Type 2 tumor sizes were 19.3 ⫾ 5.44 mm (range 9 –24 mm). Seven tumors had both plain and contrast-enhanced CT, and all demonstrated obvious heterogeneous enhancement with cystic regions (CT attenuation ⱕ20 Hu); the cystic regions became more recognizable on contrast CT. On sonography, these 7 cases showed as heterogeneously hypoechoic with an intratumoral anechoic region. With these cases, specimen his- tology showed cystic components and hemorrhage within the tumor (Figs 2 and 4). The remaining case (case 17) without contrast CT and sonography showed homogeneously attenu- ation on a plain CT scan. The specimen histology confirmed uniform tumorous tissue structure within the tumor.
In the inferior tumor group, there were seven men and three women, with a mean age of 53.9 years (range, 36-75 years). Eight of these tumors were located in the left parotidgland, and two were located in the right gland. The average disease duration before surgery was 23.4 ± 36.7 months. Except for a local mass, there were no other clinical symptoms. The ultrasonographic features were similar to those of the superior tumors. The average maximum diameter of the tumors on CT was 22.1 ± 12.5 mm. Of the 10 tumors, 3 (33.3%) exhibited cys- tic degeneration (Table 1). The surgical treat- ment involved dissection of the facial nerve and excision of the tumor and superficial lobe of the parotidgland. Five patients (50%) under- went FNAB preoperatively, and two of these patients (20%) were diagnosed with BCA. The diagnosis was confirmed on intraoperative fro- zen-section examination in three patients and on postoperative pathological examination in other patients. In one patient (10%), the facial nerve function deteriorated to House-Brack- mann (HB) grade II after the surgery, but recov- ered after 6 months. No patient developed recurrence after the operation (Table 2; Figure 2C, 2D).
Few imaging findings of BCA of the parotidgland have been reported. 6-9 In our cases, the morphology of BCAs was a well-defined margin and rounded contour, as with cases in previous reports. High-grade malignant tumors can easily be differentiated from BCAs by the infiltrative margins of malig- nant tumors. The differential diagnosis of BCA includes pleo- morphic adenoma, Warthin tumor, and low-grade malignant tumors. Most pleomorphic adenomas have an area containing abundant fibromyxoid stroma, which shows bright SI on T2WI as well as marked enhancement on postcontrast images. These areas show delayed enhancement on dynamic study. In addition, pleomorphic adenomas show lobulated contours and typically have a thick capsule. 9-11 These characteristic MR
scan values in patients with LEC of the salivary gland; based on the degree of enhancement, they classified the CT values into three ranks: (i) mildly enhanced (post-enhancement increment in CT value <15 HU); (ii) moderately enhanced (15-30 HU); (iii) significantly enhanced (>30 HU). All seven cases of primary LEC of the sali- vary gland studied by Zhang showed significant enhancement. In contrast, the present case showed only mild enhancement. Histopa- thological findings for this case were typical of LEC of the salivary gland. Extensive stromal infiltration of lymphocytes and plasma cells, accompanied by formation of lymphoid follicles was observed. Immunohistochemical examina- tion showed positivity for CK5/6 and p63 (+). These findings are consistent with the diagno- sis of LEC of the salivary gland. We also carried out a Ki-67 immunohistochemical analysis in this patient. Ki-67, a substance found in the macromolecular protein in the cell nucleus, is highly sensitive to protease, and is a sensitive index of cell proliferation. In previous reports, Ki-67 levels in primary LEC of the salivary gland tended to be higher (40% to 80%) than those in secondary LEC of salivary gland (20%) [17, 18]. Although our patient had a primary LEC of the salivary gland and had no other salivary gland disease such as Sjögren syndrome, the Ki-67 level was low (15%). Indeed, it was lower than that of a secondary LEC (20%). Another distinct characteristic of this case was EBV positivity. Earlier reports of LEC of the salivary gland associated with EBV infection were confined to endemic areas , while no association with EBV infection was observed in non-endemic areas . The present patient was a resident of northern China (non-endemic area) but was EBV (+). Further, appearance of microcysts in the tumor stroma is also a rare characteristic of this pathological entity.
