Radioimmunodetection of human colon cancer in nude mice by a new monoclonal antibody A7 against human colorectal cancer

1991 ◽  
Vol 18 (8) ◽  
pp. 847-853
Author(s):  
Shuji Kojima ◽  
Noriko Shimura ◽  
Akiko Kubodera ◽  
Kazuhiko Kubota ◽  
Toshio Takahashi ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Monoclonal Antibody ◽  
Colon Cancer ◽  
Nude Mice ◽  
Human Colon ◽  
Human Colorectal Cancer ◽  
Human Colon Cancer ◽  
Monoclonal Antibody A7

Immunoscintigraphy of human colon cancer xenografts in nude mice using a second-generation TAG-72 monoclonal antibody labelled with 99Tcm

1994 ◽  
Vol 15 (5) ◽  
pp. 379-387???387 ◽  
Author(s):  
R. M. REILLY ◽  
K. NG ◽  
J. POLIHRONIS ◽  
B. SHPITZ ◽  
W. M. NGAI ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Colon Cancer ◽  
Nude Mice ◽  
Second Generation ◽  
Human Colon ◽  
Human Colon Cancer

In vitro and in vivo activities of KRN330, a fully human monoclonal antibody against colon cancer.

2011 ◽  
Vol 29 (4_suppl) ◽  
pp. 432-432 ◽  
Author(s):  
N. Sawada ◽  
E. Taguchi ◽  
M. Takahashi
Keyword(s):  
Colorectal Cancer ◽  
Monoclonal Antibody ◽  
Colon Cancer ◽  
Western Blot ◽  
Human Colon ◽  
Human Colorectal Cancer ◽  
Antitumor Activities ◽  
Reducing Condition

432 Background: KRN330 is a novel recombinant human IgG1 monoclonal antibody (mAb) targeting A33 surface differentiation antigen that is uniformly expressed on the surface of 95% of colorectal cancer (CRC) cells. In this study, we characterized the activity of KRN330 for its in vitro properties, as well as for its in vivo antitumor activity. Methods: A kinetic analysis of the interaction between KRN330 and recombinant human A33 was conducted using a Biacore 3000. Western blot analysis was conducted using A33 expressing COLO205 lysates under reducing and non-reducing conditions. Binding of KRN330 to human colorectal cancer tissues were investigated using FITC-labeled KRN330. We also developed more conventional staining methods of A33 and investigated A33 expression using human colon cancer tissue microarray (TMA). ADCC and CDC activities of KRN330 were assessed using a standard 51Cr release assay. A33 expression levels of 14 CRC cell lines were analyzed using flow cytometer. In vivo antitumor activities of KRN330 alone or in combination with chemotherapeutic agents against subcutaneous or intraperiotoneal human CRC (COLO205 and LS174T) models were investigated using mice and rats xenograft model. Results: A kinetic analysis revealed that KRN330 showed a high binding affinity to A33. Western blot analysis also showed that antibody recognized not any protein under reducing condition, but non-reducing condition. A33 staining of TMA with 204 different samples revealed the majority of tumor expressed A33. KRN330 exhibited ADCC activity against A33 expressing human colorectal cancer cell lines which include both K-ras wild and mutated types. KRN330 showed dose-dependent antitumor activities in vivo. KRN330 also significantly prolonged survival of human colon tumor bearing mice. In addition, combination treatment of KRN330 with irinotecan showed increased antitumor activitiy and prolongation of survival, compared to either irinotecan or KRN330 alone. Conclusions: These results suggest that KRN330 is a promising candidate of novel therapy for CRC. The phase I/II study of KRN330 plus irinotecan in patients with second line metastatic CRC is ongoing. [Table: see text]

Biodistribution of radiolabeled monoclonal antibody after intraperitoneal administration in nude mice with hepatic metastasis from human colon cancer

Surgery Today ◽  
1992 ◽  
Vol 22 (2) ◽  
pp. 155-158 ◽  
Author(s):  
Kazuhiko Yoshida ◽  
Touru Fujikawa ◽  
George Yoshizawa ◽  
Akihiro Tanabea ◽  
Kenji Sakurai
Keyword(s):  
Monoclonal Antibody ◽  
Colon Cancer ◽  
Nude Mice ◽  
Hepatic Metastasis ◽  
Intraperitoneal Administration ◽  
Human Colon ◽  
Human Colon Cancer

Inhibition of hepatic metastases of human colon cancer in nude mice by a chimeric SF-25 monoclonal antibody

