Ossifying fibromyxoid tumor of the soft tissue in the left upper arm and a review of the literature: A case report.

Ossifying fibromyxoid tumor (OFMT) of the soft parts is a mesenchymal neoplasm of uncertain lineage. Fibromyxoid matrix and peripheral metaplastic bone are common histological features of this type of tumor. In the present study, a case of OFMT in a 33-year-old female was reported. The patient was referred to the First Affiliated Hospital of China Medical University (Shenyan, China) in January 2018. The patient had developed a mass in the left upper arm 6 months prior to presentation, which was slowly enlarging. The tumor was 1.5 cm in diameter, with hard texture. Histologically, the tumor showed a clear boundary with no invasion into the adjacent tissue. The majority of tumor cells were round and medium-sized, with abundant pale cytoplasm, without obvious atypia and densely arranged in sheets. The tumor tissue was characterized by cartilage-like morphology and fibromyxoid and hyalinization matrix. Mitotic index was <1/10 high-power fields. Additionally, tumor cells were positive for S-100 and vimentin expression, but negative for smooth muscle actin, CD34, cytokeratin, desmin, human melanoma black 45 and melanoma A. Ki67 index was ~1%. The patient underwent surgery and the tumor was totally removed. No recurrence was observed at the final 6-year follow-up. Based on the aforementioned findings, the patient was diagnosed as typical OFMT. Slow growth and clear boundaries often suggest an indolent nature to this type of tumor. However, close follow-up should be performed due to its malignant potential.

Multiple Primary Lung Tumors of Different Pathological Types Including Squamous Cell Carcinoma, Adenocarcinoma, and Mixed Squamous Cell and Glandular Papilloma: A Case Report.

Multiple primary lung cancer (MPLC) is considered relatively rare. This report presents an unusual case of multiple pulmonary nodules in a 74-year-old man who presented with three independent synchronous tumors in the right upper lobe. The tumors were diagnosed as peripheral squamous cell carcinoma (SCC), adenocarcinoma, and pulmonary mixed squamous cell and glandular papilloma (mixed papilloma). Mixed papilloma is an extremely rare, benign pulmonary tumor with a typical papillary appearance, showing squamous and glandular epithelial differentiation. The histological and immunohistochemical features of each tumor were analyzed. In addition, molecular pathological examination for epidermal growth factor receptor (EGFR) showed no mutation in two primary cancers. Mixed papilloma showed no BRAF V600E mutation or HPV infection. The present case report provides a clinicopathological understanding of an instance in which three tumors of different pathological types are present in the same lung lobe. Furthermore, it provides a literature review regarding multiple lung nodules, focusing on the clinicopathological diagnosis, clinical treatment, and prognostic assessment of these nodules. This is the first case report of mixed papilloma arising in MPLC.

The Role of Ki67 in Evaluating Neoadjuvant Endocrine Therapy of Hormone Receptor-Positive Breast Cancer.

Ki67 is a proliferation marker. It has been proposed as a useful clinical marker for breast cancer subtype classification, prognosis, and prediction of therapeutic response. But the questionable analytical validity of Ki67 prevents its widespread adoption of these measures for treatment decisions in breast cancer. Currently, Ki67 has been tested as a predictive marker for chemotherapy using clinical and pathological response as endpoints in neoadjuvant endocrine therapy. Ki67 can be used as a predictor to evaluate the recurrence-free survival rate of patients, or its change can be used to predict the preoperative "window of opportunity" in neoadjuvant endocrine therapy. In this review, we will elaborate on the role of Ki67 in neoadjuvant endocrine therapy in breast cancer.

WBP2 negatively regulates the Hippo pathway by competitively binding to WWC3 with LATS1 to promote non-small cell lung cancer progression.

WW domain binding protein-2 (WBP2) can function as a Yes-associated protein/transcriptional co-activator with PDZ-binding motif (YAP/TAZ) co-activator and has a crucial role in promoting breast cancer progression. However, the expression and potential molecular mechanisms of WBP2 in the context of lung cancer are not fully understood. We determined that WBP2 was highly expressed in lung cancer specimens and cell lines and that this expression was closely related to the advanced pTNM stage, lymph node metastasis, and poor prognosis of patients. In addition, gain- and loss-of-function experiments revealed that WBP2 could significantly promote the proliferation and invasion of lung cancer cells both in vivo and in vitro. To elucidate the underlying molecular mechanism, we determined that wild-type WBP2 could competitively bind to the WW domain of WWC3 (WW and C2 domain-containing-3) with LATS1 (Large tumor suppressor-1) through its PPxY motifs, thus inhibiting the formation of the WWC3-LATS1 complex, reducing the phosphorylation level of LATS1, suppressing the activity of the Hippo pathway, and ultimately promoting YAP nuclear translocation. Therefore, from the aspect of upstream molecules of Hippo signaling, WBP2 promotes the malignant phenotype of lung cancer cells in a unique manner that is not directly dependent upon YAP, thus providing a corresponding experimental basis for the development of targeted therapeutic drugs for lung cancer.

