Experimental Organism Ductal Cell Adenocarcinoma

Paget’s disease of the breast is a rare type of cancer of the nipple–areola complex and that is often associated with an underlying in situ or invasive carcinoma. It is often misdiagnosed as eczema of breast and treatment is delayed. Here we present a case where a 30 year old female presented with itching ulceration and destruction of her left nipple. She was treated initially by local physicians by applying local ointments but as her condition did not improve she was admitted to department of surgery Shaheed Suhrawardy Medical College hospital where she was diagnosed as Paget’s disease with infiltrating ductal cell carcinoma. She underwent modified radical mastectomy with axillary clearance and referred to oncology department for further management. J Shaheed Suhrawardy Med Coll, June 2019, Vol.11(1); 81-83

Download Full-text

Ductal Cell Reprogramming to Insulin-Producing Beta-Like Cells as a Potential Beta Cell Replacement Source for Chronic Pancreatitis

Current Stem Cell Research & Therapy ◽

10.2174/1574888x13666180918092729 ◽

2019 ◽

Vol 14 (1) ◽

pp. 65-74 ◽

Cited By ~ 7

Author(s):

Aravinth P. Jawahar ◽

Siddharth Narayanan ◽

Gopalakrishnan Loganathan ◽

Jithu Pradeep ◽

Gary C. Vitale ◽

...

Keyword(s):

Chronic Pancreatitis ◽

Beta Cell ◽

Lineage Tracing ◽

Clinical Tool ◽

Glucose Levels ◽

Ductal Cells ◽

Pancreatic Ductal Cells ◽

Insulin Producing Cells ◽

Ductal Cell ◽

Recent Advances

Islet cell auto-transplantation is a novel strategy for maintaining blood glucose levels and improving the quality of life in patients with chronic pancreatitis (CP). Despite the many recent advances associated with this therapy, obtaining a good yield of islet infusate still remains a pressing challenge. Reprogramming technology, by making use of the pancreatic exocrine compartment, can open the possibility of generating novel insulin-producing cells. Several lineage-tracing studies present evidence that exocrine cells undergo dedifferentiation into a progenitor-like state from which they can be manipulated to form insulin-producing cells. This review will present an overview of recent reports that demonstrate the potential of utilizing pancreatic ductal cells (PDCs) for reprogramming into insulin- producing cells, focusing on the recent advances and the conflicting views. A large pool of ductal cells is released along with islets during the human islet isolation process, but these cells are separated from the pure islets during the purification process. By identifying and improving existing ductal cell culture methods and developing a better understanding of mechanisms by which these cells can be manipulated to form hormone-producing islet-like cells, PDCs could prove to be a strong clinical tool in providing an alternative beta cell source, thus helping CP patients maintain their long-term glucose levels.

Download Full-text

TAZ inhibits acinar cell differentiation but promotes immature ductal cell proliferation in adult mouse salivary glands

Genes to Cells ◽

10.1111/gtc.12879 ◽

2021 ◽

Author(s):

Yosuke Miyachi ◽

Miki Nishio ◽

Junji Otani ◽

Shinji Matsumoto ◽

Akira Kikuchi ◽

...

Keyword(s):

Cell Proliferation ◽

Cell Differentiation ◽

Salivary Glands ◽

Acinar Cell ◽

Adult Mouse ◽

Ductal Cell

Download Full-text

The PDX1 Homeodomain Transcription Factor Negatively Regulates the Pancreatic Ductal Cell-specific Keratin 19 Promoter

Journal of Biological Chemistry ◽

10.1074/jbc.m605891200 ◽

2006 ◽

Vol 281 (50) ◽

pp. 38385-38395 ◽

Cited By ~ 25

Author(s):

Therese B. Deramaudt ◽

Mira M. Sachdeva ◽

Melanie P. Wescott ◽

Yuting Chen ◽

Doris A. Stoffers ◽

...

Keyword(s):

Transcription Factor ◽

Homeodomain Transcription Factor ◽

Keratin 19 ◽

Ductal Cell ◽

Pancreatic Ductal Cell

Download Full-text

The proportion of periportal mesenchyme to ductal epithelial cells acts as a proliferative rheostat in liver regeneration

10.1101/2020.09.21.306258 ◽

2020 ◽

Author(s):

Lucía Cordero-Espinoza ◽

Timo N. Kohler ◽

Anna M. Dowbaj ◽

Bernhard Strauss ◽

Olga Sarlidou ◽

...

Keyword(s):

Cell Proliferation ◽

Tissue Injury ◽

Portal Tract ◽

Mesenchymal Cells ◽

Dependent Manner ◽

Cell Contacts ◽

Ductal Cells ◽

Ductal Cell ◽

Cell Cell

AbstractIn the homeostatic liver, ductal cells intermingle with a microenvironment of endothelial and mesenchymal cells to form the functional unit of the portal tract. Ductal cells proliferate rarely in homeostasis but do so transiently after tissue injury to replenish any lost epithelium. We have shown that liver ductal cells can be expanded as liver organoids that recapitulate several of the cell-autonomous mechanisms of regeneration, but lack the stromal cell milieu of the biliary tract in vivo. Here, we describe a subpopulation of SCA1+ periportal mesenchymal cells that closely surrounds ductal cells in vivo and exerts a dual control on their proliferative capacity. Mesenchymal-secreted mitogens support liver organoid formation and expansion from differentiated ductal cells. However, direct mesenchymal-to-ductal cell-cell contact, established following a microfluidic co-encapsulation that enables the cells to self-organize into chimeric organoid structures, abolishes ductal cell proliferation in a mesenchyme-dose dependent manner. We found that it is the ratio between mesenchymal and epithelial cell contacts that determines the net outcome of ductal cell proliferation both in vitro, and in vivo, during damage-regeneration. SCA1+ mesenchymal cells control ductal cell proliferation dynamics by a mechanism involving, at least in part, Notch signalling activation. Our findings underscore how the relative abundance of cell-cell contacts between the epithelium and its mesenchymal microenvironment are key regulatory cues involved in the control of tissue regeneration.SummaryIn the homeostatic liver, the ductal epithelium intermingles with a microenvironment of stromal cells to form the functional unit of the portal tract. Ductal cells proliferate rarely in homeostasis but do so transiently after tissue injury. We have shown that these cells can be expanded as liver organoids that recapitulate several of the cell-autonomous mechanisms of regeneration, but lack the stromal cell milieu of the portal tract in vivo. Here, we describe a subpopulation of SCA1+ periportal mesenchymal niche cells that closely surrounds ductal cells in vivo and exerts a dual control on their proliferative capacity. Mesenchymal-secreted mitogens support liver organoid formation and expansion from differentiated ductal cells. However, direct mesenchymal-to-ductal cell-cell contact, established through a microfluidic co-encapsulation method that enables the cells to self-organize into chimeric organoid structures, abolishes ductal cell proliferation in a mesenchyme-dose dependent manner. We found that it is the ratio between mesenchymal and epithelial cell contacts that determines the net outcome of ductal cell proliferation both in vitro, and in vivo, during damage-regeneration. SCA1+ mesenchymal cells control ductal cell proliferation dynamics by a mechanism involving, at least in part, Notch signalling activation. Our findings re-evaluate the concept of the cellular niche, whereby the proportions of cell-cell contacts between the epithelium and its mesenchymal niche, and not the absolute cell numbers, are the key regulatory cues involved in the control of tissue regeneration.

Download Full-text