Malignant mixed Mullerian tumour (MMMT) of uterus: Rare and aggressive Tumor

Endometriosis is one of the most common gynecological problem. Cells resulted in chronic inflammation and progressive, proliferative, invasive and even infiltrating an area that resembles the character of the malignancy. Ki-67 is an antigen on the cell nucleus that is found only in actively dividing cells. Expression of Ki-67 are associated with an aggressive tumor and metastasis. This study aims to determine the level of Ki-67 expression correlation with stage and size of the endometriosis cyst. Methods research is observational analytic cross cut method on 56 paraffin blocks of patients who have been diagnosed with endometriosis and had performed a laparotomy or laparoscopic surgery in Dr Hasan Sadikin Hospital. The results showed a significant relationship between the level of expression of Ki-67 with endometriosis cyst size (p <0.001) with a fairly strong relationship (0.55) according to statistics based on criteria Guilford. Moreover the results also showed a significant relationship between the level of expression of Ki-67 with endometriosis stage (p <0.001) with a fairly close relationship (0.564) according to statistics based on criteria Guilford. It can be concluded that the expression of Ki-67 associated with cyst size and stage of endometriosis. Keywords: Ki-67, endometriosis stage, endometriosis cyst

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Regeneration linked miRNA modify tumor phenotype and can enforce multi-lineage growth arrest in vivo

Scientific Reports ◽

10.1038/s41598-021-90009-9 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Siamak Salehi ◽

Oliver D. Tavabie ◽

Augusto Villanueva ◽

Julie Watson ◽

David Darling ◽

...

Keyword(s):

Cell Proliferation ◽

Growth Inhibition ◽

Tumor Aggressiveness ◽

Novel Treatment ◽

Tumor Phenotype ◽

Aggressive Tumor ◽

In Vivo Growth ◽

Regulation Of Regeneration

AbstractRegulated cell proliferation is an effector mechanism of regeneration, whilst dysregulated cell proliferation is a feature of cancer. We have previously identified microRNA (miRNA) that regulate successful and failed human liver regeneration. We hypothesized that these regulators may directly modify tumor behavior. Here we show that inhibition of miRNAs -503 and -23a, alone or in combination, enhances tumor proliferation in hepatocyte and non-hepatocyte derived cancers in vitro, driving more aggressive tumor behavior in vivo. Inhibition of miRNA-152 caused induction of DNMT1, site-specific methylation with associated changes in gene expression and in vitro and in vivo growth inhibition. Enforced changes in expression of two miRNA recapitulating changes observed in failed regeneration led to complete growth inhibition of multi-lineage cancers in vivo. Our results indicate that regulation of regeneration and tumor aggressiveness are concordant and that miRNA-based inhibitors of regeneration may constitute a novel treatment strategy for human cancers.

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Single-cell evaluation reveals shifts in the tumor-immune niches that shape and maintain aggressive lesions in the breast

Nature Communications ◽

10.1038/s41467-021-25240-z ◽

2021 ◽

Vol 12 (1) ◽

Author(s):

Vidya C. Sinha ◽

Amanda L. Rinkenbaugh ◽

Mingchu Xu ◽

Xinhui Zhou ◽

Xiaomei Zhang ◽

...

Keyword(s):

Breast Cancer ◽

T Cells ◽

Mouse Model ◽

Transition State ◽

Tumor Cell ◽

Single Cell ◽

Tumor Cells ◽

Breast Lesions ◽

Aggressive Tumor ◽

Insight Into

AbstractThere is an unmet clinical need for stratification of breast lesions as indolent or aggressive to tailor treatment. Here, single-cell transcriptomics and multiparametric imaging applied to a mouse model of breast cancer reveals that the aggressive tumor niche is characterized by an expanded basal-like population, specialization of tumor subpopulations, and mixed-lineage tumor cells potentially serving as a transition state between luminal and basal phenotypes. Despite vast tumor cell-intrinsic differences, aggressive and indolent tumor cells are functionally indistinguishable once isolated from their local niche, suggesting a role for non-tumor collaborators in determining aggressiveness. Aggressive lesions harbor fewer total but more suppressed-like T cells, and elevated tumor-promoting neutrophils and IL-17 signaling, disruption of which increase tumor latency and reduce the number of aggressive lesions. Our study provides insight into tumor-immune features distinguishing indolent from aggressive lesions, identifies heterogeneous populations comprising these lesions, and supports a role for IL-17 signaling in aggressive progression.

