十二指肠间质瘤的临床病理及免疫组织化学研究

目的：研究十二指肠间质瘤临床病理学特点和免疫组织化学表达特征。方法：对18例十二指肠间质瘤作了临床病理形态学观察和免疫组织化学分析。结果：18例肿瘤良性3例，恶性15例，基本细胞类型为梭形细胞，1例肿瘤细胞外基质可见丝团样纤维。免疫表型特征为：C-kit18例（100％）胞质强阳性表达；CD347例（38．9％）阳性；S－100蛋白9例（50％）呈局灶性或散在阳性，其中包括2例良性，7例恶性；SMA仅1例阳性。结论：十二指肠间质瘤恶性发生率较高，细胞类型以梭形细胞为主。C-kit因其敏感性高、特异性强成为十二指肠间质瘤的可靠标记物，但不能作为良恶性判断指标，CD34阳性表达率低；神经化生率较高平滑肌方向分化率低。     

子宫血管周上皮样细胞肿瘤临床病理观察

目的研究子宫血管周上皮样细胞肿瘤的病理学特征、诊断、鉴别诊断和生物学行为。方法对5例子宫血管周上皮样细胞肿瘤进行常规组织学和免疫组织化学（SP法）染色和观察,对患者进行随访,并复习相关文献。结果光镜下5例肿瘤均由透明或嗜酸细胞巢或宽窄不等的细胞索组成,间质有丰富的小血管和程度不等的透明变。免疫组织化学染色示5例瘤细胞均黑色素细胞标记阳性和程度不等的结蛋白和平滑肌肌动蛋白（SMA）阳性,CK和CD10阴性。5例患者现均存活。结论子宫血管周上皮样细胞肿瘤具有较特征性的组织病理及免疫组织化学特点,HMB45阳性对诊断有重要作用。该肿瘤分良性、恶性潜能不能确定和恶性三类,应与透明细胞癌和上皮样平滑肌肿瘤区别。     

伴有破骨细胞样巨细胞的胰腺未分化癌1例报道及文献复习

目的：探讨伴有破骨细胞样巨细胞的胰腺未分化癌的临床病理特点.方法：观察1例伴有破骨细胞样巨细胞的胰腺未分化癌的形态学特征,并进行免疫组织化学染色.结果：伴有破骨细胞样巨细胞的胰腺未分化癌肿瘤主要有两种细胞组成,一种为单核细胞,分为组织细胞样单核细胞和梭形或多形性瘤细胞两型;另一种为多核巨细胞,分为非肿瘤性的破骨细胞样巨细胞和瘤巨细胞两型.免疫组织化学研究显示,这两种细胞Vimentin均阳性,均不表达cytokeratin（AE1/AE3）,CK5/6,CEA,CgA;其中破骨细胞样巨细胞、组织细胞样单核细胞CD45,CD68阳性,而瘤巨细胞和梭形瘤细胞阴性.结论：伴有破骨细胞样巨细胞的胰腺未分化癌是一种罕见恶性肿瘤,可能为胰腺未分化癌的一个亚型.诊断需与胰腺恶性纤维组织细胞瘤、转移的骨巨细胞瘤或黑色素瘤等鉴别.     

原发肠道恶性纤维组织细胞瘤

1974～1985年遇到的6例原发肠道恶性纤维组织细胞瘤。男4例,女2例,发病年龄28～64岁,平均47岁。肿瘤发生小肠3例、回盲部1例、结肠2例。瘤组织是多形性,主要由纤维母细胞样细胞和组织细胞样细胞构成,以及以上二者之间的胖棱形过渡细胞。组织细胞样细胞可演变成泡沫细胞、多核及单核瘤巨细胞。另见少量未分化间叶细胞。对4例肿瘤做了α_1-抗胰蛋白酶、抗溶菌酶血清免疫组织化学(ABC法)染色观察,2例进行电镜超微结构观察。     

