Induction of epithelial-mesenchymal transition and loss of podoplanin expression are associated with progression of lymph node metastases in human papillomavirus-related oropharyngeal carcinoma.

AIMS: To examine human papillomavirus (HPV) status, the expression of podoplanin and epithelial-mesenchymal transition (EMT) markers and lymphatic vessel counts (LVC) in oropharyngeal squamous cell carcinoma (OPSCC) tissues, and to evaluate whether these factors were associated with survival and nodal status. METHODS AND RESULTS: A total of 53 OPSCC specimens were evaluated for HPV status and expression of proteins such as podoplanin and EMT markers by immunohistochemistry. E-cadherin-negative and vimentin-positive specimens were defined as EMT-positive. Twenty-two OPSCCs were HPV-positive. There was significant progression of nodal status in patients with HPV-positive tumours (P = 0.0475). HPV-positive cases had significantly lower expression of podoplanin (P = 0.0016) and were more frequently EMT-positive (P = 0.0172). Podoplanin-negative cases and EMT-positive cases showed significantly more advanced nodal status than their respective counterparts (P = 0.0082 and P = 0.0186, respectively). LVC correlated with neither HPV nor nodal status. Multivariate analyses revealed that HPV infection was an independent marker of longer disease-specific survival (P = 0.014). CONCLUSIONS: HPV-positivity in OPSCC was associated with loss of podoplanin expression and with EMT induction, which resulted in progression of nodal status. The mechanisms leading to an improved prognosis in HPV-positive OPSCC patients requires elucidation, as this is inconsistent with the aggressive phenotype with lymph node metastases.

Characteristics of hepatic fatty acid compositions in patients with nonalcoholic steatohepatitis.

BACKGROUND & AIMS: Nonalcoholic fatty liver disease (NAFLD) is closely related to insulin resistance and lipid metabolism. Recent studies have suggested that the quality of fat accumulated in the liver is associated with the development of nonalcoholic steatohepatitis (NASH). In this study, we investigated the fatty acid composition in liver tissue and its association with the pathology in NAFLD patients. METHODS: One hundred and three patients diagnosed with NAFLD [simple steatosis (SS): 63, NASH: 40] were examined and their hepatic fatty acids were measured using gas chromatography. In addition, relationships between the composition and composition ratios of various fatty acids and patient backgrounds, laboratory test values, histology of the liver, and expression of fat metabolism-related enzymes were investigated. RESULTS: The C16:1n7 content, the C16:1n7/C16:0 and C18:1n9/C18:0 ratios were increased and the C18:0/C16:0 ratio was decreased in the NASH group. The C18:0/C16:0 and C18:1n9/C18:0 ratios were associated with the steatosis score in liver tissue, and the C16:1n7/C16:0 ratio was associated with the lobular inflammation score. The expressions levels of genes: SCD1, ELOVL6, SREBP1c, FAS and PPARγ were enhanced in the NASH group. In multivariate analysis, the C18:0/C16:0 ratio was the most important factor that was correlated with the steatosis score. In contrast, the C16:1n7/C16:0 ratio was correlated with lobular inflammation. CONCLUSION: The fatty acid composition in liver tissue and expression of genes related to fatty acid metabolism were different between the SS and NASH groups, suggesting that the acceleration of fatty acid metabolism is deeply involved in pathogenesis of NASH.

Clonal profiling of mixed lobular and ductal carcinoma revealed by multiplex ligation-dependent probe amplification and fluorescence in situ hybridization.

A needle biopsy of a mass in the right breast of a 36-year-old woman revealed invasive ductal carcinoma (IDC), and approximately 20% of cancer cells showed unequivocal membranous staining with the HercepTest. After systemic therapy with trastuzumab and paclitaxel followed by FEC (fluorouracil + epirubicin + cyclophosphamide), a right mastectomy was performed. By histological and immunohistochemical examinations, the resected tumor consisted mainly of E-cadherin-negative invasive lobular carcinoma (ILC), and the rest was ERBB2-positive IDC; thus, the diagnosis was mixed ductal and lobular carcinoma. Multiplex ligation-dependent probe amplification and fluorescence in situ hybridization (FISH) analyses revealed that ILC and IDC shared high-level amplification of CCND1 in homogeneously staining regions (HSR) and that IDC had an additional HSR-type amplicon of ERBB2. These findings strongly indicate that IDC and ILC had a common precursor cell with CCND1 amplification. Review of the biopsy specimen with FISH showed IDC with gene amplifications of CCND1 and ERBB2 as a minor component, IDC without amplification of CCND1 or ERBB2 as a major component, and a minute portion of ILC with CCND1 amplification. We speculate that chemotherapy and trastuzumab caused a marked reduction in IDC; however, ILC with CCND1 amplification was resistant to chemotherapy and grew.

