Metalloestrogens exposure and risk of gestational diabetes mellitus: Evidence emerging from the systematic review and meta-analysis.

BACKGROUND: Metalloestrogens are metals and metalloid elements with estrogenic activity found everywhere. Their impact on human health is becoming more apparent as human activities increase. OBJECTIVE: Our aim is to conduct a comprehensive systematic review and meta-analysis of observational studies exploring the correlation between metalloestrogens (specifically As, Sb, Cr, Cd, Cu, Se, Hg) and Gestational Diabetes Mellitus (GDM). METHODS: PubMed, Web of Science, and Embase were searched to examine the link between metalloestrogens (As, Sb, Cr, Cd, Cu, Se, and Hg) and GDM until December 2023. Risk estimates were derived using random effects models. Subgroup analyses were conducted based on study countries, exposure sample, exposure assessment method, and detection methods. Sensitivity analyses and adjustments for publication bias were carried out to assess the strength of the findings. RESULTS: Out of the 389 articles identified initially, 350 met our criteria and 33 were included in the meta-analysis, involving 141,175 subjects (9450 cases, 131,725 controls). Arsenic, antimony, and copper exposure exhibited a potential increase in GDM risk to some extent (As: OR = 1.28, 95 % CI [1.08, 1.52]; Sb: OR = 1.73, 95 % CI [1.13, 2.65]; Cu: OR = 1.29, 95 % CI [1.02, 1.63]), although there is a high degree of heterogeneity (As: Q = 52.93, p < 0.05, I2 = 64.1 %; Sb: Q = 31.40, p < 0.05, I2 = 80.9 %; Cu: Q = 21.14, p < 0.05, I2 = 71.6 %). Conversely, selenium, cadmium, chromium, and mercury exposure did not exhibit any association with the risk of GDM in our study. DISCUSSION: Our research indicates that the existence of harmful metalloestrogens in the surroundings has a notable effect on the likelihood of GDM. Hence, we stress the significance of environmental elements in the development of GDM and the pressing need for relevant policies and measures.

Maternal Di-(2-ethylhexyl)-Phthalate exposure during pregnancy altered energy metabolism in immature offspring and caused hyperglycemia.

Di-(2-ethylhexyl)-phthalate (DEHP), as distinctive endocrine disrupting chemicals, has become a global environmental pollutant harmful to human and animal health. However, the impacts on offspring and mothers with maternal DEHP exposure are largely unknown and the mechanism remains elusive. We established DEHP-exposed maternal mice to investigate the impacts on mother and offspring and illustrate the mechanism from multiple perspectives. Pregnant mice were administered with different doses of DEHP, respectively. Metagenomic sequencing used fecal and transcriptome sequencing using placentas and livers from offspring have been performed, respectively. The results of the histopathology perspective demonstrated that DEHP exposure could disrupt the function of islets impact placentas and fetus development for maternal mice, and cause the disorder of glucose and lipid metabolism for immature offspring mice, resulting in hyperglycemia. The results of the metagenome of gut microbial communities indicated that the dysbiosis of gut microbiota in mother and offspring mice and the dominant phyla transformed through vertical transmission. Transcriptome analysis found DEHP exposure induced mutations of Ahcy and Gstp3, which can damage liver cells and affect the metabolism of the host. DEHP exposure harms pregnant mice and offspring by affecting gene expression and altering metabolism. Our results suggested that exposure of pregnant mice to DEHP during pregnancy and lactation increased the risk of metabolic disorders by altering key genes in liver and gut microbiota, and these results provided new insights into the potential long-term harms of DEHP.

Perianal Paget disease associated with non-invasive colorectal adenoma.

Perianal skin Paget disease (PPD) is an unusual subtype of extramammary Paget disease, which is usually caused by a primary intraepithelial adnexal tumor and secondary spread from colorectal adenocarcinoma. The reports of secondary PPD associated with non-invasive colorectal adenoma are rare. We report a rare case of non-invasive colorectal-adenoma-associated PPD. In this case, the intraepithelial Paget cells of perianal skin manifested with colorectal phenotype by immunohistochemistry, and adjacent adenomas had high-grade intraepithelial neoplasia but not invasion. Although this is a rare manifestation of PPD, understanding this phenomenon is important to prevent overdiagnosis and invasive overtreatment. Clinical management is variable and, therefore, close follow-up examination is necessary.