上皮样血管内皮瘤的临床病理分析

目的：探讨上皮样（组织细胞样）血管内皮瘤的临床病理学特点及其意义。方法：对9例上皮样血管内皮瘤进行光镜和免疫组织化学SP法检测,1例作电镜观察,结果：年龄16－47岁,平均32岁,男女性别差异无显著性意义。部位：头面部4例,上肢3例,下肢2例,形态特征：瘤细胞具有上皮样或组织细胞样的形态;瘤细胞圆形或多角开,三五成群呈小巢状,索状,不规则状排列,分布于粘液间质中;间质可显著或少量粘液样变或玻璃样变,瘤细胞内含有原始血管腔,核分裂角,多形性及坏死少见,部分病例伴有梭形细胞血管内皮瘤改变,1例见破骨细胞样的多核巨细胞,免疫组织化学检测7例,7例波形蛋白均阳性,5例第八因子相关抗原,CD31,CD34阳性,2例细胞角蛋白弱阳性,1例CD68和a1-抗胰蛋白酶阳性,电镜观察1例见胞质内含丰富的微丝和少许的W－P小体,6例随访－8年,3例在原发部位有1或2次复发,但未见有转移,结论：上皮样血管内皮瘤是一种低度恶性的软组织肉瘤,其病因学尚不清楚,熟悉其形态特征对避免误诊为其他类似病变具具有重要意义。     

骨软化或佝偻病相关的间叶组织肿瘤临床病理分析

目的 探讨骨软化或佝偻病相关的间叶组织肿瘤的临床病理特点。方法 回顾分析10例患者的临床资料,观察10例骨软化相关的肿瘤组织的形态和免疫表型[免疫组织化学SP法染色,所用抗体包括波形蛋白、S-100、平滑肌肌动蛋白（SMA）、结蛋白、CD34、AE1／AE3、Ki-67、HMB45]。结果 患者男性6例,女性4例,年龄范围28～69岁（平均45．6岁）;患者均有2～27年（平均9．6年）骨痛、关节痛和活动困难的病史,检查发现低血磷、高尿磷;肿瘤最大径1～7cm不等（平均3．5cm）;瘤组织为间叶组织来源（仅2例颌骨病变中见不明显的条索状上皮）,可见多少不等的梭形纤维母细胞样细胞、脂肪细胞、软骨样细胞、黏液样细胞等,瘤组织富于血管,8例病变中有少见的絮状或不规则砂砾样钙盐沉积,2例发生于软组织的肿瘤周边见骨壳形成。3例组织中可见非尿酸盐结晶：9例细胞分裂象少见,1例核分裂象多见并且异型性明显;瘤细胞波形蛋白阳性,5例SMA部分阳性,3例CD34部分瘤细胞阳性,结蛋白、S-100、AE1／AE3均阴性,Ki-67指数（8例≤4％,仅1例为30％）;AB／PAS染色：8例肿瘤黏液基质和血管周围黏液样变呈AB染色阳性。结论 骨软化相关的肿瘤多为良性或低度恶性的间叶组织肿瘤,因组织学具有多样性而易误诊,掌握其共性特征并结合临床资料方能正确诊断。     

胃肠道间质瘤临床病理及免疫组织化学特征

目的 探讨胃肠道间质瘤的免疫组织化学特征，为其诊断及鉴别诊断和预后提供依据。方法 对消化道内169例间叶源性肿瘤进行免疫组织化学标记和形态学观察，确诊113例胃肠道间质瘤。结果 肿瘤多见于胃，临床常见首发症状为消化道出血及腹部包块。瘤细胞主要有梭形细胞及上皮样细胞两种形态，梭形细胞型70例，上皮样细胞型10例，混合细胞型33例。相对良性33例，交界性26例，恶性54例。免疫表型：CD117阳性112例，CD34阳性102例，阳性率分别为99．1％及90．2％，且呈弥漫强阳性表达。结论 胃肠道间质瘤是消化道最常见间叶源性肿瘤，以胃内多见；主要有2种细胞形态和3种组合形式；确诊需要依靠CD117、CD34等免疫标记物配合。     

软组织骨化性纤维粘液样瘤八例临床病理分析

目的：研究软组织骨化性纤维粘液样瘤（OFT）的病理形态学特点和免疫组织化学表型,并探讨其组织发生,方法：采用光镜观察（HE）和免疫组织化学标记（LSAB法）结合临床资料对8例软组织骨化性纤维粘液样瘤进行临床病理学分析。结果：8例患者均为中老年人,年龄43－78岁,平均63岁,临床上多表现为四肢近端皮下缓慢性生长的肿块,组织学上,该肿瘤归纳起来有以下3个持征性的形态,比较独特,具有诊断性意义：（1）肿瘤境界清楚,有一层厚的纤维性假包围绕,多数病例于包膜内可见一层薄的不连续性骨壳,由成熟的化生性板层骨组成;（2）肿瘤的实质由多个大小不一,细胞密度不均的小叶组成,小叶内的瘤细胞呈圆形,卵圆形或短梭形,胞质淡染或呈嗜伊红色,核染色质细致,核分裂象偶见;（3）瘤细胞呈特征性的巢状,条束状或纤细的网格六排列,肿瘤的基质呈特征性的纤维粘液样,7例行免疫组织化学标记,结果显示瘤细胞强阳性表达波形蛋白和神经元特性烯醇化酶（7／7）,多数表达S－100蛋白（6／7）,部分表达结蛋白（2／7）,7例均有随访资料,2例分别于术后2年及15年复发。结论：软组织骨化性纤维粘液样瘤是一种好发于中老年人的具潜在低度恶性的软组织肿瘤,其特征性的骨壳结构,独特的细胞形态及其排列方式具有诊断意义。免疫组织化学检测结果支持OFT起源于雪旺细胞。     

