Histologic Variant (histologic + variant)

Distribution by Scientific Domains


Selected Abstracts


Clinical curiosity: Cribriform-morular variant of papillary thyroid carcinoma,

HEAD & NECK: JOURNAL FOR THE SCIENCES & SPECIALTIES OF THE HEAD AND NECK, Issue 5 2006
Kimberly M. Dalal MD
Abstract Background. There is an increasing awareness of the association of papillary thyroid carcinoma and familial adenomatous polyposis (FAP). Although the incidence is rare, most tend to occur in women. Several authors have described a distinctive histologic variant of papillary thyroid carcinoma, the cribriform-morular variant, which is associated with FAP but also may be encountered in patients with non-FAP. This diagnosis may precede the symptoms of colorectal polyposis. Methods. A healthy 36-year-old woman was seen with a left thyroid nodule, and a 34-year-old woman with FAP was seen with a right thyroid nodule; both masses were suspicious for papillary thyroid carcinoma. Both patients underwent total thyroidectomy. Results. Pathologic examination of both specimens revealed papillary thyroid carcinoma, cribriform-morular variant. The first patient subsequently underwent colonoscopy, which was negative for polyposis. Conclusions. Patients diagnosed with the cribriform-morular variant of papillary thyroid cancer should be screened for the presence of FAP. © 2006 Wiley Periodicals, Inc. Head Neck28: 471,476, 2006 [source]


Follicular porokeratosis: distinct clinical entity or histologic variant?

JOURNAL OF CUTANEOUS PATHOLOGY, Issue 11 2009
M. Pongpudpunth
Various clinical subtypes of porokeratosis, clinically characterized by annular plaques with a normal or atrophic center and a distinctive keratotic ridge, are described based on the age of onset, size, number and distribution of the lesions. Follicular involvement, identified by follicular localization of cornoid lamellae, is uncommon and has only been reported in association with other subtypes such as disseminated superficial actinic porokeratosis and porokeratosis of Mibelli. We present a case of follicular porokeratosis in a 40-year-old male who presented initially with scaly red "papules" in a follicular distribution on the upper extremity. Microscopic examination of a punch biopsy specimen revealed parakeratosis confined to the follicle and mild interface change. A repeat biopsy performed in 2008 revealed identical histologic features. In terms of etiopathogenesis, a clone of cells at the base of the follicle demonstrating abnormal keratinization is not a novel concept and has been demonstrated in other porokeratotic dermatoses. However, the presence of lesions that are solely follicular based, in terms of clinical presentation and histologic findings, and static over a 3-year period favors the concept that follicular porokeratosis is a distinct clinical entity and not merely a histologic variant of the porokeratotic dermatoses described in the literature thus far. [source]


Focal Acral Hyperkeratosis: A Rare Cutaneous Disorder within the Spectrum of Costa Acrokeratoelastoidosis

PEDIATRIC DERMATOLOGY, Issue 2 2004
Emel Erkek M.D.
These disorders are distinguished solely on the basis of the absence of elastorrhexis in the latter. We present a case of focal acral hyperkeratosis in a 9-year-old girl. The lesions consisted of translucent polygonal papules clustered on the thenar regions of the palms and over the metacarpophalangeal and interphalangeal joints. Histopathologic examination revealed orthohyperkeratosis within focal clavus-like depressions of the epidermis and prominent hypergranulosis. There was no evidence of alterations in elastic tissue. The clinicopathologic distinction between focal acral hyperkeratosis and acrokeratoelastoidosis is blurred. There is enough evidence to consider the former as a histologic variant of Costa acrokeratoelastoidosis syndrome, and a better nomenclature for this disorder would be "acrokeratoelastoidosis without elastorrhexis." [source]


Tubular Carcinoma of the Breast: A Population-Based Study of Nodal Metastases at Presentation and of Patterns of Relapse