Diagnosis and treatment of low-grade osteosarcoma: experience with nine cases.

BACKGROUND: Low-grade osteosarcoma, including low-grade central osteosarcoma and parosteal osteosarcoma, is an extremely rare variant, and the diagnosis is occasionally difficult. In this article we present cases of low-grade osteosarcomas that should be reviewed by a clinical oncologist. PATIENTS AND METHODS: Nine cases of histologically diagnosed Broder grade 1 osteosarcoma were retrospectively reviewed. The pathological diagnoses included parosteal osteosarcoma, low-grade central osteosarcoma, and low-grade chondroblastic osteosarcoma in four, four, and one cases, respectively. RESULTS: Duration from initial surgical intervention including biopsy to final diagnosis as low-grade osteosarcoma was a mean of 9.4 months. The initial benign diagnoses on biopsy specimens included fibrous dysplasia in three cases, chondroblastoma in one case, and a giant cell tumor in one case. The average number of histological examinations was 1.8. Low-grade osteosarcomas are well suited for biological reconstruction: seven cases were reconstructed by frozen autografts, distraction osteogenesis, or vascularized bone grafts. CONCLUSION: Low-grade osteosarcomas can be misdiagnosed as benign lesions, especially fibrous dysplasia. If the diagnosis of a low-grade osteosarcoma is not established on the basis of radiologic findings, care should be exercised, even when a biopsy suggests a benign lesion. Low-grade osteosarcomas should be treated with wide excision, even after an intralesional excision. Biological reconstruction might be a better option for low-grade osteosarcomas.

Gene amplification of ESR1 in breast cancers--fact or fiction? A fluorescence in situ hybridization and multiplex ligation-dependent probe amplification study.

Oestrogen receptor-alpha (ERα), encoded by the ESR1 gene located on 6q25, is a nuclear transcription factor. Since it was reported in 2007 that more than 20% of breast cancers show ESR1 gene amplification, there has been considerable controversy about its frequency and clinical significance. We set out to assess the frequency and levels of ESR1 amplification in breast cancers. In a total of 106 breast needle biopsy specimens examined by immunohistochemistry, 78 tumours contained more than 10% ERα-positive cancer cells. In fluorescence in situ hybridization (FISH) analysis with an ESR1-specific probe, variously extended ESR1 signals were found in ERα-expressing cells. Some of these were indistinguishable from large clustered signals generally accepted to mean high-level gene amplification in homogeneously staining regions (HSRs), and could be considered to represent gene amplification. However, with RNase treatment, the 'HSR-like' signals changed to small compact signals, and are thus thought to represent concentrated RNA. FISH using two differently labelled probes corresponding to the non-overlapping 5'- and 3'-end portions of the ESR1 gene on touch smears showed a preserved spatial relationship of the 3' to 5' sequence of ESR1, therefore strongly suggesting that the RNA consisted of primary transcripts. Using touch smears obtained from 51 fresh tumours, precise enumeration of ESR1 signals with a correction by the number of centromere 6 on FISH after RNase A treatment revealed that three tumours (5.9%) had tumour cells with one to three additional copies of ESR1 as predominant subpopulations. This infrequent and low level of gene amplification of ESR1 was also detected as a 'gain' of the gene by analysis with multiplex ligation-dependent probe amplification (MLPA). The consistent results from immunohistochemistry, FISH, and MLPA in the present study settle the long-standing debate concerning gene amplification of ESR1 in breast carcinoma.

A serum amyloid A-positive hepatocellular neoplasm arising in alcoholic cirrhosis: a previously unrecognized type of inflammatory hepatocellular tumor.