肾脏上皮样色素性透明细胞肿瘤病理形态观察

目的 探讨上皮样色素性透明细胞肾脏肿瘤形态学特点,加强对该肿瘤的认识,减少误诊.方法 回顾性分析2000余例肾脏肿瘤,符合上皮样色素性透明细胞肿瘤3例,通过HE、免疫组织化学EnVision法观察3例肿瘤形态学特点,对其中1例行超微结构观察,同时复习相关文献.结果 女性2例,男性1例,2例形态学表现为透明细胞癌样,1例见透明细胞和嗜酸性细胞构成乳头结构.免疫组织化学上皮标记及S-100蛋白均为阴性,HMB45均为阳性,2例Melan A阳性.电镜末见黑色素小体结构.结论 色素性透明细胞上皮样肿瘤是非常罕见的肾脏肿瘤,病理学特征兼有肾细胞癌、上皮样血管平滑肌脂肪瘤与黑色素瘤等肿瘤特征,免疫组织化学有利于鉴别诊断.其可能是上皮样血管平滑肌脂肪瘤的一种亚型.     

子宫和卵巢腺瘤样瘤的临床病理分析

目的 探讨女性生殖系统腺瘤样瘤的发生、免疫组织化学表达的特征及鉴别诊断。方法 对24例子宫和卵巢腺瘤样瘤进行临床病理及免疫组织化学观察。结果 24例患者中腺瘤样瘤发生于子宫者21例,卵巢者2例,子宫与卵巢同时发生者1例,分别占本院同期子宫及卵巢肿瘤及瘤样病变的0.34%和0.06%。免疫组织化学染色显示：波形蛋白及细胞蛋白（AE1／AE3）均为阳性,呈双相表达;第八因子相关抗原（FⅧRAg)均为阴性;S－100蛋白20例阳性（83.3%),上皮膜抗原（EMA）4例阳性（16.7%);其中10例行calretinin蛋白染色,均为阳性表达。结论 女性生殖系统腺瘤样瘤为间皮起源,子宫为最常见部位。免疫组织化学染色结果可作为诊断及鉴别诊断的重要参考依据。其生物学行为为良性,预后良好。     

Occurrence of hyaline droplets in renal biopsy specimens: an ultrastructural study

Hyaline droplets are apical cytoplasmic vesicles containing an accumulation of electron-dense amorphous materials surrounded by a unit membrane. Hyaline droplets may originate from apical vesicles after conversion to osmotic vesicles and loss of internally lined glycocalyx. They are found in the proximal tubular epithelium in biopsies from patients with renal diseases; however, their biological importance is not well understood. We reviewed ultrastructural pathology records of 140 renal biopsy patients to determine the occurrence and relevance of hyaline droplets. Of the cases, 14 (10%) showed the presence of hyaline droplets in proximal tubular epithelium. The distribution of cases were 8 of the 19 (42%) with minimal change nephritic syndrome, 2 of the 37 (5%) with IgA nephropathy, 2 of the 4 (50%) with membranous glomerulonephropathy, 1 of the 4 (25%) with tubulointerstitial nephritis, and 1 of the 1 (100%) with acute renal failure. The droplets were frequently found in male patients (86%), never in children, and were mostly associated with tubular necrosis (8 of 14 cases; 56%). Many hyaline droplets were observed in the cytoplasm of necrotic proximal tubular epithelial cells, and even when tubular necrosis was not evident, the proximal tubular epithelial cells containing hyaline droplets showed degenerated microvilli and decreased basal interdigitations. These results suggest that hyaline droplets could be one marker of renal tubular necrosis and a sign of functional disorder of protein reabsorption by degenerating proximal tubular epithelium.     

