POSTER ESSO 41 BORDEAUX- 0525 supplementary data and updates  by Sinziana Ionescu*

1.Consultant Surgeon at the General and Oncological Surgery Clinic I of the “Prof.Dr. Al. Trestioreanu ” Bucharest Oncology Institute, Bucharest, Romania;

2. University lecturer at -“Carol Davila” University of Medicine and Pharmacy, Bucharest, Romania

Pathology images depicting tumor response to radiotherapy in rectal cancer, images offered courtesy of dr Mihai Ceausu, associate professor at the Carol Davila University of Medicine and Pharmacy, Bucharest , Romania

Figure legend:
Moderately differentiated colo-rectal adenocarcinoma (G2):
-left panel: biopsy specimen – compact back-to-back tubulo-glandular structures with cribriform architecture, HE, 100x
-right panel: surgical excision specimen after radiotherapy – tumour necrosis associated with reactive fibrosis with residual adenocarcinoma outgrowing fibrosis (Mandard grade 4)

Preliminary results from our study

Our research focused on a  batch formed out of 29 patients diagnosed with rectal cancer(adenocarcinoma) which had received radiochemotherapy before the surgical intervention, under the form of a  neoadjuvant treatment. The post-radic changes of the following immunohistochemical markers were analyzed: MMP1, MMP2, MMP3, MMP9, MMP11, MMP13, p63, TIMP1, TIMP2, TIMP3, BCL- 2, Cycline D1, Vimentin, CEA, E-cadherin, p53, CK-7, CK-20.

Table with Statistics and marker  variation with radiochemotherapy in our batch (29 pts)


•  In conclusion, from the analysis of the group of 29 patients in whom other immunohistochemical markers were studied and their modifications with radiotherapy, the following markers showed significant variation:

•P53 varied the expression, involving the modification of the cellular repair behavior in case of cellular exposure to stress, in this case the “threat” of cellular injury being brought by the radiotherapy itself.

•MMP1 has increased expression with radiotherapy, also of statistically relevant value and since MMP1 is involved in extracellular matrix degradation and metastasis, then the immediate clinical involvement would be to be able to detect if radiotherapy does not increase the metastatic potential of cells, through this mechanism

•MMP13 was negative (became positive – »0) in most tumor cell nuclei of the tumor stroma, which would demonstrate an opposite effect to the previous one, namely the involvement of radiotherapy in decreasing the oncogenic potential.

•TIMP-1 can promote cell proliferation and in some cases may even acquire anti-apoptotic function; In our group, TIMP 1 was slightly positive with tumor radiotherapy, a result that is consistent with the results related to MMP-1

•TIMP-3 showed negativity (most values ​​became positive- »0) with statistical variation in both tumor and tumor stroma, and how the expression of this gene was generally correlated with the mitogenic response, then its decrease with Radiation therapy would lead to the reasoning that radiation therapy would inhibit tumor cell proliferation through this mechanism.

•The study is currently underway, with all the above presented elements being preliminary results.