased substantially over the recent decades. It has generally been assumed that early diagnosis may in fact be responsible for a part of incidence increase. The aim of the study was to analyze the prevalence and distribution of primary cutaneous melanoma among biopsy specimens during the 1991-2000 period. The Surgical Pathology computerized registry was used to identify patients with primary cutaneous melanoma. The distribution of primary cutaneous melanoma according to Clark showed an increased number of melanoma in situ diagnosed during the 1997-2000 period. It could not be definitely concluded whether these data resulted from more common excision of suspicious pigmented skin lesions or there was an increase in the melanoma rate as a consequence of environmental changes. Fortunately, nowadays new patients with cutaneous melanoma are mostly diagnosed early in the clinical course of disease when it can be successfully managed by simple surgical treatment.
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PMID:The rise in melanoma incidence in Croatia. 1213 24

Oncogenic human papillomavirus (HPV) types such as HPV 16 are known to play a crucial role in the development of anogenital carcinomas. The etiology of anogenital malignant melanoma is unknown. We report two case of vulvar malignant melanoma in which multiple HPV types including HPV 16 and putative novel HPV types (alb-1, alb-2, alb-7, and alb-10) were identified by degenerated nested polymerase chain techniques (polymerase chain reaction) in both the malignant melanoma and surrounding skin. One melanoma was associated with lichen sclerosus, and the other, with melanoma in situ and pigmented vulvar squamous papillomatosis. These melanomas harbored HPV types alb-7, and HPV 16 as well as alb-1, respectively. HPV types 16, 20, 21, 36, alb-2, and AJ001060 were detected in vulvar skin affected by lichen sclerosus. Vulvar squamous papillomatosis harbored HPV types 28 and alb-10. HPV 16 was physically integrated into the host genome in lichen sclerosus skin and possibly in the melanoma associated with pigmented vulvar squamous papillomatosis. Twenty-two percent (4 of 18) of normal control specimens from skin tumor excisions were found to harbor HPV DNA (HPV types 3, 54, and alb-7); none of these control samples harbored multiple HPV DNA. These findings of multiple HPV DNA and integrated HPV 16 in skin associated with vulvar malignant melanoma indicate that HPV may play a role in the development of vulvar malignant melanoma. The role of HPV could be either direct through infection of melanocytes or indirect as a cofactor with free radicals in chronic fibroinflammatory vulvar disorders such as lichen sclerosus.
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PMID:Vulvar malignant melanoma associated with human papillomavirus DNA: report of two cases and review of literature. 1214 Apr 40

We report a case of a 24-year-old woman with multiple pigmented lesions on her vulva. Histologically the lesions showed a heterogeneous pattern: the majority consisted of melanoma in situ and invasive melanoma; in a few lesions a much less clear-cut picture was found with only melanocytic dysplasia of various degrees. Our case shows the relationship between anomalous melanocytic proliferation of the vulva and vulvar melanoma and underlines the necessity of a thorough check of all melanocytic vulvar lesions also in young patients.
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PMID:Melanocytic dysplasia and multiple melanoma of the vulva. 1221 33