[Role of R-Spondin1 in the activation of hepatic stellate cells].

OBJECTIVE: To investigate the role of R-Spondinl in the activation of hepatic stellate cells (HSCs). METHODS: Twenty-four healthy male Kunming mice were randomly divided into the following two groups:fibrosis model group (n=16) and control group (n=8). Hepatic fibrosis was induced by subcutaneous injections of CC14 (20% in olive oil) at a dose of 5 ml/kg twice per week. After 10 weeks, the animals were sacrificed by CO(2) over-exposure and liver tissues were harvested.The protein and mRNA levels of R-Spondin1, alphat-SMA,and collagen I were examined by Western blot assay and real-time PCR respectively. Additionally,HSCs were isolated from the mice liver tissues to examine the time-series expression changes of R-Spondinl, alpha-SMA, and nuclear beta-catenin.TCF activity was analyzed by luciferase reporter assay.Moreover,HSCs were cocultured with recombinant R-Spondin1 and DKK1 to evaluate dose-response. RESULTS: R-Spondinl expression was significantly higher in the fibrosis model group than in the control group (protein level:3.16 ± 0.18 vs. 0.99 ± 0.16, t =13.31, P < 0.01; mRNA level:4.36 ± 0.26 vs. 0.98 ± 0.12, t =21.46, P < 0.01).The culture-activated mouse HSCs showed up-regulated TCF activity (5.33 ± 0.34 vs. non-activated: 1.03 ± 0.09, t =20.93, P < 0.01), nuclear beta-catenin expression (4.47 ± 0.21 vs. 0.97 ± 0.14, t =25.25, P < 0.01), and R-Spondin1 expression (protein level: 4.54 ± 0.18 vs. 1.04 ± 0.12, t =31.17, P < 0.01; mRNA level:5.13 ± 0.15 vs. 1.01 ± 0.16, t=38.06, P < 0.01). Exogenous stimulation of freshly isolated mouse HSCs with recombinant R-Spondin1 induced a dose-dependent increase in both TCF activity and the expression of nuclear beta-catenin and alphat-SMA. DKK1 down-regulated activities of factors in the WNT signaling pathway and repressed activation of HSCs. Conclusion R-Spondin1 may promote HSC activation by enhancing the canonical WNT signaling pathway.

R-spondin2 activates hepatic stellate cells and promotes liver fibrosis.

BACKGROUND: The development of liver fibrosis is the fundamental stage toward a number of mortal complications of liver diseases, including cirrhosis and hepatocellular carcinoma. Canonical Wnt pathway is crucial in diverse biological processes and mediates the progression and regression of liver fibrosis. As a potent Wnt pathway agonist, the role of roof plate-specific spondin-2 (R-Spondin2) in the hepatic fibrosis has not been well elucidated. AIMS: The purpose of this study was to investigate whether R-Spondin2 contributes to hepatic stellate cells (HSCs) activation, the key event in liver fibrogenesis. METHODS: Human liver tissues, hepatic fibrosis mouse model, and freshly isolated mice HSCs were used. Protein expression and transcriptional level were analyzed by Western-blot assays and real-time PCR, respectively. Exogenous stimulation with recombinant R-Spondin2 and knockdown of R-Spondin2 were performed to investigate functionality. Nuclear ß-catenin level and T cell-specific transcription factors activity were analyzed, and HSC proliferation was tested by MTT assay. RESULTS: Overexpression of R-Spondin2 was observed in both human fibrotic liver tissues and hepatic fibrosis mouse model. Exogenous stimulation with R-Spondin2 in the freshly isolated mice HSCs induced a dose-dependent increase in Wnt pathway activities, HSC proliferation, and the expression of α-smooth muscle actin (α-SMA) and Collagen I. Additionally, Wnt pathway activities, HSC proliferation, and the expressions of α-SMA and Collagen I decreased in the R-Spondin2 knockdown HSCs. CONCLUSIONS: These findings suggest that R-Spondin2 may promote HSC activation by enhancing the canonical Wnt pathway.