ATF4 promotes lung cancer cell proliferation and invasion partially through regulating Wnt/ß-catenin signaling.

Activating transcription factor 4 (ATF4) is a member of the cAMP response element binding (CREB) protein family and has been reported to participate in cancer progression; however, its molecular mechanism is not fully understood. In this study, we investigated the function of ATF4 in non-small cell lung cancer and its molecular regulation. We detected cytoplasmic and nuclear ATF4 expression in lung cancer A549, H1299, and LK2 cells, and the total expression of ATF4 was higher than that in HBE cells (p < 0.05). Higher nuclear ATF4 expression was detected in all these cells compared to cytoplasmic ATF4 expression (p < 0.05). Overexpression of ATF4 in A549 cells significantly promoted cancer cell growth and invasion (p < 0.05). Expression of Wnt signaling molecules, including ß-catenin, MMP7, and cyclin D1, and the activity of canonical Wnt signaling were also significantly promoted by ATF4 (p < 0.05). ICG001, a canonical Wnt signaling inhibitor that selectively inhibits ß-catenin/ cyclic adenosine monophosphate response element binding protein (CBP) interaction, significantly inhibited cancer cell invasion and Wnt signaling. The function of ATF4 was also significantly inhibited by ICG001 (p < 0.05). However, compared to treatment with ICG001, the invasion ability of cancer cells treated with both ICG001 and ATF4 cDNA significantly increased (p < 0.05), which indicates that the function of ATF4 was not dependent only on Wnt/ß-catenin signaling. The function of ATF4 in the regulation of ß-catenin expression was not significantly affected by ICG001 (p > 0.05). The function of ATF4 to promote the activity of Wnt/ß-catenin signaling in cancer cells was abolished by treatment with ICG001 (p > 0.05). These results indicate that ATF4 may contribute to lung cancer progression at least partly by regulating Wnt/ß-catenin signaling.

A retrospective observational study of intraductal breast papilloma and its coexisting lesions: A real-world experience.

BACKGROUND: Breast intraductal papilloma is a heterogeneous group. The aim of the study is to investigate the intraductal breast papilloma and its coexisting lesions retrospectively in real-world practice. METHODS: We retrospectively identified 4450 intraductal breast papilloma and its coexisting lesions. RESULTS: About 18.36% of intraductal papilloma coexisted with malignant lesions of the breast, 37.33% coexisted with atypia hyperplasia (AH), 25.24% coexisted with benign lesions, and only 19.10% coexisted without concomitant lesions. In addition, 36.80% of intraductal breast papilloma had nipple discharge, 51.46% had a palpable breast mass, and 16.45% had both nipple discharge and a palpable breast mass. About 28.18% experienced discomfort or were asymptomatic. Furthermore, 98.99% had ultrasound abnormalities, and 53.06% had intraductal hypoechogenicity upon ultrasound. 31.89% had mammographic distortion, and 14.45% had microcalcification upon mammography. Intraductal breast papilloma with malignancy had significant correlations with clinical manifestations. CONCLUSION: Coexisting malignancy was also related to ultrasound abnormality (BIRADS 4C and 5), mammographic distortion, and microcalcification upon mammography but was not related to the intraductal hypoechoic upon ultrasound. Coexisting atypical hyperplasia correlated with nipple discharge but not palpable mass, mammographic distortion, or intraductal hypoechoic upon ultrasound. The coexisting AH was also related to abnormality upon ultrasound or microcalcification compared with the benign lesions. The intraductal papilloma coexists with malignancy or AH accounted for more than 50%, and the clinical information on papilloma and its coexisting lesions is nonspecific. We recommended surgical treatment for benign intraductal papillary lesions.

Ube2S regulates Wnt/ß-catenin signaling and promotes the progression of non-small cell lung cancer.