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Sinonasal FUS-ERG-Rearranged Ewing’s Sarcoma Mimicking Glomangiopericytoma

Case Reports in Oncology ◽

10.1159/000511415 ◽

2020 ◽

Vol 13 (3) ◽

pp. 1393-1396

Author(s):

Maggie Zhou ◽

Yen Chen Kevin Ko ◽

Gregory W. Charville ◽

Kristen N. Ganjoo

Keyword(s):

Ewing’S Sarcoma ◽

Ewing's Sarcoma ◽

Staining Pattern ◽

Gene Arrangement ◽

Round Cell ◽

The Family ◽

History Of ◽

Blue Cell ◽

Aggressive Tumor ◽

Membranous Staining

Ewing’s sarcoma is a rare and aggressive tumor that typically arises in the long bones of the extremities. It belongs in the family of small round blue cell tumors and is characterized immunohistochemically by diffuse CD99 expression and molecularly by one of several oncogenic translocations, most commonly t(11;22)(q24;q12) between the EWSR1 gene and the FLI1 gene. Here we present a rare case of Ewing’s sarcoma in the sinonasal tract with FUS-ERG gene arrangement that was regarded for almost a decade as a sinonasal-type hemangiopericytoma (glomangiopericytoma). This case illustrates the surprisingly prolonged natural history of Ewing’s sarcoma that did not receive therapy for many years and the importance of considering alternative genetic translocations. Our experience suggests that the presence of diffuse CD99 membranous staining pattern in a small blue round cell tumor with morphology typical for Ewing’s sarcoma but FISH negative for EWSR1 rearrangement should prompt consideration of FUS-ERG fusion.

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RASSF1A inhibits PDGFB-driven malignant phenotypes of nasopharyngeal carcinoma cells in a YAP1-dependent manner

Cell Death and Disease ◽

10.1038/s41419-020-03054-z ◽

2020 ◽

Vol 11 (10) ◽

Author(s):

Ying-Ying Liang ◽

Xu-Bin Deng ◽

Xian-Tao Lin ◽

Li-Li Jiang ◽

Xiao-Ting Huang ◽

...

Keyword(s):

Nasopharyngeal Carcinoma ◽

Underlying Mechanism ◽

Carcinoma Cells ◽

Dependent Manner ◽

Transcriptional Coactivator ◽

Actin Remodeling ◽

Aggressive Tumor ◽

Subunit B

Abstract Nasopharyngeal carcinoma (NPC) is a highly aggressive tumor characterized by distant metastasis. Deletion or down-regulation of the tumor suppressor protein ras-association domain family protein1 isoform A (RASSF1A) has been confirmed to be a key event in NPC progression; however, little is known about the effects or underlying mechanism of RASSF1A on the malignant phenotype. In the present study, we observed that RASSF1A expression inhibited the malignant phenotypes of NPC cells. Stable silencing of RASSF1A in NPC cell lines induced self-renewal properties and tumorigenicity in vivo/in vitro and the acquisition of an invasive phenotype in vitro. Mechanistically, RASSF1A inactivated Yes-associated Protein 1 (YAP1), a transcriptional coactivator, through actin remodeling, which further contributed to Platelet Derived Growth Factor Subunit B (PDGFB) transcription inhibition. Treatment with ectopic PDGFB partially increased the malignancy of NPC cells with transient knockdown of YAP1. Collectively, these findings suggest that RASSF1A inhibits malignant phenotypes by repressing PDGFB expression in a YAP1-dependent manner. PDGFB may serve as a potential interest of therapeutic regulators in patients with metastatic NPC.