Formaldehyde biodegradation by immobilized Methylobacterium sp. XJLW cells in a three-phase fluidized bed reactor.

In the present study, the ability of a newly isolated strain, Methylobacterium sp. XJLW to degrade formaldehyde was investigated in shake flasks and in a bioreactor. The resting cells of Methylobacterium sp. XJLW showed high formaldehyde tolerance (60 g L(-1)) and high degradation rate (1,687.5 mg L(-1) h(-1)) in shake flasks. This biodegradation was initiated by a dismutation reaction since formic acid was formed and caused significant dropping of pH in the media. The addition of CaCO(3) to the media was found as an effective strategy to control the pH and keep the cells in high degradation bioactivity. A three-phase fluidized bed reactor (TPFBR) was designed to test the formaldehyde-biodegrading ability of immobilized Methylobacterium sp. XJLW. Using a repeated-batch degradation mode, the immobilized cells were able to degrade 5 g L(-1) formaldehyde (with a maximal degradation rate of 464.5 mg L(-1) h(-1) under the optimum conditions) and showed stable bioactivity after 20 batches of reuse in the TPFBR.

[Expression and significance of c-Jun activation domain binding protein 1 in human colorectal carcinoma].

OBJECTIVE: To explore the association of Jab1 (c-Jun activation domain binding protein 1) expression during carcinogenesis and clinicopathological characteristics of colorectal carcinoma (CRC) . METHODS: Tissue specimens were obtained from 80 cases of CRC from January 2007 to December 2008. And the expression of Jab1 protein for each specimen was detected by immunohistochemistry (EnVision). Six representative paired samples of cancerous and paired adjacent normal tissues were collected for Western blot. The relationships between the expression level of Jab1 protein and the clinicopathological characteristics of primary CRC were retrospectively analyzed. RESULTS: A high-level expression of Jab1 was present in cancerous tissues but not in paired adjacent normal tissues. The positive expression rate of Jab1 protein was as high as 96.3% (77/80) . And its high expression rate was 82.5% (66/80) , low expression rate 17.5% (14/80) and 8.8% (7/80) in cancerous and paired adjacent normal tissues respectively (P < 0.05) . Its expression was correlated with differentiation, invasion depth, TNM stage and lymph node metastasis (all P < 0.05) . Jab1 was significantly correlated with Ki-67 (r = 0.548, P < 0.01) and inversely with p27(kip1) (r = -0.461, P < 0.01). CONCLUSIONS: An over-expression of Jab1 protein might play an important role in the pathogenesis of CRC. Thus it may become a novel diagnostic marker and a therapeutic target in patients with CRC.

Influence of gut microbiome on metabolic diseases: a new perspective based on microgravity.

Purpose: Microgravity, characterized by gravity levels of 10-3-10-6g, has been found to significantly impair various physiological systems in astronauts, including cardiovascular function, bone density, and metabolism. With the recent surge in human spaceflight, understanding the impact of microgravity on biological health has become paramount. Methods: A comprehensive literature search was performed using the PubMed database to identify relevant publications pertaining to the interplay between gut microbiome, microgravity, space environment, and metabolic diseases. Results: This comprehensive review primarily focuses on the progress made in investigating the gut microbiome and its association with metabolic diseases under microgravity conditions. Microgravity induces notable alterations in the composition, diversity, and functionality of the gut microbiome. These changes hold direct implications for metabolic disorders such as cardiovascular disease (CVD), bone metabolism disorders, energy metabolism dysregulation, liver dysfunction, and complications during pregnancy. Conclusion: This novel perspective is crucial for preparing for deep space exploration and interstellar migration, where understanding the complex interplay between the gut microbiome and metabolic health becomes indispensable.

Primary adrenal anastomosing haemangioma.

Not required for Clinical Vignette.