Ubiquitin conjugating enzyme E2S (Ube2S) plays important roles in cancer development in some malignant tumors. However, the functions and related molecular network of Ube2S in non-small cell lung cancer are not fully understood. In the current study, we examined the expression of Ube2S in non-small cell lung cancer and its clinicopathological significance. We also investigated the molecules and pathways regulated by Ube2S. An immunostaining study showed that the positive rate of Ube2s expression in lung cancer tissues was higher than that in normal lung tissues (p < 0.05). Upregulated Ube2S expression in cancer tissues significantly correlated with clinical progression (TNM III versus I + II), lymph node metastasis, and shorter survival time of the patients (p < 0.05). When Ube2S was overexpressed in A549 cells, the abilities of these cells to proliferate and migrate were increased (p < 0.05). Moreover, Ube2S significantly upregulated the expression of ß-catenin, cyclin D1, and MMP7 (novel molecules of the Wnt/ß-catenin pathway), and the activity of this pathway (p < 0.05). In addition, a Wnt/ß-catenin signaling inhibitor effectively abolished the function of Ube2S. These results indicate that Ube2S may be a novel marker contributing to lung cancer development, possibly through regulating canonical Wnt signaling.

Timescale of tumor volume of a young breast cancer patient with luminal B subtype: A case report.

RATIONALE: It is largely unknown about the tumor growth of breast cancer naturally. We devised and analyzed an appropriate mathematical tool of the equations that describe how fast tumors grow without treatment on the basis of the ellipsoid shape of solid breast cancer. PATIENT CONCERNS: A 31-year-old woman presented with a painless palpable lump in her left breast for 5 months. DIAGNOSIS: Infiltrated ductal breast cancer (histologic grade II) of luminal B INTERVENTIONS:: The patient did not receive any therapy due to her private reasons for 2 years, the analysis of the tumor volume growth was done regarding the growth rate of the tumor in the absence of intervention. OUTCOMES: After 2 years of diagnosis of breast cancer, the tumor mass occupied the whole left breast with skin implanted and nipple abnormality. As this case indicated that the tumor's early growth rate was very slow. When the tumor volume reached 300 cm, its fast growth began without treatment. Later growth approached the maximum, when the tumor volume was more than 800 cm. LESSONS: The tumor growth is segmental without therapy. Early diagnosis and treatment is the key to good prognosis for every breast cancer patient.

FAM163A, a positive regulator of ERK signaling pathway, interacts with 14-3-3ß and promotes cell proliferation in squamous cell lung carcinoma.

PURPOSE: FAM163A, also called neuroblastoma-derived secretory protein (NDSP) or C1ORF76, was newly found on chromosome 1q25.2. Previous studies of FAM163A focused on its expression and function in neuroblastoma. However, using an online database, we found that FAM163A may predict poor prognosis in lung squamous cell carcinomas (LUSC). Therefore, the role of FAM163A plays in LUSC needs to be further clarified. PATIENTS AND METHODS: Western blots, immunofluorescence and immunohistochemistry were used to detect the effect of FAM163A on mediating cell proliferation in vitro and in vivo. Co-immunoprecipitation and immunofluorescence were utilized to evaluate the interaction and co-localization of FAM163A with 14-3-3ß and ERK. RESULTS: In this study, our data revealed that FAM163A overexpression increased the levels of ERK and p90RSK phosphorylation and promoted the expression of cyclin D1. Incorporation with U0126 reversed the effects of FAM163A overexpression. FAM163A directly interacted with both 14-3-3ß and ERK and regulated the phosphorylation of ERK by upregulating the protein level of 14-3-3ß. Immunohistochemistry results also showed that FAM163A expression significantly correlated with larger tumor size (P=0.023), TNM staging (P=0.015) and regional lymph node metastasis (P=0.016). Kaplan-Meier survival analysis implied the mean survival time of patients with positive FAM163A expression (49.72±3.97 months) was much shorter than the patients with negative FAM163A expression (63.36±3.14 months, P=0.011). CONCLUSION: In summary, the present study identified a novel mechanism that FAM163A, through binding and upregulating 14-3-3ß, facilitated ERK phosphorylation that led to an increase of cellular proliferation of LUSC cells. FAM163A may be a useful marker to predict poor prognosis of patients with LUSC.

Identifying UBA2 as a proliferation and cell cycle regulator in lung cancer A549 cells.