A Japan ALOKA (model: α10) color ultrasound scanner was used for the examination of the bilateral parotidgland with a probe frequency of 8~13 MHz. The results of the evaluation of the parotidultrasound were assessed using a scoring system , 0 points: normal gland, ec- ho uniform; 1 point: substantial echo is weak- ened, mildly uneven, a little high echo line can be seen; 2 points: obvious echo of uneven echo, diffuse distribution of hypoechoic nod- ules, diameter < 2 mm, high echo line Increased; 3 points: nodular hypoechoic area increased fusion, diameter 2~6 mm, high echo line distri- bution disorder; 4 points: hypoechoic nodules > 6 mm, or gland atrophy (gland up and down diameter < 5.0 cm, left and right the diameter was < 3.0 cm and the thickness was < 1.0 cm), and there were many high echo lines (Figure 1). Statistical analysis
ISCM is a rare complication of several types of cancers. The prognosis of ISCM is poor with an overall surviv- al of 6 months in surgically treated patients, and opti- mum management remains controversial. In the pres- ent study, the case des- cribed a patient with ISCM from parotidgland CXPA, who underwent surgical resection successfully and survived for 8 months. In the authors’ opinion, it is extremely rare that a pa- tient with ISCM from parot- id gland CXPA can survive as long as 8 months, indi- cating that early diagnosis and surgical resection are vitally important when IS- CM is suspected.
The differential diagnosis includes benign and malignant parotid tumors, especially Warthin tumors and adenoid cystic carcinomas, which may also have a solid cystic appearance. These tumors rarely occupy the total gland parenchyma. In particular, Warthin tumors are bilateral in up to 10% of cases reported. They present as well-circum- scribed, partly cystic and partly solid lesions on MRI and are often located in the tail of the parotidgland. Adenoid cystic carcinoma usually presents as an infiltrating mass with a high propensity for perineural invasion. On MRI adenoid cystic carcinoma has an irregular contour, poorly defined margins, and a strong enhancement after the administration of contrast medium .
According to the ROC curve, and comprehensive ana- lysis of AUC, sensitivity, and speci ﬁ city, it could be con- cluded that energy and energy-mean were the ideal texture parameter or joint diagnostic model to identify parotid PA and malignant epithelial tumors because of their good diagnosis ef ﬁ ciency, with the AUC of 0.887 and 0.888, respectively. The sensitivity of energy was the highest (0.970), and the speci ﬁ city of energy-correlation was the highest (0.970).The energy represents the stability of the lesion texture gray scale change and re ﬂ ects the gray scale distribution uniformity and texture thickness. The higher the energy is, the more regular and stable the current texture change becomes. In this study, the energy of par- otid epithelial malignancy was statistically higher than that of PA. This may be closely related to the histopathological characteristics of PA, such as complicated histological structure and diverse cell types, including glandular epithelium, myoepithelium, mucus, mucoid tissue, and chondroid tissue.
Two-time surgery was indicated to avoid bilateral facial nerve palsy. In May 2011, the left tumor was excised by total parotidectomy with facial nerve preservation under general anesthesia. Six months later no recurrence or facial palsy of the left side were observed. In February 2012, surgical enucleation of the right tumor was per- formed preserving the fibrous capsule integrity with no facial injury. We chose this approach in relation to the early age of our patient and the small size of the right lesion. Histopathology exam confirmed the diagnosis of pleomorphic adenoma in both specimens (Figure 4). One year after the second surgery, no recurrence was ob- served in both parotid areas and no neural dysfunction was reported.
ber 2014 and May 2015. The institutional revi- ew board at the Kyungpook National University College of Medicine, Daegu, Korea, reviewed and approved the study protocol and exempted informed consent for this study (IRB no: 2014- 09-002-001). We performed all procedures by the tenets of the World Medical Association’s Declaration of Helsinki. All patients underwent salivary gland resection for their tumor, and their clinical data was collected from medical records. The histologic type of the collected tumor sample was confirmed by a pathologist (Table 1). Histologic types of thirty-two cases were divided into three groups: 19 PAs, 8 WTs, and 5 carcinomas. The five instances of carci- noma consisted of adenosquamous carcino- ma, poorly differentiated adenocarcinoma, epi- thelial-myoepithelial carcinoma, adenoid cystic carcinoma, and salivary duct carcinoma. After curative resection, some part of the tumor was sampled for this study and underwent DNA extraction. DNA was isolated using an Absolute TM DNA Extraction kit (BioSewoom, Inc., Seoul, Korea), according to the manufacturer’s proto- col. DNA quantity and quality were measured using NanoDrop 1000 (Thermo Fisher Scientic, Inc., Pittsburgh, PA, USA).