Expression of T-cell antigens on Reed-Sternberg cells in a subset of patients with nodular sclerosing and mixed cellularity Hodgkin's disease

Expression of T-cell antigens by Reed-Sternberg (RS) cells has not been detected in most studies of Hodgkin's disease (HD). The authors employed an improved method of fixation (paraformaldehyde-lysine-periodate), which sharply defined cell borders and revealed T-cell antigens on RS cells in 8 of 30 (27%) cases of HD. Antigen-specific staining was confirmed by immunoelectron microscopy. RS cells expressed T11 (8/8 cases), Leu-3 or T4 (4/8 cases), Leu-4 or T3 (3/8 cases), but not other T-cell specific antigens (Leu-1, T8, T6, 3A1). RS cells were negative for leukocyte common antigen (LCA/T200), in contrast to positive LCA/T200 staining of RS-like cells in T-cell lymphomas. RS cells in all HD cases were positive for Ki-1 and/or Leu-M1 antigens. The percentage of RS cells expressing T-cell antigens was less than 20% (2 cases), 20-50% (3 cases), or greater than 50% (3 cases). This percentage and the specific T-cell antigens expressed varied in tissues from different sites in each of 2 cases. Expression of T-cell antigens by RS cells was found in nodular sclerosis (6 of 20 cases) and mixed cellularity (2 of 5 cases) but not in lymphocyte predominance (2 cases), lymphocyte depletion (1 case), or unclassified types (2 cases). Two cases of nodular sclerosis contained areas of necrosis surrounded by sheets of lacunar cells (syncytial variant of NSHD). Two other cases were associated with cutaneous lymphoma. One of these cases was mixed cellularity HD, which appeared to be confined to the skin. In a second case, tumor cells of similar phenotype (T4+, Ki-1+) were found in skin and lymph nodes of a patient with coexistent mycosis fungoides and HD. These results are consistent with an origin of RS cells from T cells in some cases of nodular sclerosing and mixed cellularity HD. They also suggest that the same cell type, an activated helper T-cell, is involved in the pathogenesis of both skin lesions and lymphadenopathy of some patients with coexistent mycosis fungoides and HD.     

Multipoint interphase FISH in childhood T-acute lymphoblastic leukemia detects subpopulations that carry different chromosome 3 aberrations

We examined chromosome 3 in 32 childhood acute lymphoblastic leukemia (ALL) bone marrow samples. Using interphase multipoint FISH (mp-FISH), which was developed by our group, with 42 chromosome 3-specific probes, we detected clonal chromosome 3 aberrations in 4 T-cell ALL (T-ALL) cases. Four out of seven T-ALL cases carried 3q trisomies. One T-ALL case carried either trisomy 3 (in 15% of the cells) or a 23-megabase (Mb) 3p13 approximately p12 deletion in a different subpopulation of cells of 32%. Another T-ALL case had either 3q trisomy in 11% or a 12-Mb 3p12 approximately p13 deletion in 19% of the cells. The deletions were overlapping. In both cases, the majority of the bone marrow cells (47 and 70%, respectively) were normal chromosome 3 disomics. The interstitial deletions detected harbor a known homozygous deletion region between 72.6 and 78.8 Mb, which has been described in lung and breast tumors and contains the DUTT1/ROBO1 tumor suppressor gene. These deletions detected by mp-FISH would have remained unnoticed by conventional cytogenetics and multiplex FISH, as well as by current methods based on total tumor DNA analysis such as comparative genomic hybridization (CGH), array CGH, and loss of heterozygosity (LOH).     

Assessment of Epstein-Barr virus association with pediatric non-hodgkin lymphoma in immunocompetent and in immunocompromised patients in Argentina