Sclerosing extramedullary hematopoietic tumor of the colon: A case report and literature review.

Sclerosing extramedullary hematopoietic tumor (SEMHT) is a rare tumor that can occur in association with some chronic myeloproliferative neoplasms, particularly myelofibrosis. The morphology of SEMHT can mimic that of a wide variety of other lesions, both macroscopically and microscopically. SEMHT originating from the colon is extremely rare. The present study reports a case of SEMHT in the colon with involvement of the peri-intestinal lymph nodes. On the basis of the clinical symptoms and endoscopic results, a malignant tumor of colon was suspected. Pathological examination revealed the deposition of collagen and hematopoietic components in the fibrous mucus background. Immunohistochemical staining for CD61 confirmed the presence of atypical megakaryocytes, while immunohistochemical staining for myeloperoxidase and glycophorin A highlighted the existence of granulocyte and erythrocyte precursors, respectively. These findings combined with a clinical history of myelofibrosis led to the final diagnosis of SEMHT. The presence of atypical megakaryocytes with immature hematopoietic cell morphology and a good understanding of the clinical history of the patient are essential to prevent misdiagnosis. The present case emphasizes the necessity of reviewing previous hematological history and considering clinical findings together with the associated pathological results.

Mediastinal cavernous angioleiomyoma: A case report and review of literature.

Angioleiomyoma is a type of pericyte tumor with a benign biological behavior. It typically features proliferation of mature perivascular smooth muscle cells around blood vessels. Angioleiomyoma may be categorized into solid, cavernous or venous subtypes. Usually, it occurs in the dermis or subcutaneous tissue, while the rare cavernous subtype is most common in the upper extremities. Only a small number of cases of angioleiomyoma located in the mediastinum have been reported to date. In addition, there are few reports of mediastinal angioleiomyoma described as a cavernous histopathological subtype. The present study reported a case of mediastinal angioleiomyoma presenting as an unusual cavernous histopathological subtype. The histopathological and immunohistochemical features, based on which a diagnosis of cavernous angioleiomyoma was confirmed, were desmin- and smooth muscle actin-positive expression in spindle tumor cells, as well as ETS-related gene (ERG)- and CD31-positive expression in vascular endothelial cells. Cavernous angioleiomyoma of the mediastinum rarely occurs in the clinical setting but should be considered as a differential diagnosis of mediastinal tumors.

Axillary Lymph Node Dissection Can Be Omitted in Breast Cancer Patients With Mastectomy and False-Negative Frozen Section in Sentinel Lymph Node Biopsy.

Background: The IBCSG 23-01 and AMAROS trials both reported that axillary lymph node dissection (ALND) did not change survival rates in breast cancer patients with positive nodes detected by sentinel lymph node biopsy (SLNB). The aim of this study was to determine whether breast cancer patients with mastectomy and false-negative frozen section (FS) in SLNB could forgo ALND. Materials and Methods: This was a retrospective study of cN0 patients diagnosed with primary invasive breast cancer treated by mastectomy and SLNB at our institute between January 2010 and December 2014. Patients with false-negative FS in SLNB were separated by the following management of axillary lymph node dissection in the non-ALND group (nonprocess or axillary radiation only) and ALND group (with or without radiation). Results: A total of 212 patients were included, 86 and 126 patients in the non-ALND and ALND groups, respectively. The positive rate of non-sentinel lymph nodes (SLNs) was 15.87% (20/126) in the ALND group. In multivariate analysis, we found that patients with larger tumor size (>2 cm) (OR, 1.989; p = 0.030) and multifocal lesions (OR, 3.542; p = 0.029) tended to receive ALND. The positivity of non-SLNs in the ALND group was associated with SLN macrometastasis (OR, 3.551; p = 0.043) and lymphovascular invasion (OR, 6.158; p = 0.003). Also, removing more SLNs (≥3) was related to negativity in non-SLNs (OR, 0.255; p = 0.016). After a median follow-up of 59.43 months, RFS and OS of the two groups were similar (p = 0.994 and 0.441). In subgroup analysis, we found that 97 patients who met the inclusive criteria of the IBCSG 23-01 trial had similar RFS and OS between the non-ALND and ALND groups (p = 0.856 and 0.298). The positive rate of non-SLNs was 9.62% (5/52). Also, in 174 patients who met the criteria of the AMAROS trial, RFS and OS in the non-ALND and ALND groups were similar (p = 0.930 and 0.616). The positive rate of non-SLNs was 18.27% (19/104). Conclusion: ALND can be carefully omitted in selected breast cancer patients with mastectomy and false-negative FS in SLNB. SLNB is relatively sufficient in the IBCSG 23-01-eligible patients, and axillary radiation was an effective option in the AMAROS-eligible patients.