Final pathology revealed high grade mucoepidermoid carcinoma arising from a pleomorphic adenoma. The primary tumor was resected with negative margins. Al- though only one of thirteen nodes excised was positive, the level II node was determined to be metastatic MEC. The patient was referred to radiation oncology for inten- sity-modulated radiation therapy, but decided against radiation treatment for fear of side effects despite exten- sive communication about its post-operative indications. The patient has been compliant with serial surveillance examinations and PET scans, which have remained nor- mal after two years.
CNS involvement has a significant impact on survival rates. Hollender & colleagues who studied up to 170 cases with systemic central nervous system involvement of non-Hodgkin's lymphoma reports a very poor prognosis following secondary central nervous system lymphoma, with an overall median survival of 2.6 months, and with only 12/140 patients (8.6%) being in a complete remission at the last follow-up . While Seiichi Yoshida & colleagues found the overall median survival of the 58 CNS lymphoma patients was only 13.4 months (ranging from 1 to 32 months) .
recurrence rates, which vary between 50 and 90% after conservative treatment, several authors have supported surgical resection with safety margins for the treatment of solid or multicystic ameloblastomas and have advocated bone resection in the affected area with at least 15 mm of healthy adjacent tissue beyond the radiographic borders of the lesion , as performed in both of the above mentioned cases. The second patient is currently free of recurrences and was rehabilitated with reconstruction plate fixation , as well as reported in other cases . In addition to the low radiosensitivity of this neoplasm, the intraosseous location of the ameloblastoma prevents the use of radiotherapy as an effective therapeutic option because radiation increases the potential development of secondary tumors 24 .
The well-differentiated ACC with lymphoid stro- ma has a low proliferative activity with MIB1 indices between 0.5% and 3.7% (mean, 1.7%). In contrast, the conventional ACC revealed higher proliferative activity with MIB1 indices between 3.4% and 45% (mean, 17%) . Other immunohistochemical profiles are the same as conventional ACC that are nonspecific and are rarely of diagnostic value. Although the zymo- gen granules of normal salivary glands stain consistently for anti-alpha amylase, those in ACC show very variable reactivity . It has been reported immunoreactive for cytokera- tins, transferrin, lactoferrin, alpha 1-antitrypsin, alpha 1-antichymotrypsin, IgA, carcinoembry- onic antigen, Leu M1 antigen [21-24], vasoac- tive intestinal polypeptide , cyclooxygen- ase-2 , amylase and bone morphogenic protein 6 . Some tumors are positive for estrogen and progesterone receptors , and prostate-specific antigen . Although about 10% of ACCs are positive for S-100 protein , there appears to be no evidence of basalcell or myoepithelial differentiation [30, 31]. In a recent study, cytokeratin 14 and P63, which has been used as myoepithelial marker, is detected in a wide range of salivary tumors but was not a feature of ACC [32, 33].
tion section. The submandibular and parotid glands were specifically evaluated and largest diameter was measured on transverse images. Decisions regarding the CTfeatures were deter- mined in consensus, with particular attention to the location and number of lesions, internal architecture, enhancement patterns, presence of calcification, vascular occlusion or compres- sion, and cervical lymph nodes. On post-con- trast CT images, the enhancement pattern of the lesions was categorized as either homoge- neous or heterogeneous, and specific patterns were described. Lymph nodes were considered enlarged if their maximal short-axis diameters were greater than 1 cm on axial images. The groups with different imaging features were compared. The CT characteristics of the sub- mandibular glands were also compared to the histological features.