1995 ◽  
Vol 108 (1) ◽  
pp. 172-182 ◽  
Author(s):  
Hiroshi Takahashi ◽  
Tetsuya Nakada ◽  
Motoe Nakaki ◽  
Jack R. Wands
Keyword(s):  
Monoclonal Antibody ◽  
Colon Cancer ◽  
Nude Mice ◽  
Hepatic Metastases ◽  
Human Colon ◽  
Human Colon Cancer

Immunohistochemical detection of biotinlabeled murine monoclonal antibody in nude mice transplanted with human colon cancer

1989 ◽  
Vol 24 (1) ◽  
pp. 22-24
Author(s):  
Takashi Yokota ◽  
Toshio Takahashi ◽  
Toshiharu Yamaguchi ◽  
Kazuya Kitamura ◽  
Kiyoshi Sawai
Keyword(s):  
Monoclonal Antibody ◽  
Colon Cancer ◽  
Nude Mice ◽  
Human Colon ◽  
Murine Monoclonal Antibody ◽  
Immunohistochemical Detection ◽  
Human Colon Cancer

scholarly journals Olaparib-mediated enhancement of 5-fluorouracil cytotoxicity in mismatch repair deficient colorectal cancer cells

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Helena de Castro e Gloria ◽  
Laura Jesuíno Nogueira ◽  
Patrícia Bencke Grudzinski ◽  
Paola Victória da Costa Ghignatti ◽  
Temenouga Nikolova Guecheva ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Colon Cancer ◽  
Dna Damage ◽  
Cancer Cells ◽  
Mismatch Repair ◽  
Cell Cycle Progression ◽  
Combined Therapy ◽  
Combined Treatment ◽  
Human Colon ◽  
Human Colon Cancer

Abstract Background The advances in colorectal cancer (CRC) treatment include the identification of deficiencies in Mismatch Repair (MMR) pathway to predict the benefit of adjuvant 5-fluorouracil (5-FU) and oxaliplatin for stage II CRC and immunotherapy. Defective MMR contributes to chemoresistance in CRC. A growing body of evidence supports the role of Poly-(ADP-ribose) polymerase (PARP) inhibitors, such as Olaparib, in the treatment of different subsets of cancer beyond the tumors with homologous recombination deficiencies. In this work we evaluated the effect of Olaparib on 5-FU cytotoxicity in MMR-deficient and proficient CRC cells and the mechanisms involved. Methods Human colon cancer cell lines, proficient (HT29) and deficient (HCT116) in MMR, were treated with 5-FU and Olaparib. Cytotoxicity was assessed by MTT and clonogenic assays, apoptosis induction and cell cycle progression by flow cytometry, DNA damage by comet assay. Adhesion and transwell migration assays were also performed. Results Our results showed enhancement of the 5-FU citotoxicity by Olaparib in MMR-deficient HCT116 colon cancer cells. Moreover, the combined treatment with Olaparib and 5-FU induced G2/M arrest, apoptosis and polyploidy in these cells. In MMR proficient HT29 cells, the Olaparib alone reduced clonogenic survival, induced DNA damage accumulation and decreased the adhesion and migration capacities. Conclusion Our results suggest benefits of Olaparib inclusion in CRC treatment, as combination with 5-FU for MMR deficient CRC and as monotherapy for MMR proficient CRC. Thus, combined therapy with Olaparib could be a strategy to overcome 5-FU chemotherapeutic resistance in MMR-deficient CRC.

scholarly journals Animal models of gastrointestinal and liver diseases. New mouse models for studying dietary prevention of colorectal cancer

2014 ◽  
Vol 307 (3) ◽  
pp. G249-G259 ◽  
Author(s):  
James C. Fleet
Keyword(s):  
Colorectal Cancer ◽  
Colon Cancer ◽  
Mouse Models ◽  
Human Colon ◽  
Low Grade ◽  
Preclinical Models ◽  
Dietary Interventions ◽  
Single Model ◽  
Human Colon Cancer ◽  
Molecular Etiology

Colorectal cancer is a heterogeneous disease that is one of the major causes of cancer death in the U.S. There is evidence that lifestyle factors like diet can modulate the course of this disease. Demonstrating the benefit and mechanism of action of dietary interventions against colon cancer will require studies in preclinical models. Many mouse models have been developed to study colon cancer but no single model can reflect all types of colon cancer in terms of molecular etiology. In addition, many models develop only low-grade cancers and are confounded by development of the disease outside of the colon. This review will discuss how mice can be used to model human colon cancer and it will describe a variety of new mouse models that develop colon-restricted cancer as well as more advanced phenotypes for studies of late-state disease.

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