[Establishment and characterization of serial subpopulations with highly metastatic potential via different metastatic routes].

OBJECTIVE: To establish the serial cell lines, derived from the same parental gallbladder cancer cell line GBC-SD, with highly metastatic potential via different routes and characterize their biological behaviors to understand the different metastasis mechanisms via lymph and blood. METHODS: The spleen-liver metastasis model and footpad-inguinal lymph node metastasis model were established. GBC-SD was injected into spleen or footpad of nude mice. Then the highly metastasized subpopulations via lymph and blood were isolated. Their differences in morphology, genetic background, proliferation, migration, invasion and adhesion were revealed by comparing the lymphatic-disseminating and hematogenous-disseminating subpopulations with parental cells. RESULTS: The lymphatic-disseminating and hematogenous-disseminating subpopulations were successfully isolated and designated as GBC-SD/HL and GBC-SD/M3 respectively. They demonstrated the identical genetic background with GBC-SD. In comparison with parental cells, the hematogenous-disseminating subpopulation was morphologically characterized with epithelial-mesenchymal transition (EMT) while it was not shown in the lymphatic-disseminating subpopulation. Furthermore, the hematogenous-disseminating subpopulation showed the strongest migrating capacity but the lymphatic-disseminating subpopulation demonstrated a stronger invasive and adhesive ability. CONCLUSION: The whole parental cell GBC-SD, hematogenous-metastasized subpopulation GBC-SD/M3 and lymphatic-disseminating subpopulation GBC-SD/HL is an ideal tool for metastatic mechanism study of gallbladder cancer. EMT plays an important role in hematogenous metastasis while lymphatic metastasis relies more on enhanced invasiveness and adhesion. It may be a target for interfering the lymphatic metastasis of gallbladder cancer.

High expression of USP18 is associated with the growth of colorectal carcinoma.

AIM: To investigate whether USP18 can be used as a predictive marker for the diagnosis and development of colorectal cancer. METHODS: The Gene Expression Omnibus (GEO) Dataset and the Cancer Genome Atlas (TCGA) database were used to select differential proteins for the ubiquitin-specific peptidases (USPs). The extensive target prediction and network analysis methods were used to assess the association with the USP18 interacting proteins, as well as the statistical correlation between USP18 and the clinical pathology parameters. The effects of USP18 on the proliferation of colorectal cancer were examined using CCK8. The effects of USP18 on the migration of colorectal cancer were examined using wound healing assays. Immunohistochemistry (IHC) was performed on the tissue microarray. RESULTS: The results showed that the expression of USP18 was related to age (P=0.014). The positive rates of the USP18 protein in T1, T2, T3, and T4 were 0.00%, 22.92%, 78.38%, and 95.35%, respectively (P<0.00). The positive rates of the USP18 protein in I, II, III, and IV were 47.43%, 83.12%, 66.67%, and 100.00%, respectively (P<0.00). The Western blot assay showed that the expression of USP18 in colorectal cancer tissues was significantly higher than that in matched paracancerous tissues (P<0.05). The CCK8 experiments suggested that USP18 promoted the migration of CRC cells. Wound healing assays suggested that USP18 promoted the proliferation of CRC cells. CONCLUSION: This study showed that USP18 can promote the proliferation of colorectal cancer cells and might be a potential biomarker for the diagnosis of CRC.