Ubiquitin activating enzyme 2 (UBA2) is a basic component of E1-activating enzyme in the SUMOylation system. Expression and function of UBA2 in human cancers are largely unknown. In this study we investigate UBA2 expression the function in human non-small-cell lung cancer. Immunochemistry study showed that UBA2 was overexpressed in cancer tissues (53.3%, 40 of 75) compared with normal lung tissues (14.3%, 4 of 28) (P < 0.05). Immunostaining of UBA2 was mainly detected in nucleus. Overexpression of UBA2 in cancer tissues was significantly associated with poor differentiation, large tumor size ( > 5.0 cm), higher T stages (T3 + 4), lymph node metastasis and advanced TNM stages (III + IV). In vitro study showed that UBA2 was expressed in A549, 95D, H1975, and H1299 cells. Knockdown of UBA2 in A549 cells significantly inhibited cancer cell proliferation and upregulated cancer cell apoptosis (P < 0.05). Cell cycle analysis showed that knockdown of UBA2 in A549 cell significantly increased the G1 and G2/M phase cells and reduced the S phase cells (P < 0.05). Gene expression profile after knockdown of UBA2 in A549 cells showed that the most related function was cell cycle, cell death and survival, and cellular growth and proliferation. Western blot analysis study showed that knockdown of UBA2 significantly inhibited expression of poly(ADP-ribose) polymerase 1, mini-chromosome maintenance 7 (MCM7), MCM2, MCM3 and MCM7. These results indicated that UBA2 was a critical cell cycle and proliferation regulator and may be a novel cancer marker in this malignant tumor.

Hes3 Enhances the Malignant Phenotype of Lung Cancer through Upregulating Cyclin D1, Cyclin D3 and MMP7 Expression.

Hes3 is a basic helix-loop-helix factor gene, which was found to be involved in neural cell differentiation. Expression and clinicopathological significance of Hes3 in non-small cell lung cancer was not clear. In this study, we used immunohistochemistry to examine Hes3 expression in normal human lung and non-small cell lung cancer tissues. Hes3 expression was detected in cytoplasm and nucleus. Hes3 expression in bronchial epithelial cells and epithelial cells of submucosal glands was relatively weak and the positive rate was of 30.3% (10/33). Hes3 expression in non-small cell lung cancer tissues (51.8% (58/112)) was significantly higher than that in normal lung tissues (p < 0.05). Hes3 expression in cancer tissues was significantly associated with poor differentiation, advanced TNM stages, lymph node metastasis, and a shorter patient survival time (p < 0.05). In vitro study showed that overexpression of Hes3 in A549 cells significantly promoted cancer cell proliferation and invasion, while inhibition of Hes3 expression significantly downregulated cancer cell proliferation and invasion (p < 0.05). Western blotting showed that overexpression of Hes3 significantly upregulated expression of Cyclin D1, Cyclin D3, and MMP7 in A549 cells, while inhibition of Hes3 expression in LK2 cells significantly downregulated the expression of these molecules (p < 0.05). These results indicated that Hes3 may contribute to the malignant phenotype of non-small cell lung cancer, possibly through regulation of Cyclin D1, Cyclin D3, and MMP7, and may be a promising cancer marker.

The function of BED finger domain of Zbed3 in regulating lung cancer cell proliferation.

Zbed3, a BED finger domain-containing protein was found to promote cancer proliferation by regulating ß-catenin expression through interacting with Axin. But whether and how BED finger domain function in regulating cancer proliferation is unknown. We constructed five mutants of Zbed3, which lacks the Axin-Zbed3 binding site, and the 43 to 52, 69 to 77, 87 to 92, and 97 to 104 sequences in BED finger domain, respectively and named them as Z-A, Z1, Z2, Z3, and Z4. Transfection of both wild-type of Zbed3 and the mutants Z1, Z3, and Z4 (P < 0.05), but not Z2 (P > 0.05) significantly upregulated ß-catenin expression in NCI-H1299 cells. Overexpression of both wild-type of Zbed3 and the mutants Z1, Z3, and Z4 (P < 0.05) but not Z2 (P > 0.05) significantly promoted cancer cell proliferation and invasion. The ability of proliferation (P < 0.05) but not invasion (P < 0.05) of cancer cells transfected with Z1 and Z4 was significantly lower than that with wild-type Zbed3 and Z3. Overexpression of wild-type Zbed3 (P < 0.05) but not the mutant Z-A, which lacks the binding site with Axin and Z2 (P > 0.05) significantly upregulated the interaction of Axin and Zbed3, ß-catenin expression and the activity of Wnt signaling. Both overexpression of wild-type Zbed3 and the mutant Z1 and Z4 significantly upregulated the activity of Wnt signaling and promoted cancer cell proliferation (P < 0.05) but only overexpression of wild-type Zbed3 (P < 0.05), but not the mutant Z1, and Z4 (P > 0.05), significantly upregulated the expression of proliferating cell nuclear antigen (PCNA) in NCI-H1299 cells. These results indicate that Zbed3 may promote lung cancer cell proliferation through regulating PCNA expression besides regulating ß-catenin expression and BED finger domain can impact on this function.