THE BREAST JOURNAL, Issue 1 2001
H. A. Kader MD
Abstract: Tubular carcinoma of the breast (TCB) is a recognized histologic variant of infiltrating ductal carcinoma (IDC) and has been considered to have a comparatively favorable prognosis. However, previous studies have been based on small numbers of cases, some pure TCB and some mixed histology, or have not employed an appropriate comparison group. In this study 171 pure TCB cases and a comparison group of 386 cases with grade I (well differentiated) IDC were identified in a population-based database maintained by the British Columbia Cancer Agency (BCCA). The proportion of cases with axillary nodal involvement at presentation was lower in TCB cases than in the grade I IDC comparison group (12.9% and 23.9%, respectively; p < 0.05). Low-risk tumors (T1 and without vascular lymphatic or perineural invasion) were more prevalent in the TCB patients than in the grade I IDC patients (66.7% and 60.0%; p < 0.05). Low-risk TCB cases had a significantly lower rate of nodal metastases at presentation than low-risk grade I IDC cases (7.0% and 13.2%; p < 0.05). Kaplan,Meier and log-rank analyses indicated a statistically significantly lower rate of local recurrence in TCB cases than among IDC cases (p < 0.05) and a trend toward a lower rate of systemic relapse in TCB cases (p = 0.07). However, no difference in disease-specific survival was observed between TCB cases and grade I IDC comparisons. We conclude that the biologic behavior of TCB was more favorable than that of a comparison group of IDC cases. In view of the low incidence of axillary node metastases at presentation in the low-risk TCB subset (7%), axillary dissection may be omitted as part of the initial surgical management in these patients. [source]


Small cell astrocytoma: An aggressive variant that is clinicopathologically and genetically distinct from anaplastic oligodendroglioma

CANCER, Issue 10 2004
Arie Perry M.D.
Abstract BACKGROUND Small cell glioblastoma (GBM) is a variant with monomorphous, deceptively bland nuclei that often is misdiagnosed as anaplastic oligodendroglioma. METHODS To elucidate its clinicopathologic and genetic features, the authors studied 71 adult patients (median age, 57 years), including 22 patients who were identified from a set of 229 GBMs (10%) that had been characterized previously by epidermal growth factor receptor (EGFR)/EGFR-vIII variant immunohistochemistry. Tumors also were analyzed by fluorescence in situ hybridization for 1p, 19q, 10q, and EGFR copy numbers. RESULTS Radiologically, 37% of tumors that were not selected for grade showed minimal to no enhancement. Similarly, 33% of tumors had no endothelial hyperplasia or necrosis histologically, qualifying only as anaplastic astrocytoma (Grade III) using World Health Organization criteria. Nevertheless, such tumors progressed rapidly, with mortality rates that were indistinguishable from their Grade IV counterparts. The median survival for 37 patients who were followed until death was 11 months. Oligodendroglioma-like histology included chicken-wire vasculature (86%), haloes (73%), perineuronal satellitosis (58%), and microcalcifications (45%), although mucin-filled microcystic spaces were lacking. No small cell astrocytomas had 1p/19q codeletions, whereas EGFR amplification and 10q deletions were present in 69% and 97% of small cell astrocytomas, respectively. The tumors expressed EGFR and EGFR-vIII more commonly than nonsmall cell GBMs (83% vs. 35% [P < 0.001]; 50% vs. 21% [P < 0.001] respectively). CONCLUSIONS Small cell astrocytoma is an aggressive histologic variant that behaved like primary GBM, even in the absence of endothelial hyperplasia and necrosis. Despite considerable morphologic overlap with anaplastic oligodendroglioma, clinicopathologic and genetic features were distinct. Fifty percent of small cell astrocytomas expressed the constitutively activated vIII mutant form of EGFR, and molecular testing for 10q deletion improved the diagnostic sensitivity over EGFR alone. Cancer 2004. © 2004 American Cancer Society. [source]