Screening of Breast Cancer Methylation Biomarkers Based on the TCGA Database.

OBJECTIVE: Breast cancer has become a fatal disease for women world-wide. Its incidence in China has been increasing yearly, and the identification of early-stage biomarkers is urgently required. METHODS: ANOVA was carried out in the case of a primary tumor, adjacent normal tissue, and tumor metastasis of breast cancer, and on pan-cancer samples using the genome-wide methylation data of 31 solid tumor Illumina Methylation 450K chips downloaded from The Cancer Genome Atlas (TCGA) website in September 2018. Methylation sites showing a significant difference (P ≤ 0.05) were screened and compared with the whole-genome methylation data of 31 other solid tumor species in the TCGA database using t-tests in order to screen the methylation sites of breast cancer-specific expression. The expression of the screened methylation sites was confirmed through pyrosequencing in 45 cases of breast cancer, lung cancer, gastric cancer, and colorectal cancer. RESULTS: A total of 10 specific breast cancer methylation sites (cg13683194, cg07996594, cg21646032, cg07671949, cg21185686, cg03625109, cg16429070, cg23601468, cg24818566, and cg01240931) were analyzed; nine genes (C9orf125, RARB, ESR1, RUNX3, PCDHGB7, DBC1, PDGFRB, TIMP3, and APC) were involved. The overall effect was excellent; a total of 4 methylation sites (2 in the DBC1 gene [cg03625109 and cg24818566], 1 in the C9orf125 gene [cg13683194], and 1 in the PDGFRB gene [cg16429070]) could effectively distinguish breast cancer from 31 other cancer species. The pyrosequencing results revealed that 7 screened methylation sites could significantly distinguish between breast cancer, lung cancer, gastric cancer, and colorectal cancer samples; these sites could also specifically distinguish between luminal A, luminal B, HER2, and Basal-like types of breast cancer. CONCLUSION: The 10 breast cancer methylation sites screened in the present study can effectively distinguish breast cancer from 31 other solid tumors, and they are expected to be used as biomarkers for early screening of breast cancer.

Multiple Microinvasion Foci in Ductal Carcinoma In Situ Is Associated With an Increased Risk of Recurrence and Worse Survival Outcome.

BACKGROUND: Ductal carcinoma in situ with microinvasion (DCISM) was defined as one or more foci of invasion beyond the basement membrane within 1 mm. The size of primary lesion is associated with axillary status and prognosis in patients with invasive breast cancer; thus, it is of interest to determine whether multiple foci of microinvasion are associated with a higher risk of positive axillary status or worse long-term outcomes in patients with DCISM. METHODS: This study identified 359 patients with DCISM who had undergone axillary evaluation at our institute from January 2006 to December 2015. Patients were categorized as one focus or multiple foci (≥2 foci) according to the pathological results. Clinicopathological features, axillary status, and disease-free survival rate were obtained and analyzed. RESULTS: Of 359 patients, 233 (64.90%) had one focus of microinvasion and 126 (35.10%) had multiple foci. Overall, 242 (67.41%) and 117 (32.59%) patients underwent sentinel lymph nodes biopsy (SLNB) and axillary lymph nodes dissection (ALND), respectively. Isolated tumor cells were found in four (1.11%) patients and axillary metastasis rate was 2.51%. Neither axillary evaluation methods (P = 0.244) nor axillary metastasis rate (P = 0.559) was significantly different between patients with one focus and multiple foci. In univariate analysis, patients with multiple foci tended to have larger tumor size (P < 0.001), higher nuclear grade (P = 0.001), and higher rate of lymphatic vascular invasion (P = 0.034). Also, the proportion of positive HER2 (P = 0.027) and Ki67 level (P = 0.004) increased in patients with multiple foci, while in multivariate analysis, only tumor size showed significant difference (P = 0.009). Patients with multiple foci were more likely to receive chemotherapy (56.35 vs 40.77%; P = 0.028). At median 5.11 years follow-up, overall survival rate was 99.36%. Patients with multiple microinvasive foci had worse disease-free survival rate compared with one-focus patients (98.29 vs 93.01%, P = 0.032). CONCLUSION: Even though the numbers of microinvasion were different and patients with multiple foci of microinvasion tended to have larger tumor size, there was no higher risk of axillary involvement compared with patients with one focus of microinvasion, while patients with multiple microinvasive foci had worse DFS rate. Thus, DCISM patients with multiple foci of microinvasion may be the criterion for more aggressive local-regional treatment. Optimization of adjuvant therapy in DCISM patients is required.