ZCCHC9 promotes proliferation and invasion of lung cancer through regulating the JNK pathway.

ZCCHC9 is a type of CCHC type zinc-finger containing protein which was found to be expressed in some tissues including brain and testicles in mice. Expression and function of ZCCHC9 in human tissues including cancer was largely unknown. In this study, we investigated the expression and function of ZCCHC9 in human non-small cell lung cancer (NSCLC) and the related molecular mechanism. Immunochemistrical standing showed that ZCCHC9 was mainly located in the nucleus in bronchial epithelial cells and epithelial cells of submucosal glands (58.3% [14/24]). But in NSCLC cells ZCCHC9 was mainly located in the cytoplasm and the positive rate was 54.5% (60/110). Ectopic cytoplasmic expression of ZCCHC9 in cancer tissues was significantly associated with advanced TNM stages (III+IV), lymph node metastasis, and poor clinical outcome (P < 0.05). Overexpression of cytoplasmic ZCCHC9 using transfection of ZCCHC9 cDNA in A549 and NCI-H1299 cells significantly upregulated the proliferation and invasion of these cancer cells in vitro (P < 0.05). Western blot study showed that overexpression of cytoplasmic ZCCHC9 significantly upregulated expression of p-JNK, Cyclin D1, and MMP7 (P < 0.05). Next we used the inhibitor of JNK pathway to inhibit the activity of the JNK pathway and the results showed that co-addition of SP600125 significantly abolished the function of ZCCHC9 to promote the proliferation and invasion of cancer cells. These results indicate that cytoplasmic ZCCHC9 could promote the proliferation and invasion of NSCLC through the JNK pathway and may be a promising cancer maker.

TIMM50 promotes tumor progression via ERK signaling and predicts poor prognosis of non-small cell lung cancer patients.

TIMM50 (Translocase of the inner mitochondrial membrane 50), also called TIM50, plays an essential role in mitochondrial membrane transportation. The existing literature suggests that TIMM50 may perform as an oncogenetic protein in breast cancer. However, the molecular mechanism, especially in human non-small cell lung cancer (NSCLC), is uncertain to date. In the present study, using immunohistochemistry, we found that TIMM50 expression significantly correlated with larger tumor size (P = 0.049), advanced TNM stage (P = 0.001), positive regional lymph node metastasis (P = 0.007), and poor overall survival (P = 0.001). Proliferation and invasion assay showed that TIMM50 dramatically promoted the ability of proliferation and invasion of NSCLC cells. Subsequent Western blotting results revealed that TIMM50 enhanced the expression of Cyclin D1 and Snail, and inhibited the expression of E-cadherin. Moreover, TIMM50 facilitated the expression of phosphorylated ERK and P90RSK. Incorporation of ERK inhibitor counteracted the upregulating expression of CyclinD1, and Snail, and downregulating expression of E-cadherin expression induced by TIMM50 overexpression. In conclusion, our data indicated that TIMM50 facilitated tumor proliferation and invasion of NSCLC through enhancing phosphorylation of its downstream ERK/P90RSK signaling pathway. We speculated that TIMM50 might be a useful prognosis marker of NSCLC patients.

Zbed3 promotes proliferation and invasion of lung cancer partly through regulating the function of Axin-Gsk3ß complex.

