Detection of bone marrow metastases in prostate cancer: Role of trephine biopsy and Immunohistochemistry

Bone marrow-derived mesenchymal stem cells (BMSCs) are an integral part of cancer microenvironment. We intend to clarify BMSC-derived exosomes’ role in prostate cancer. The exosomes miR-200c secreted by BMSCs were identified by electron microscopy. The mice tumor model was used to explore the role of miR-200c’s in tumor mice. Cell invasion was assessed by transwell assay and Wnt/β-catenin expression was measured by western blot. Exosomes miR-200c derived from BMSCs promoted tumor cell invasion and activated Wnt/β-catenin signaling. miR-200c targets CTTN-mediated cell signal transduction, and blocking CTTN expression can suppression miR-200c-mediated Wnt/β-catenin signal transduction and inhibit cell invasion. In conclusion, miR-200c regulates CTTN, thereby inducing Wnt/β-catenin signaling to enhance tumor growth.

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Expression of BCL-2 Oncoprotein and P53 Protein Accumulation in Bone Marrow Metastases of Androgen Independent Prostate Cancer

The Journal of Urology ◽

10.1097/00005392-199702000-00042 ◽

1997 ◽

pp. 569-574 ◽

Cited By ~ 2

Author(s):

Timothy J. McDonnel ◽

Nora M. Navone ◽

Patricia Troncoso ◽

Louis L. Pisters ◽

Claudio Conti ◽

...

Keyword(s):

Prostate Cancer ◽

Bone Marrow ◽

P53 Protein ◽

Protein Accumulation ◽

Bone Marrow Metastases ◽

Androgen Independent

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9240 POSTER Role of Routine Bone Marrow Trephine Biopsy and Flow Cytometry in Patients With Marginal Zone Lymphoma – a Comparative Analysis and Clinical Implications

European Journal of Cancer ◽

10.1016/s0959-8049(11)72505-9 ◽

2011 ◽

Vol 47 ◽

pp. S651

Author(s):

S.X. Koo ◽

G. Lai ◽

K. Tay ◽

S.T. Lim

Keyword(s):

Bone Marrow ◽

Flow Cytometry ◽

Comparative Analysis ◽

Marginal Zone ◽

Marginal Zone Lymphoma ◽

Clinical Implications ◽

Trephine Biopsy ◽

Bone Marrow Trephine ◽

Bone Marrow Trephine Biopsy

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Tyrosine Kinases Expressed in Vivo by Human Prostate Cancer Bone Marrow Metastases and Loss of the Type 1 Insulin-Like Growth Factor Receptor

American Journal Of Pathology ◽

10.1016/s0002-9440(10)65229-7 ◽

1999 ◽

Vol 155 (4) ◽

pp. 1271-1279 ◽

Cited By ~ 117

Author(s):

Andreas Chott ◽

Zijie Sun ◽

Daniel Morganstern ◽

Jing Pan ◽

Tong Li ◽

...

Keyword(s):

Prostate Cancer ◽

Bone Marrow ◽

Growth Factor ◽

Tyrosine Kinases ◽

Growth Factor Receptor ◽

Human Prostate ◽

Human Prostate Cancer ◽

Bone Marrow Metastases

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Diffuse bone marrow metastases from glioblastoma multiforme: The role of dural invasion

Human Pathology ◽

10.1016/s0046-8177(96)90376-7 ◽

1996 ◽

Vol 27 (2) ◽

pp. 197-201 ◽

Cited By ~ 18

Author(s):

B.K Kleinschmidt-Demasters

Keyword(s):

Bone Marrow ◽

Glioblastoma Multiforme ◽

Bone Marrow Metastases

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Prostate Cancer Dormancy and Reactivation in Bone Marrow

Journal of Clinical Medicine ◽

10.3390/jcm10122648 ◽

2021 ◽

Vol 10 (12) ◽

pp. 2648

Author(s):

Deepak K. Singh ◽

Vaibhav G. Patel ◽

William K. Oh ◽

Julio A. Aguirre-Ghiso

Keyword(s):

Prostate Cancer ◽

Bone Marrow ◽

Cancer Cells ◽

Unique Challenge ◽

Disease States ◽

Metastatic Cells ◽

Cancer Dormancy ◽

Major Organ ◽

Dynamic Interplay

Prostate cancer has a variable clinical course, ranging from curable local disease to lethal metastatic spread. Eradicating metastatic cells is a unique challenge that is rarely met with the available therapies. Thus, targeting prostate cancer cells in earlier disease states is a crucial window of opportunity. Interestingly, cancer cells migrate from their primary site during pre-cancerous and malignant phases to seed secondary organs. These cells, known as disseminated cancer cells (DCCs), may remain dormant for months or decades before activating to form metastases. Bone marrow, a dormancy-permissive site, is the major organ for housed DCCs and eventual metastases in prostate cancer. The dynamic interplay between DCCs and the primary tumor microenvironment (TME), as well as that between DCCs and the secondary organ niche, controls the conversion between states of dormancy and activation. Here, we discuss recent discoveries that have improved our understanding of dormancy signaling and the role of the TME in modulating the epigenetic reprogramming of DCCs. We offer potential strategies to target DCCs in prostate cancer.

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