Hepatocellular adenoma usually arises in the absence of significant fibrosis. Herein, we report seven patients with serum amyloid A-positive hepatocellular neoplasm, which shares features with inflammatory hepatocellular adenoma arising in alcoholic cirrhosis. Seven patients (two women and five men, age range 41-67 years) with hypervascular hepatocellular nodules associated with alcoholic cirrhosis were retrieved from our pathological files (1997-2011). The hepatocellular nodules were multiple (>3) in all patients and 17 nodules were histologically examined. We surveyed the immunoreactivity for serum amyloid A, glutamine synthetase, and glypican-3 in the hepatocellular nodules and control lesions, including 5 focal nodular hyperplasia, 18 dysplastic nodules, and 54 hepatocellular carcinomas in various background diseases. In all, 15 of 17 nodules showed strong and distinct immunoreactivity for serum amyloid A, sharing features with inflammatory hepatocellular adenoma. The serum amyloid A-positive hepatocellular neoplasms showed increased cellular density, inflammatory infiltrate, sinusoidal dilatation, and ductular reaction to various degrees. Although about a half of dysplastic nodules and hepatocellular carcinomas showed focal immunoreactivity for serum amyloid A, the extent of serum amyloid A expression was significantly higher in serum amyloid A-positive hepatocellular neoplasms, than in control nodules. The serum amyloid A-positive hepatocellular neoplasms did not show the overexpression of glutamine synthetase or immunoreactivity for glypican-3. In contrast, most hepatocellular carcinomas showed the overexpression of glutamine synthetase and immunoreactivity for glypican-3, irrespective of background diseases. In conclusion, this study highlights a characteristic group of hepatocellular neoplasms arising in alcoholic cirrhosis, which share features with inflammatory hepatocellular adenomas. These serum amyloid A-positive hepatocellular neoplasms may be a new type of inflammatory hepatocellular tumors in alcoholic patients.

Lymphangiogenesis in regional lymph nodes predicts nodal recurrence in pathological N0 squamous cell carcinoma of the tongue.

AIMS: Cancer cells induce de-novo lymphatic vessel growth within draining lymph nodes before they metastasize. The aim of this study was to retrospectively evaluate lymph node lymphangiogenesis before the establishment of nodal recurrence in squamous cell carcinoma (SCC) of the tongue. METHODS AND RESULTS: Surgical specimens from 28 patients with pT2-T3N0M0 SCC of the tongue after local excision with supraomohyoid neck dissection were studied by immunohistochemistry. Intranodal lymphatic endothelium was highlighted by podoplanin staining to evaluate lymphatic vessel counts (LVCs). Primary tumour sections were examined for the expression of lymphangiogenic factors: vascular endothelial growth factor (VEGF)-C and VEGF-D. LVCs in regional lymph nodes were significantly increased in the cases with nodal recurrence (P=0.0013). Simultaneous increases in VEGF-C and VEGF-D expression were significantly associated with both an increase in LVC in regional lymph nodes (P=0.0001) and a decrease in the rate of survival without nodal recurrence (P=0.016). CONCLUSIONS: Knowing the status of lymphangiogenesis in the regional pN0 lymph nodes in tongue cancer would help in predicting which patients will develop nodal recurrence. The use of a therapeutic approach which blocks lymphangiogenic factors, such as VEGF-C and VEGF-D, may be beneficial in suppressing the lymphatic spread of tongue cancer with intense intranodal lymphangiogenesis.

Duodenal adenocarcinoma with neuroendocrine features in a patient with acromegaly and thyroid papillary adenocarcinoma: a unique combination of endocrine neoplasia.

A 67-year-old woman with familial clustering of thyroid papillary adenocarcinoma was diagnosed with acromegaly due to pituitary macroadenoma. She had multiple skin vegetations, but had no parathyroid and pancreas diseases. Before transsphenoidal surgery, she was further diagnosed as having a duodenal tumor and multiple hypervascular liver nodules. Biopsy specimens from the duodenal tumor and liver nodules were diagnosed histologically as moderately differentiated adenocarcinoma. Immunohistochemically, the tumor cells were positive for chromogranin, synaptophysin and somatostatin receptor 2a, suggestive for neuroendocrine features. After surgery, the patient was not in biochemical remission, and octreotide treatment was initiated. The duodenal cancer was treated with chemotherapy (neoadjuvant cisplatin and S-1). After 24 months, the patient's insulin-like growth factor I level had been normalized, and her liver tumors had not progressed macroscopically. This is a rare case of acromegaly associated with multiple endocrine tumors, not being categorized as conventional multiple endocrine neoplasia. Octreotide treatment might have had beneficial effects on our patient's duodenal adenocarcinoma and liver metastases, both directly via SSTR2a and indirectly via GH suppression, thereby contributing to their slow progression.

[Clinical evaluation of a novel multiplex HPV genotyping reagent using the luminex xMAP technology].