CONTEXT: Epstein-Barr virus (EBV) has been classically associated with 3 malignancies, Burkitt lymphoma, B-cell lymphoproliferative syndromes, and nasopharyngeal carcinoma, and more recently with Hodgkin disease, T-cell lymphomas, and gastric and breast carcinomas, as well as with leiomyosarcoma and leiomyoma associated with immunosuppression. OBJECTIVE: To compare EBV expression in Argentine tumor samples with those reported elsewhere, we analyzed EBV expression in an Argentine pediatric population with non-Hodgkin lymphoma and correlated these results with clinical course and outcome. METHODS: We studied EBV presence by latent membrane protein-1 protein labeling by immunohistochemistry, by in situ hybridization, and by polymerase chain reaction for Epstein-Barr-encoded RNAs (EBERs) in formalin-fixed and paraffin-embedded non-Hodgkin lymphoma tissue samples (collected retrospectively) from 32 pediatric patients at Ricardo Gutiérrez Children's Hospital from 1993 to 2000. RESULTS: Eight out of the 32 (25%) non-Hodgkin lymphoma cases showed latent membrane protein-1 and EBERs by in situ hybridization positive staining in tumor cells. Among EBERs and latent membrane protein-1-positive cases, there were 5 immunocompromised patients, with either human immunodeficiency virus infection or primary immunodeficiency. The EBERs in situ hybridization results were confirmed by EBERs polymerase chain reaction in good-quality DNA from 11 samples, with 3 proving positive and 8 negative. CONCLUSIONS: The association of EBV with non-Hodgkin lymphoma in the Argentine pediatric population was low (25%), and this figure rose to 100% when only the immunocompromised patients subgroup was considered, confirming that the virus is probably a cofactor in the lymphomagenesis of some but not all pediatric non-Hodgkin lymphoma. So far, no differences in clinical outcome are discernible between EBV-positive and EBV-negative non-Hodgkin lymphoma patients.     

Impaired clonogenic potential of CD25 positive T cells in lymph nodes involved by B cell non-Hodgkin's lymphomas

In vivo activated T cells (CD25+) present in lymph nodes involved by B-non-Hodgkin's lymphomas (B-NHL) were investigated here for their ability to proliferate in vitro. CD25-/CD25+ T cells were isolated using a rosette method with magnetic beads, then the frequency of proliferating T lymphocyte-precursors (PTL-P) in both populations was assessed by limiting dilution experiments, in the presence of IL2, PHA and allogeneic spleen cells as feeders. In a total of 16 cases studied, growing microcultures were observed in all cases for CD25- T cells (mean value of PTL-P frequency: 1/32; range 1/10 - 1/2899) but in 6 cases only for CD25+ T cells (mean value of PTL-P frequency: 1/441; range 1/119 - 1/3736); the absence of any proliferative cultures in the 10 other cases indicated that the number of PTL-P was inferior to 1/12480. These results suggest that the proliferative potential of CD25+ T cells infiltrating lymph nodes involved by B-NHL is paradoxically decreased.     

Dysplasia of the gallbladder. Its histogenesis and correlation to gallbladder adenocarcinoma

A total of 50 cases of gallbladder dysplasia found adjacent to carcinoma were examined histologically and immunohistochemically for metaplastic changes in order to elucidate the characteristics of the dysplasia of the gallbladder. The incidence of metaplastic changes in the dysplastic mucosa such as the occurrence of endocrine cells, lysozyme-immunoreactive cells, goblet cells, and Paneth cells were 58%, 74%, 32%, and 22%, respectively. Based on the presence or absence of metaplastic changes, these 50 cases of dysplasia were divided into 40 cases (80%) of metaplastic type dysplasia showing at least one marker of metaplasia and 10 cases (20%) of non-metaplastic type dysplasia showing no metaplasia. On the other hand, these 50 cases of carcinoma were divided into 10 cases of non-metaplastic type carcinoma and 40 cases of metaplastic type carcinoma based on the presence or absence of metaplasia in the tumor tissue. The incidence of metaplastic changes in the dysplastic lesions was compared between the dysplasia adjacent to non-metaplastic type carcinoma and that adjacent to metaplastic type carcinoma. The incidence of metaplasia in the dysplastic mucosa adjacent to metaplastic type carcinoma was higher than that adjacent to non-metaplastic type carcinoma with a statistically significant difference. Moreover, the presence or absence of metaplastic changes was also examined in the surrounding dysplasia and non-tumorous mucosa in each case. Most cases of metaplastic type carcinoma were surrounded by dysplasia with metaplastic changes and by metaplastic epithelium, whereas most cases of non-metaplastic type carcinoma were surrounded by dysplasia without metaplasia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Extrapulmonary small cell carcinomas express K homology domain containing protein overexpressed in cancer, but carcinoid tumors do not