Large congenital melanocytic nevi (CMN) are at an increased risk of developing melanoma. Several forms of secondary proliferations can arise in congenital nevi on rare occasions. Although some of these closely resemble melanoma both clinically and histologically, metastasis is rare. We used comparative genomic hybridization to analyze chromosomal aberrations in different types of proliferations arising in CMN and compared them to typical congenital nevi, clear-cut melanomas arising in congenital nevi, as well as primary cutaneous melanomas that were not associated with a CMN. Cases of CMN and CMN with secondary proliferations were assigned to six groups according to the predominant histological pattern: group I, bland congenital nevi (n = 6); group II, congenital nevi with foci of increased cellularity (n = 4); group III, CMN with a proliferation simulating superficial spreading melanoma in situ (n = 3); group IV, CMN with a proliferation simulating nodular melanoma (n = 9); group V, proliferating neurocristic hamartoma (n = 1); and group VI, melanoma arising in congenital nevus (n = 6). No aberrations were found in groups I to III, whereas seven of nine cases of group IV, and one of one case of group V, showed aberrations. In group IV six of seven cases with aberrations (86%) showed numerical aberrations of whole chromosomes exclusively. This pattern differed significantly from the findings in melanoma that arose within CMN (n = 6), group VI, or independent of CMN (n = 122) in which only 5% showed numerical changes only. The single case in group V showed aberrations similar to melanoma. The finding of frequent numerical chromosomal aberrations in atypical nodular proliferations arising in CMN identifies these as clonal neoplasms with a genomic instability consistent with a mitotic spindle checkpoint defect. This difference compared to the aberration pattern found in melanoma might explain their more benign clinical behavior and may be of diagnostic value in ambiguous cases.
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PMID:Genetic changes in neoplasms arising in congenital melanocytic nevi: differences between nodular proliferations and melanomas. 1236 90

It is clear that much of what has been taught over the years concerning the pathology of melanoma may have little validity. Melanoma is viewed simply as a malignant neoplasm comprised initially of a proliferation of atypical melanocytes within the surface epithelium (epidermis). It has many features in common, regardless of anatomic site. It spreads within the epidermis first for months, possibly years or even for decades. At this stage (melanoma in situ) it is wholly curable if completely surgically excised. What determines how long a given melanoma remains in situ is not clear. It is probably a combination of factors, including host response to the neoplasm; physical barriers to growth and metastasis (perhaps solar damage); chemical or humoral growth factors or inhibitors (perhaps genetically determined); and other as yet undiscovered factors. Once a given neoplasm penetrates into the subjacent dermis, there are whole ranges of ill-defined events that act on its ability to continue to grow and develop the competence for metastasis (growth factors and inhibitors, neoangiogenesis factors and inhibitors, host immune responses, and so forth). Let us throw out all of our prejudices that may have developed or nurtured over the years. There is much to learn about the pathobiology of melanoma. Clinicians should keep their minds open to new concepts and try to separate what makes sense from that which does not.
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PMID:The pathology of malignant melanoma. 1238 53

The coexistence of 2 types of malignant neoplasms is relatively uncommon. We report a pigmented melanocytic lesion occurring adjacent to a previously treated basal cell carcinoma. Histology showed melanoma (lentigo maligna type) colonizing basal cell carcinoma demonstrated by hematoxylin-eosin and immunocytochemistry stains. It is unclear whether this lesion has the metastatic potential of an invasive melanoma of similar thickness, or simply reflects melanoma in situ extending into an epidermal-derived tumor analogous to appendageal extension of lentigo maligna. We review the literature on melanoma colliding with basal cell carcinoma. Therapeutic and prognostic problems are posed by this unique situation.
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PMID:Parasitism of basal cell carcinoma by lentigo maligna melanoma. 1273 89

The histopathological diagnosis of cutaneous melanocytic lesions may be difficult to assess. Frequently encountered diagnostic problems include: 1) Dysplastic nevus or melanoma in situ?; 2) Melanoma in situ or superficial spreading melanoma?; 3) Lentigo maligna or lentigo maligna melanoma?; 4) Compound nevocellular nevus or nevoid melanoma?; and 5) Spitz nevus or Spitzoid melanoma? Moreover, less frequently encountered diagnostic challenges are discussed: 1) Deep penetrating nevus or nodular melanoma?; and 2) Cellular blue nevus or melanoma metastasis? In this contribution, these problems are discussed after a systematic approach involving a concise histopathological description of the classic lesions considered in the differential diagnoses, a presentation of the deviating histopathological features that give rise to the diagnostic problems, and finally diagnostic recommendations on the classification of the problematic lesions. We also briefly discuss the contribution of additional immunohistochemistry and molecular pathology in aiding to establish a correct diagnosis.
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PMID:Current diagnostic problems in melanoma pathology. 1277 12


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