Of the more than 100 strains of human papillomavirus (HPV) reported to date, 13 strains are clinically significant due to the highly associated risk of cervical cancer. HPV test reagents are currently being developed to aid detection of these strains. The present study compared a novel HPV genotyping reagent using a Luminex device, which enables simultaneous quantitation of multiple targets using fluorescent beads, and gene-specific multiplex polymerase chain reaction (Luminex method) with approved in vitro diagnostics. Subjects comprised 256 patients examined at our hospital for either secondary cervical cancer testing or follow-up (mean age, 40 years; age range, 20-85 years) and specimens were obtained using a cervical brush and lavage fluid. The HPV-positive rate with the Luminex method was 51.4%(132/256), of which single and multiple strain infections constituted 65.9% (87/132) and 34.1% (45/132), respectively. Correlation testing of 50 positive and 50 negative Luminex method specimens was conducted using the HPV DNA Hybrid Capture II (HCII), revealing high overall (97%[97/100]), positive(100% [47/47]) and negative(94.3% [50/53]) concordance rates. Correlation was also high for the Clinichip HPV (Clinichip), with overall, positive and negative concordance rates of 98% (98/100), 100%(48/48) and 96.2%(50/52), respectively. Furthermore, the detection concordance rate with the Clinichip was 95.8% (46/48). Sequencing of the seven specimens showing result discrepancies (HCII, n = 3; Clinichip, n = 4) confirmed concordance with the Luminex method results in all cases, indicating the validity of the present method. The present findings suggest that the Luminex method has sufficient response capability for clinical application.

Epidermal growth factor induces cytokeratin 19 expression accompanied by increased growth abilities in human hepatocellular carcinoma.

Cytokeratin (CK) 19-positive hepatocellular carcinoma (HCC) has been reported to have a poor prognosis. The mechanism of the development of CK19-positive HCC remains to be studied. To clarify this, in vitro experiments were performed using human HCC cell lines (PLC-5, HepG2), and the phenotypic changes after stimulation with several growth factors were examined using quantitative reverse transcriptase PCR, western blotting, and immunofluorescence staining. In vivo experiments using human HCC specimens obtained from a total of 78 patients and clinicopathological analysis were also performed. Among the growth factors tested, epidermal growth factor (EGF) had prominent effects on inducing CK19 expression in PLC-5 and HepG2, which was accompanied by the reduced expression of α-fetoprotein in PLC-5. The induction of CK19 expression after EGF stimulation was accompanied by the phosphorylation of c-Jun-N-terminal kinase (JNK)/stress-activated protein kinase, which was blocked by the addition of JNK inhibitors. EGF also increased proliferative abilities and invasive properties of the HCC cell lines. In vivo, 9 (12%) of 78 HCC cases showed positive immunohistochemical staining of CK19. The extent of positive immunohistochemical signals of EGF, EGF receptor (EGFR), and JNK expression was significantly intense in CK-19-positive HCC than those of CK19-negative HCC. Clinicopathological analysis showed that CK19-positive HCC had a high incidence of portal vein invasion, extrahepatic metastasis and an early relapse, which was associated with the worsened 2-year disease free survival. These results indicate that the activation of the EGF-EGFR signaling pathway is associated with the development of CK19-positive HCC, and the EGF-induced increase in growth abilities of HCC may account for the poor prognosis of the patients.

Chondroblastoma with pulmonary metastasis in a patient presenting with spontaneous bilateral pneumothorax: Report of a case.

Chondroblastoma is a benign bone tumor with a relatively high incidence in older children and adolescents. Although it is generally regarded as a benign neoplasm, it sometimes grows aggressively or recurs but rarely metastasizes to the lung. We herein present a very rare case of a bilateral pneumothorax due to a pulmonary metastasis from a chondroblastoma. A 21-year-old man developed a bilateral pneumothorax 20 months after an operation for a chondroblastoma of the right ischium. A pertinent literature review revealed similar cases of chondroblastoma with pulmonary metastasis, but revealed no reports of a pneumothorax caused by a metastatic chondroblastoma.

Endothelial to mesenchymal transition via transforming growth factor-beta1/Smad activation is associated with portal venous stenosis in idiopathic portal hypertension.