Our previous work showed that Zbed3 is overexpressed in nonsmall cell lung cancer and that down-regulation of Zbed3 inhibited ß-catenin expression and cancer cell proliferation and invasiveness. Here, we investigated Zbed3's ability to promote lung cancer cell proliferation and invasion and the involvement of the Axin/TPC/glycogen synthase kinase 3ß (Gsk-3ß) complex to the response. Coimmunoprecipitation assays showed that wild-type Zbed3 bound to Axin but a Zbed3 mutant lacking the Axin binding site did not. In A549 and H1299 lung cancer cells, Zbed3 overexpression promoted cancer cell proliferation and invasiveness, as well as Wnt signalling and expression of downstream mediators, including ß-catenin, cyclin D1 and MMP7 (P < 0.05). In contrast, the Zbed3 mutant failed to enhance ß-catenin expression (P > 0.05), and its ability to promote cancer cell proliferation and invasiveness was much less than wild-type Zbed3 (P < 0.05). The ability of Zbed3 to increase ß-catenin levels was abolished by Axin knockdown in A549 cells (P > 0.05). Similarly, treating the cells with a GSK-3ß inhibitor abolished Zbed3's ability to increase ß-catenin levels and Wnt signalling. These results indicate that Zbed3 enhances lung cancer cell proliferation and invasiveness at least in part by inhibiting Axin/adenomatous polyposis coli/GSK-3ß-mediated negative regulation of ß-catenin levels.

NDRG1 Downregulates ATF3 and Inhibits Cisplatin-Induced Cytotoxicity in Lung Cancer A549 Cells.

N-myc downstream regulated gene 1 (NDRG1) plays a variety of roles in human cancers. Our previous studies showed that NDRG1 expression is elevated in non-small cell lung cancer and contributes to cancer growth. However, its function in apoptosis and chemoresistance in malignant tumors, including lung cancer, is not yet fully understood. In this study, we investigated the roles of NDRG1 in chemoresistance to cisplatin in lung cancer cells. We found that overexpression of NDRG1 significantly reduced cisplatin-induced cytotoxicity in lung cancer A549 cells, while overexpression of activating transcription factor 3 (ATF3), a stress-inducible gene found to be associated with apoptosis in some human cancers, significantly promoted cytotoxicity (P < 0.05). Further investigation showed that overexpression of NDRG1 significantly downregulated ATF3 and P53 expression in A549 cells, while overexpression of ATF3 significantly upregulated P53 expression (P < 0.05). In addition, cisplatin significantly upregulated ATF3, phospho-P53(ser46), and cleaved caspase 3 expression in lung cancer cells, but overexpression of NDRG1 in the presence of cisplatin reduced the level of these proteins elevated by cisplatin (P < 0.05). While, overexpression of ATF3 significantly promoted the cytoxicity induced by cisplatin in 1299 cells (p<0.05) (Figure 4), but overexpression of NDRG1 didn't regulate the cytoxicity induced by cisplatin (p>0.05). These results indicate that NDRG1 may contribute to cisplatin-resistance in lung cancer, possibly due to its function in the regulation of ATF3 expression.

Alveolar architectures preserved in cancer tissues may be potential pitfalls for diagnosis and histological subtyping of lung cancer: Three case reports.

RATIONALE: Lung cancer is a leading cause of cancer-related deaths globally. Appropriate histopathological diagnosis and subtyping form the basis and are critical for clinical therapies. PATIENT CONCERNS: Here, we report about 3 patients who had a nodule in the lung. Cancer cells grow in the alveolar cavity in many lung carcinomas. In all our 3 cases preserved alveolar architectures were found in tumor tissues which may lead to diagnostic pitfalls. DIAGNOSES: Three patients had tumors that were diagnosed as nonsmall cell lung cancers, including large-cell carcinoma, peripheral squamous cell carcinoma, and large-cell neuroendocrine carcinoma, all of which contained structures of preserved alveolar cells that could be mistaken as malignant glandular components. The preserved alveolar cells formed acinar or duct-like structures enwrapped in the lung cancer tissues or surrounded the nests of cancer cells. Proliferative alveolar cells adjacent to cancer tissues were observed, and papillary structures and marked atypia, both of which may be mistaken as part of adenocarcinoma or carcinoma with glandular differentiation, were also observed. INTERVENTIONS: All patients underwent surgery and postoperative chemotherapy. OUTCOMES: The patients had no recurrence at 5-, 8-, or 10-month follow-up after the last surgery. LESSONS: Preserved alveolar cells with different architectures may be observed in various lung cancer tissues and may be mistaken as adenocarcinoma or carcinoma with glandular differentiation. Distinct morphological and immunohistochemical features may help distinguish preserved alveolar cells from tumor components.

Long period of relative quiescence in distal-type epithelioid sarcoma of the forearm with recurrence after surgery: A case report.

