Meet Inspiring Speakers and Experts at our 3000+ Global Conference Series Events with over 1000+ Conferences, 1000+ Symposiums
and 1000+ Workshops on Medical, Pharma, Engineering, Science, Technology and Business.

Explore and learn more about Conference Series : World's leading Event Organizer

Back

Peter Stoemmer

Peter Stoemmer

Pathologie Augsburg, Germany

Title: Tumorbudding in Colorectal Carcinoma - Difficulties in Graduation and some Solutions

Biography

Biography: Peter Stoemmer

Abstract

Infiltration of tumorcells into the peritumoral tissue is one of the most outstanding features of malignancy and, in small tumors/ early tumorstages probably  of eminent prognostic relevance.

In colorectal carcinomas (CRCs), the graduation of the invasive potential is difficult and shows high interobserver variability, leading to several –not very convincing- attempts of standardization as a result of mixing different morphological and biochemical modes of invasion.

We analysed different morphological  patterns of invasion  in CRCs  in respect of morphogenous features and biological consequences: The expression of  proliferation markers, cell adhesion molecules adherins, and regulators  catenins,  and invadopia- associated markers like matrix metalloproteinases vinculin and the perinfiltrative  tumorstroma.

Materials and methods:

20 hot spots of tumorbuds  in  20 cases of CRCs  (400 POIs) were analysed in  FFPE,  5 ym

 IHC. Analysis of  E-Cadherin, N-Cadherin  withMoAbs   I5626  M0735-  DAKO North America, Carpinteria California); Ki-67,  CD44  with MoAb  (  IS2541  M0753   DAKO Denmark Glostrup)    Vinculin (PoAb E18720, Spring Bioscience, California)

Results

Tumorbudding (TB) in CRCs is part of the much more complex phenomenon of epithelial- mesenchymal transformation (EMT/TEM). Morphologically tumorbuds were classified in 4 different type:   monocellular and oligocellular , (2) trabecular, (3) tubular,  (4) irregular and sheetlike. They show different IHC results:

E-Cadherin expression and membranous ß.catenin are lost in (1)  and  (2) and diiminished in (3); it is well-expressed in (4)

N-Cadherin and nuclear ß-catenin are ncreased in (1), (2) and (3)

Vinculin and  CD 44,  markers of invadopodia ,  appperently do not play a significant role in tumorbudding.

Ki-67, a marker of  mitotic ability is highly  diminished  in (1) – (3)  and low in (4).

 

Conclusion

TB is not a simple  phenomenon of tumor- cellpropagation but  the result of a complete change of intracellular organisations with shift of cadherins and catenins;  these changes apparently block the mitotic activity of invading cells. Invasion by TB is in strict contrast to proliferation.

Devellopment of new therapies should keep in mind, that one can either block proliferation or propagation of malignant tumors.