Idiopathic portal hypertension (IPH) represents noncirrhotic portal hypertension of unknown etiology, mainly due to stenosis of peripheral portal veins. This study was performed to clarify the mechanism of portal venous stenosis in IPH from the viewpoint of the contribution of the endothelial to mesenchymal transition of the portal vein endothelium via transforming growth factor-beta1 (TGF-beta1)/Smad activation. In vitro experiments using human dermal microvascular endothelial cells demonstrated that TGF-beta1 induced myofibroblastic features in human dermal microvascular endothelial cells, including spindle cell morphology, reduction of CD34 expression, and induction of S100A4, alpha-smooth muscle actin, and COL1A1 expression, as well as the increased nuclear expression of phospho-Smad2. Bone morphogenic protein-7 preserved the endothelial phenotype of human dermal microvascular endothelial cells. Immunohistochemical analysis showed that endothelial cells of the peripheral portal veins in IPH were characterized by the decreased expression of CD34 and the enhanced nuclear expression of phospho-Smad2; these results also confirmed the expression of S100A4 and COL1A1 in the portal vein endothelium. Serum TGF-beta1 levels in patients with IPH were significantly higher than those of healthy volunteers and patients with chronic viral hepatitis/liver cirrhosis, while an elevation of serum bone morphogenic protein-7 levels was not observed. These results suggest that the endothelial to mesenchymal transition of the portal venous endothelium via TGF-beta1/Smad activation is associated with portal venous stenosis in IPH, and bone morphogenic protein-7 may therefore be a suitable therapeutic candidate for IPH.

A case of neurosarcoidosis with necrotizing granuloma expressing angiotensin-converting enzyme.

We described a case of neurosarcoidosis with necrotizing sarcoid granulomatosis in a 22-year-old man. Contrast-enhanced brain computed tomography scan and magnetic resonance imaging showed intracerebral multiple nodular lesions. Noncaseating and partial necrotizing granulomas were detected in the specimen resected by neurosurgery. In addition, immunohistochemical examination revealed the expression of angiotensin-converting enzyme in necrotizing granuloma. Thus, these findings were consistent with neurosarcoidosis. Clinical and pathological presentation, immunological features, and treatment modalities of neurosarcoidosis are discussed.

[Combined chemotherapy with cisplatin plus vinorelbine showed efficacy in a case of metastatic primary cutaneous adenoid cystic carcinoma].

We report a case of a 65-year-old man with metastatic primary cutaneous adenoid cystic carcinoma that was effectively treated by combination chemotherapy with cisplatin (CDDP) plus vinorelbine(VNR). He detected a tumor mass on the anterior surface of his left patella in 2003 and underwent a tumorectomy in October 2008. He was given a diagnosis of primary cutaneous adenoid cystic carcinoma with metastatic lesions to multiple lungs and left tibial bone and then given chemotherapy combining CDDP plus VNR as the first treatment in December 2008. By this treatment for six cycles, the lung metastatic tumors gradually reduced on chest CT. We reported the efficacy of combined treatment with CDDP plus VNR for primary cutaneous adenoid cystic carcinoma, because this clinical condition was very rare and the standard treatment has still not been established.

Temporary spontaneous regression of male breast cancer: a case report.

BACKGROUND: Spontaneous regression (SR) of a malignant tumor is the partial or complete disappearance of primary or metastatic tumor tissue in the absence of treatment, which can be temporary or permanent. Here, we report an extremely rare case of male breast cancer that exhibited temporary SR followed by reappearance 8 months after tumor disappearance. CASE PRESENTATION: A 70-year-old man presented at our hospital with a primary complaint of pain and a lump in his left breast. Ultrasonography revealed a hypoechoic lesion measuring 12 mm × 10 mm × 8 mm. Fine-needle aspiration cytology revealed numerous necrotic and degenerated cells and few sheet-like clusters of atypical ductal epithelial cells. The atypical cells had mildly enlarged nuclei with nucleoli, were focally overlapped and formed tubular patterns. The cytological diagnosis indicated a suspicion of malignancy. Core needle biopsy (CNB) revealed necrotic and degenerated cells with microcalcification. The pathological diagnosis was indeterminate because there was no area of viable atypical cells. An excisional biopsy of the left breast lesion was scheduled one month later. However, it was difficult to detect the tumor during physical examination and ultrasonography performed 1 month after the patient's first visit. The operation was canceled, and the patient received follow-up observation. After 8 months of follow-up, ultrasonography and computed tomography (CT) revealed reappearance of a 0.6-cm-diameter breast tumor in the same place. CNB was performed again and revealed invasive ductal carcinoma. A total mastectomy with sentinel lymph node biopsy was performed 13 months after the first tumor disappeared. Histopathological examination revealed invasive cribriform carcinoma without sentinel lymph node metastasis. The patient did not have any complications, and adjuvant therapy with tamoxifen was started. The patient was alive without recurrence 7 months after surgery. CONCLUSIONS: Temporary SR followed by tumor reappearance can occur in breast cancer cases, and it is important to follow patients even if their breast tumor has seemingly disappeared. When breast tumors disappear without treatment, clinicians must be aware of the possibility of SR of cancer and should follow the patient for early detection of tumor reappearance.