BACKGROUND: Epithelioid sarcoma (ES) is a rare malignant mesenchymal tumor that only accounts for 0.6% to 1.0% of all cases of sarcomas. ES with a relative quiescent state of more than 10 years is extremely rare.Here, we present a rare case of ES in the forearm of a 17-year-old girl. The patient had a congenital mass in her forearm that measured approximately 1cm; it grew rapidly starting 5 years ago. The mass was not treated until last year when she underwent the first surgery. The mass was located in the middle and lower part of the left forearm and involved the dorsal muscle group, intermuscular space, and subcutaneous tissues without clear boundaries.The patient underwent surgery, and the tumor recurred twice within 1 year postoperatively. METHODS: The tumor samples were examined via hematoxylin-eosin (HE) and immunohistochemistry staining. RESULTS: Histopathologically, the tumor comprised large polygonal epithelioid cells with abundant eosinophilic cytoplasm arranged in cell nests. Central necrosis and focal myxoid change could be seen in the tumor tissues. Immunostaining showed that the tumor cells were positive for CD34, CK, EMA, and vimentin but negative for CD31, S-100, and INI-1. CONCLUSION: Based on these findings, the tumor was diagnosed as ES of distal form. Distal-type ES could have a long period of relative quiescence, after which it could grow rapidly and relapse multiple times over a short duration.

TMEM17 promotes malignant progression of breast cancer via AKT/GSK3ß signaling.

PURPOSE: Current knowledge of TMEM17, a recently identified protein of the transmembrane (TMEM) family, is limited, especially with respect to its expression and biological functions in malignant tumors. This study analyzed TMEM17 expression in invasive breast cancer tissue and breast cell lines and its relevance to clinicopathological factors, and investigated the mechanisms underlying the biological effects of TMEM17 on breast cancer cells. PATIENTS AND METHODS: TMEM17 protein expression was determined in 20 freshly harvested specimens (tumor and paired normal tissues) by Western blotting. Immunohistochemical analysis was performed to determine the expression and subcellular localization of TMEM17 in samples from 167 patients (mean age, 49 years) diagnosed with invasive ductal carcinoma (38 with triple-negative breast cancer; 129 with non-triple-negative breast cancer) who underwent complete resection in the First Affiliated Hospital of China Medical University between 2011 and 2013. Furthermore, TMEM17 was knocked down by small interfering RNAs in breast cancer cell lines. RESULTS: TMEM17 was found to be significantly upregulated in breast cancer tissues compared to the corresponding normal breast tissues by Western blotting (p=0.015). Immunohistochemical analysis revealed that TMEM was significantly upregulated in invasive breast cancer cells compared to adjacent normal breast duct glandular epithelial cells (10.78% vs 76.05%, p<0.001), and its expression was closely related to the patient's T-stage (p=0.022), advanced TNM stages (p=0.007), and lymph node metastasis (p=0.012). After TMEM17 knockdown or overexpression in breast cancer cell lines, TMEM17 upregulated p-AKT, p-GSK3ß, active ß-catenin, and Snail, and downstream target proteins c-myc and cyclin D1, and downregulated E-cadherin, resulting in increased cancer cell proliferation, invasion, and migration. These effects were reversed by the AKT inhibitor LY294002. CONCLUSION: Our results indicate that TMEM17 is upregulated in breast cancer tissues and can promote malignant progression of breast cancer cells by activating the AKT/GSK3ß signaling pathway.

Endometriosis in the rectum accompanied by hemorrhoids leading to diagnostic pitfalls: a rare case report.

BACKGROUND: Hemorrhoid is a common anorectal disease. Hemorrhoids accompanied by endometriosis are unusual. As endometriosis in the rectum may mimic many other diseases, including cancer and inflammation, its diagnosis may be difficult, especially when it is combined with other diseases. CASE PRESENTATION: Here, we present a rare case of a patient with hemorrhoids accompanied by endometriosis in the rectum. The endometriosis mass was detected by digital rectal examination and CT scan and confirmed by pathological examination. The mass was approximately 0.8 cm × 0.6 cm and located in the muscularis and submucosa of the rectum 8 cm from the anus. CONCLUSIONS: In this case, hemorrhoid is a common disease of rectum and anal canal. However, when it is complicated by another rare disease, the rare one can be easily neglected because of the existence of the common one, especially when the two diseases have similar lesions or symptoms. We suggest that strict physical examination, such as the digital rectal examination in the current case, is critical for correct disease diagnosis.