[Relationship between epithelial-mesenchymal transition and basal cell-like phenotype in breast cancer].

OBJECTIVES: To evaluate the relationship between epithelial-mesenchymal transition and basal cell-like phenotype breast cancer (BLBC). METHODS: Three hundred and eighty two cases of breast cancers including basal cell-like, luminal A, luminal B and Her-2 subtypes were collected from 458 cases of invasive breast cancers based on their immunophenotypes. They were then stained immunohistochemically with FOXC-2, vimentin, Syndecan-1 and E-cadherin. The relationship of these markers with the basal cell-like phenotype of breast cancer was studied. RESULTS: Of the 41 BLBC cases, FOXC-2, vimentin and Syndecan-1 were positive in 14 cases (34.1%), 18 cases (43.9%) and 36 cases (87.7%) respectively; E-cadherin expression was reduced in 26 cases (63.4%). The positive rates of FOXC-2 and vimentin were higher in BLBC than in other subtypes of breast cancer (P < 0.01). The expression of E-cadherin was the lowest among the 4 subtypes of breast cancers (P < 0.01). Syndecan-1 was positive in the stromal cells adjacent to cancer cells in 17 cases (41.5%) BLBC and the expression was higher than that in other subtypes (P = 0.007). There existed a correlation between FOXC-2 and vimentin expression in BLBC (r = 0.607, P < 0.01). The rates of positive lymph nodes in FOXC-2 and vimentin positive BLBC cases were 71.4% and 66.7% respectively, and both were higher than those of FOXC-2 and vimentin negative BLBC cases (P = 0.002 and P = 0.001). CONCLUSION: Epithelial-mesenchymal transition is probably related to the basal cell-like phenotype of breast cancers, and this may be one of the reasons accounting for the different biological behavior of BLBC from other subtypes of breast cancer.

[Clinicopathologic characteristics of breast cancer with basal-like immunophenotype].

OBJECTIVE: To study the clinicopathologic characteristics of basal-like immunophenotype breast cancer (BLBC). METHODS: 458 cases of female infiltrative breast cancer were studied using immunohistochemical staining with an antibody panel of ER, PR, HER2, Ki-67, CK5/6, CK14 and epidermal growth factor receptor (EGFR) and were classified basing on the immunophenotypes. The clinicopathologic characteristics were compared with other immunophenotypes of breast cancer. 228 of 458 cases of breast cancer were followed up. RESULTS: 46 cases of BLBC were screened out among the 458 breast cancers. And histological features of BLBC were analysed including the larger diameter of cancer foci (average 3.3 cm), appearance of squeezing phenomenon of neighboring cell borders (58.7%, 27/46), geography-like distribution of necrosis (52.2%, 24/46), central zone fibrosis (30.4%, 14/46) and lymphoplasmacytic infiltration at the margin and stroma (63.0%, 29/46). There were nuclear pleomorphism with numerous mitoses. The cancer cells were closely arranged, forming irregular solid architectures. There was a high expression (> 25%) of Ki-67 (43.5%, 20/46). CK5/6, CK14 and EGFR were positive in 58.7% (27/46), 43.5% (20/46) and 65.2% (30/46) respectively. 3-year survival rate of BLBC was 66.9%, lower than the luminal A breast cancer and similar to HER2 over-expression breast cancer. CONCLUSIONS: The proportion of BLBC in the group of breast cancers is 10%. BLBC has its distinct histological and cytological features. Currently, it is still necessary to depend on immunophenotyping in making a BLBC diagnosis. BLBC is the one of breast cancer subtypes with the poorest prognosis.