Microscopic examination of incisional biopsy specimen showed principally basaloid cells arranged in clumps with hyperchromatic nuclei and increased nu- clear-cytoplasmic ratio. A probable diagnosis of benign monomorphic adenoma of salivary gland was made. Surgery was planned and tumor was excised along with a safe margin after ligating greater palatine vascular bundle and the defect was repaired by buccal fat pad (BFP). The excised pathology was submitted to the de- partment of Oral and Maxillofacial Pathology where the routine tissue processing was carried out. The histo- pathological examination of the excised specimen re- vealed well-encapsulated tumormass which was com- posed of monomorphic basaloid cells arranged in the form of solid nests and trabeculae pattern in the loose connective tissue stroma. The peripheral cuboidal cells
The mechanism of congenital cholesteatoma has not been clarified yet. Usually, middle ear cholesteatoma (congenital and acquired) is a progressive and destructive disease that requires surgery for complete cure. In recent years, early detection of congenital cholesteatomas has become more frequent due to advances in endoscopy and microscopy. Along with these developments, there have been reports of congenital cholesteatoma regressing spontaneously, as seen by tympanic and computed tomography findings over time. Herein, we report two cases of spontaneous regression of cholesteatoma, both with ossicular chain malformation. One cholesteatoma was close to the ossicles. In the other case, the cholesteatoma and ossicle were separated; however, the ossicular morphology was inconsistent with that of congenital ossicular malformation. Further similarities and differences between these two cases are discussed herein.
Under microscopic examination, the tumor ap- peared to be made up of eosinophilic adeno- epithelial cells, adipose tissue, sporadic lym- phocytes, and the remnants of salivary gland epithelial cells. Eosinophil and lipocytes were the main components, occupying about 40% and 50% respectively. The eosinophilic cells showed adenomatoid hyperplasia, with a flaky and nest-like distribution (Figure 4). The cells were large, square or polygonal, and were ar- ranged into luminal structure with eosinophi- lic secretions in certain areas (Figure 5). The boundary between the adipocyte components and the eosinophils was unclear, and some adi- pocytes were scattered between fibrous con- nective tissues and eosinophilic components (Figure 6), and many lymphocytes and a few Figure 1. MR showed a parotidgland mass with het-
Abstract: Objective: Recent studies revealed the existence of ectopic gene at t(6;9)(q22-23;p23-24) in adenoid cys- tic carcinoma (ACC), resulting in MYB-NFIB fusion gene formation. In this study, we discuss the expression of MYB of ACC in salivary gland and its clinicopathological significance. Methods: We examined 98 samples of salivary gland adenoid cystic carcinoma and 68 samples of salivary non-ACC neoplasms among patients at the Department of Oral Pathology, Nanjing Stomatological Hospital, Medical School of Nanjing University (China). The expression of Ki67 and MYB was analyzed by immunohistochemical analysis and followed up with survival analysis. Results: Of the 98 cases of salivary ACC, 87 (88.8%) stained positive for MYB, including 59.2% (58/98) strongly positive and 29.6% (29/98) weakly positive. Among the non-ACC neoplasms, 11.8% (8/68) cases stained weakly positive for MYB. No salivary gland tissue adjacent to ACC (0/20) or salivary gland tissue of non-neoplastic lesions (including subman- dibular gland calculus and inflammation) (0/5) was MYB positive. No significant relation was seen between MYB expression and age, gender, size, site, histological type, distant metastasis, Ki67 proliferation index and prognosis. Conclusion: Immunohistochemical analysis of MYB facilitates clinical pathological diagnosis and differential diagno- sis of ACC in salivary gland. A strong positive expression of MYB is a significant ACC-specific marker in salivary gland.
The tumors in 4 of the patients showed homogeneous en- hancement. Heterogeneous enhancement was demonstrated in the remaining 6 patients (60%), in whom a central nonen- hancing curvilinear cleft was seen in 4 (Fig 4A, -B) and a cystic component, in the other 2 (Fig 5). None of the tumors showed calcification. Cut sections of the gross specimens of the tumors showing central non-enhancing curvilinear clefts on CT re- vealed central gray-white scars, which correlated microscopi- cally with hyalinized and fibrous tissue. Cystic degeneration was noted histopathologically with respect to the 2 tumors demonstrated to have nonenhancing cystic components on CT. We concluded that these central scars and areas of cystic degeneration would most likely be responsible for the nonen- hancing curvilinear cleft and cystic component detected on CT, respectively.