Testicular "Tumor" of the adrenogenital syndrome

Adesokan, Adekunle; Adegboyega, Patrick A.; Cowan, Daniel F.; Kocurek, Jeffrey N.; Neal, Durwood E.

doi:10.1002/(sici)1097-0142(19971201)80:11<2120::aid-cncr11>3.0.co;2-0

Cited by 22 publications

(1 citation statement)

References 17 publications

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“…These lesions have been found in the liver, lung, mediastinum, mesentery, stomach, spleen, pelvis, and most commonly the retroperitoneal presacral region [4, 5]. Our review of the literature demonstrates there have been 45 reported cases of extra-adrenal myelolipomas, some with multiple lesions and locations including: 16 presacral, 9 retroperitoneal, 8 thoracic/mediastinal, 7 perirenal, 3 pelvic, 2 renal, 2 hepatic, 1 gastric, and 1 perivesicular [1, 6–23].…”

Section: Discussionmentioning

confidence: 99%

Extra-Adrenal Myelolipoma Presenting as Efferent Limb Obstruction

Conley

Klein

Edhayan

et al. 2012

Case Reports in Surgery

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Myelolipomas are rare benign lesions composed of mature adipose tissue and immature hematopoetic cells. The adrenal gland is the most common location for these lesions, but cases of extra-adrenal myelolipomas have been described. The predominant location for extra-adrenal myelolipomas is the retroperitoneum, and very few reported cases describe these lesions in the peritoneal cavity. Typically these lesions are incidental findings and asymptomatic, but occasionally can present with symptoms secondary to mass effect. We present the case of a 72 year old man presenting with a gastric outlet obstruction secondary to an epigastric mass. The mass was resected and pathology was consistent with myelolipoma. This case illustrates an atypical location and presentation of a myelolipoma. These are rare tumors with only 5 intra-abdominal myelolipomas reported in the literature. This article is a review of the surgical literature and a discussion on myelolipomas. Knowledge of these rare entities can help ensure proper management of these patients, which may include early surgical intervention.

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Section: Discussionmentioning

confidence: 99%

Extra-Adrenal Myelolipoma Presenting as Efferent Limb Obstruction

Conley

Klein

Edhayan

et al. 2012

Case Reports in Surgery

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Syndromic aspects of testicular carcinoma

Holzik

Sijmons

Sleijfer

et al. 2003

Cancer

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BACKGROUNDIn patients with hereditary or constitutional chromosomal anomalies, testicular carcinoma can develop sporadically or on the basis of an underlying hereditary genetic defect. Greater knowledge of these genetic defects would provide more insight into the molecular pathways that lead to testicular carcinoma. To the authors' knowledge, little attention has been paid to date to the comorbid occurrence of testicular carcinoma in patients with hereditary disorders or constitutional chromosomal anomalies.METHODSThe authors performed a review of the literature.RESULTSTwenty‐five different hereditary disorders or constitutional chromosomal anomalies have been reported in patients who developed seminomatous or nonseminomatous testicular carcinoma.CONCLUSIONSAlthough most of these malignancies were too rare to enable the detection of statistically significant correlations between the chromosomal/hereditary disorder and the testicular tumor, it was striking that many of the patients had also other urogenital abnormalities. Susceptibility to urogenital abnormalities seems to disrupt normal urogenital differentiation and suggests a correlation with testicular dysgenesis and, thus, also with testicular carcinoma. Other evidence of causal involvement has been found in the field of tumor cytogenetics. Some of the genes responsible for hereditary disorders have been mapped to regions that are of interest in the development of sporadic testicular carcinoma. Molecular studies on candidate genes will be required to provide definite answers. Completion of the human gene map and the availability of advanced gene arrays and bioinformatics are expected to greatly facilitate further exploration of the role of hereditary genetic defects in testicular carcinoma. Cancer 2003;97:984–92. © 2003 American Cancer Society.DOI 10.1002/cncr.11155

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