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Primary Nongestational Choriocarcinoma of the Ovary

Journal of Enam Medical College ◽

10.3329/jemc.v4i1.18070 ◽

2014 ◽

Vol 4 (1) ◽

pp. 56-59

Author(s):

AMM Shariful Alam ◽

Syeda Nurjahan Bhuiyan ◽

Md Rashid Un Nabi

Keyword(s):

Germ Cell ◽

Combination Chemotherapy ◽

Single Agent ◽

Ovarian Pregnancy ◽

Cell Neoplasm ◽

Aggressive Tumor ◽

Single Agent Chemotherapy ◽

Disease Free ◽

Worse Prognosis ◽

Unmarried Girl

Pure primary ovarian choriocarcinoma is an extremely rare and aggressive tumor. It can be of gestational or nongestational in origin. The gestational type can arise from an ovarian pregnancy or can be of metastatic origin from uterine choriocarcinoma. The nongestational type is a very rare germ cell neoplasm. It is important to distinguish between two types of choriocarcinomas as nongestational origin is highly malignant and has worse prognosis than gestational type. But it is very difficult to differentiate by routine histological examination. Nongestational choriocarcinoma has been found to be resistant to single agent chemotherapy. It occurs usually around 13 years of age and is mainly confined to females under 20. Here we report a case of primary pure nongestational choriocarcinoma of the ovary in an unmarried girl of 14 years, diagnosed in 2001 and treated successfully with surgery and combination chemotherapy and remained disease-free till last reporting in September 2013. DOI: http://dx.doi.org/10.3329/jemc.v4i1.18070 J Enam Med Col 2014; 4(1): 56-59

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Glioma Revisited: From Neurogenesis and Cancer Stem Cells to the Epigenetic Regulation of the Niche

Journal of Oncology ◽

10.1155/2012/537861 ◽

2012 ◽

Vol 2012 ◽

pp. 1-20 ◽

Cited By ~ 17

Author(s):

Felipe de Almeida Sassi ◽

Algemir Lunardi Brunetto ◽

Gilberto Schwartsmann ◽

Rafael Roesler ◽

Ana Lucia Abujamra

Keyword(s):

Stem Cells ◽

Cancer Stem Cells ◽

Cellular Proliferation ◽

Survival Rates ◽

Comprehensive Analysis ◽

Heterogeneous Population ◽

Aggressive Tumor ◽

Epigenetic Modulation ◽

The Brain

Gliomas are the most incident brain tumor in adults. This malignancy has very low survival rates, even when combining radio- and chemotherapy. Among the gliomas, glioblastoma multiforme (GBM) is the most common and aggressive type, and patients frequently relapse or become refractory to conventional therapies. The fact that such an aggressive tumor can arise in such a carefully orchestrated organ, where cellular proliferation is barely needed to maintain its function, is a question that has intrigued scientists until very recently, when the discovery of the existence of proliferative cells in the brain overcame such challenges. Even so, the precise origin of gliomas still remains elusive. Thanks to new advents in molecular biology, researchers have been able to depict the first steps of glioma formation and to accumulate knowledge about how neural stem cells and its progenitors become gliomas. Indeed, GBM are composed of a very heterogeneous population of cells, which exhibit a plethora of tumorigenic properties, supporting the presence of cancer stem cells (CSCs) in these tumors. This paper provides a comprehensive analysis of how gliomas initiate and progress, taking into account the role of epigenetic modulation in the crosstalk of cancer cells with their environment.

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Temporal gliosarcoma: case report and review of literature

Romanian Neurosurgery ◽

10.1515/romneu-2015-0014 ◽

2015 ◽

Vol 22 (1) ◽

pp. 112-116

Author(s):

Amit Agrawal ◽

Vissa Shanthi ◽

Baddukonda Appala Ramakrishna ◽

Kuppili Venkata Murali Mohan

Keyword(s):

Case Report ◽

Median Survival ◽

Glial Cells ◽

Primary Tumor ◽

Clinical Presentation ◽

Spindle Cell ◽

Review Of Literature ◽

Future Studies ◽

Aggressive Tumor ◽

The Brain

Abstract First characterized by Stroebe, the gliosarcomas are highly malignant and rare primary tumor of the brain composed of neoplastic glial cells in association with spindle cell sarcomatous elements (biphasic tissue patterns). In spite of being recognized as two different pathologies studies have not shown any significant differences between gliosarcoma and glioblastoma with regard to age, sex, size, clinical presentation, and median survival. In summary, gliosarcoma is an aggressive tumor with a propensity to recur and re-grow with poor outcome. Future studies are needed to understand the true pathology of these biphasic tumors.

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