A number of malignancies, including high-grade neuroendocrine carcinomas of the lung, have been reported to express K homology domain containing protein overexpressed in cancer (KOC), a member of the insulin-like growth factor messenger RNA-binding protein (IMP) family also known as L523S and IMP3. KOC acts to promote tumor cell proliferation by enhancing insulin-like growth factor-II protein expression. This study aimed to examine KOC expression pattern in extrapulmonary neuroendocrine tumors. Seventy-five extrapulmonary neuroendocrine tumors that were surgically resected or had undergone biopsy, including 53 small cell carcinomas (uterine cervix, 21; bladder, 10; colorectum, 13; prostate, 7; stomach, 1; and esophagus, 1) and 22 carcinoid tumors (colorectum, 10; appendix, 5; ileum, 4; duodenum, 2; and stomach, 1), were immunohistochemically studied using a monoclonal antibody against KOC. Our results demonstrated that 47 small cell carcinomas (89%) showed moderate to strong positive staining for KOC, with 25 cases (53%) showing positivity in more than 90% of tumor cells and 22 cases (47%) in 40% to 80% of tumor cells. Three cases showed weak staining in 5% to 10% of the tumor cells. The remaining 3 cases (uterine cervix, 2; bladder, 1) showed completely negative immunoreactivity. No KOC immunostaining was detected in 22 carcinoid tumors. These findings indicate that KOC may play an important role in the regulation of biologic behavior of extrapulmonary small cell carcinomas. In addition, immunohistochemical detection of KOC expression may serve as a useful diagnostic tool in the distinction between small cell carcinoma and carcinoid tumor, particularly when the diagnostic material is a small biopsy with crushing artifact.     

The role of cell cycle regulatory protein, cyclin D1, in the progression of thyroid cancer.

Cell cycle progression is facilitated by cyclin-dependent kinases that are activated by cyclins including cyclin D1 and inactivated by cyclin-dependent kinase inhibitors (CDKIs) such as p27. Our previous studies have demonstrated decreased p27 expression in both papillary and more aggressive carcinomas of the thyroid compared to thyroid adenoma and almost similar level of cyclin D1 expression between thyroid adenoma and papillary carcinoma. These results indicate that CDKIs may have an important role in the carcinogenesis of the thyroid and that they probably have a limited role in malignant progression of the thyroid cancer. The role of cyclin D1 in malignant progression of thyroid carcinoma has yet to be established. We studied the expression of cyclin D1 by immunohistochemistry in 34 cases of conventional papillary carcinoma (CPC), 10 cases of minimally invasive follicular carcinoma (MIFC), and 32 cases of more aggressive thyroid carcinoma (ATC), which included 11 tall cell variants, one columnar cell variant of papillary carcinoma, seven insular carcinomas, and 13 anaplastic carcinomas. Cyclin D1 staining was classified by staining score as 0, negative; 1+, less than 25%; 2+, 25 to 50%; and 3+, more than 50% tumor cells staining positive. Kruskal-Wallis one-way ANOVA and Wilcoxon Rank Sum/Mann-Whitney U Test was used to assess the difference in the expression of cyclin D1 between the study groups. Twenty-eight out of the 34 CPCs were cyclin D1 positive, 24 (70%) were 1+, 3 (9%) were 2+, and one (3%) were 3+ positive. Seven of 10 MIFCs were cyclin D1 positive, five (71%) were 1+, and the remaining two (29%) were 2+ positive. On the other hand, 28 of 32 ATCs showed cyclin D1 immunostaining. Of these, three (9%) were 1+, five (13%) were 2+, and 20 (63%) were 3+ positive. This study demonstrates a significant overexpression of cyclin D1 in ATC compared CPC (P < .001) and MIFC (P < .005), suggesting that the cyclin D1 expression may play a role in tumor progression and may have prognostic significance in thyroid cancer.     

Adenoid cystic carcinoma of the breast: Diagnosis by fine-needle aspiration

Adenoid cystic carcinoma rarely occurs as a primary breast malignancy. When seen in fine-needle aspiration (FNA) material, it is identical to its counterpart in the salivary glands. We report six cases diagnosed by aspiration in patients aged 32-82 yr. The smears were highly cellular and featured extracellular spheres of metachromatic material. These were surrounded by small, uniform cells with bland nuclei and very little cytoplasm. Numerous similar cells occurred singly in the background. The cytologic differential diagnosis of adenoid cystic carcinoma includes other entities that produce extracellular metachromatic spheres including collagenous spherulosis. We describe and illustrate similar material originating in inspissated secretions or stromal fragments from fibrocystic change and fibroadenoma, as well as infiltrating ductal carcinoma. Diagnostic criteria for adenoid cystic carcinoma and the clinical relevance of distinguishing this rare tumor from typical infiltrating ductal carcinoma are discussed.