Thiamine-responsive pyruvate dehydrogenase deficiency in two patients caused by a point mutation (F205L and L216F) within the thiamine pyrophosphate binding region.

The human pyruvate dehydrogenase complex (PDHC) catalyzes the thiamine-dependent decarboxylation of pyruvate. Thiamine treatment is very effective for some patients with PDHC deficiency. Among these patients, five mutations of the pyruvate dehydrogenase (E1)alpha subunit have been reported previously: H44R, R88S, G89S, R263G, and V389fs. All five mutations are in a region outside the thiamine pyrophosphate (TPP)-binding region of the E1alpha subunit. We report the biochemical and molecular analysis of two patients with clinically thiamine-responsive lactic acidemia. The PDHC activity was assayed using two different concentrations of TPP. These two patients displayed very low PDHC activity in the presence of a low (1 x 10(-4) mM) TPP concentration, but their PDHC activity significantly increased at a high (0.4 mM) TPP concentration. Therefore, the PDHC deficiency in these two patients was due to a decreased affinity of PDHC for TPP. Treatment of both patients with thiamine resulted in a reduction in the serum lactate concentration and clinical improvement, suggesting that these two patients have a thiamine-responsive PDHC deficiency. The DNA sequence of these two male patients' X-linked E1alpha subunit revealed a point mutation (F205L and L216F) within the TPP-binding region in exon 7.

Ghrelin concentration in cord and neonatal blood: relation to fetal growth and energy balance.

To investigate the relationship between ghrelin and both fetal and neonatal growth parameters and energy balance, we measured plasma ghrelin concentrations in 54 cord blood samples (male, n = 34; female, n = 20; gestational age, 37.0-41.6 wk; birth weight, 2206-4326 g) and 47 neonatal blood samples (male, n = 27; female, n = 20; postnatal d 3-8). The plasma ghrelin concentrations in cord blood ranged from 110.6-446.1 pmol/liter (median, 206.7 pmol/liter), which were equal to or higher than those in normal weight adults. These values were inversely correlated with birth weight (r = -0.40; P = 0.002), birth length (r = -0.36; P = 0.007), placental weight (r = -0.35; P = 0.01), and IGF-I concentration (r = -0.49; P = 0.0002), but were not significantly correlated with the GH concentration (r = 0.22; P = 0.12). The ghrelin concentrations in small for gestational age newborn were significantly higher than those in appropriate for gestational age newborns (P = 0.0008). The ghrelin concentrations in the vein were significantly higher than those in the artery in 8 cord blood samples (P = 0.01), which suggests that the placenta is an important source of fetal ghrelin. In neonates, the ghrelin concentrations ranged from 133.0-481.7 pmol/liter (median, 268.3 pmol/liter), which were significantly higher than those in cord blood (P < 0.0001). These results suggest that ghrelin may contribute to fetal and neonatal growth.

Magnetic resonance imaging features of breast cancer according to intrinsic subtypes: correlations with neoadjuvant chemotherapy effects.

PURPOSE: The purpose of this study was to evaluate the magnetic resonance imaging (MRI) features of breast cancer according to intrinsic subtypes and to investigate whether the MRI and immunohistochemical findings were related to neoadjuvant chemotherapy (NAC) effects. MATERIALS AND METHODS: The MRI in 116 women with breast cancers who underwent NAC was reviewed. The mass margin, presence of intratumoral necrosis, tumor extension around the mass, relative signal enhancement (RSE), and kinetic curve pattern were analyzed. We investigated the possible correlations between MRI findings and the effects of NAC. RESULTS: An irregular mass margin was significantly associated with luminal-A cancers, while a smooth mass margin was associated with human epidermal growth factor receptor2 (HER2) cancers. Intratumoral necrosis was significantly associated with triple-negative cancers. Tumor extension around the mass was significantly infrequent in luminal-B cancers and frequent in HER2 cancers. Luminal-B and HER2 cancers showed a significantly higher RSE at 2 min than Luminal-A cancers. Estrogen receptor (ER)-positive cancers, HER2-negative cancers, and presence of intratumoral necrosis were significantly associated with the NAC non-response. CONCLUSIONS: Several MR features can be used to predict the intrinsic subtype of breast cancers. ER-positivity, HER2-negativity, and presence of intratumoral necrosis were significantly associated with NAC non-response.