Assessment of microsatellite instability in colorectal carcinoma at an Indian center

Pandey, Vijay; Prabhu, Jyothi S; Payal, K; Rajan, Veena; C, Deepak; Barde, Shubhada; Jagannath, P.; Borges, Anita M.; Sridhar, T.S.

doi:10.1007/s00384-006-0241-3

Cited by 18 publications

(7 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…25 A recent study from north India by Dubey et al reported MSI-high in 22% patients. 26 Earlier, two studies from India by Pandey et al 27 and Malhotra et al 28 have reported MMR protein loss from 17.8-19.9%. But both had reported their study with only 2 antibodies, i.e.…”

Section: Discussionmentioning

confidence: 96%

Pattern of mismatch repair protein loss and its clinicopathological correlation in colorectal cancer in North India

et al. 2018

View full text Add to dashboard Cite

Background: To determine the mismatch repair (MMR) protein loss in colorectal cancer (CRC) in north Indian patients and its clinicopathological correlation. Methods: A prospective study on patients with colorectal cancer from a tertiary level hospital conducted between May 2014 and June 2015. MMR protein loss was determined using immunohistochemistry for MLH1, MSH2, PMS2 and MSH6. Results: 52 patients (38 male and 14 females) of CRC, with median age of 52.5 years who underwent resection form the study group. 18 (35%) patients were < 50 years of age. Family history of malignancy was present in 3 (6 %) patients. A total of 15 (29%) patients had loss of MMR protein of which 7 (46%) were < 50 years. Most common MMR loss was combined loss of MSH2 + MSH6 [6 (11.5%)] followed by isolated loss of PMS2 [5 (9.6%)]. MMR protein loss was more frequent in patients with right side colon cancer [12 (42%)] compared to left [3 (13%)] (p = 0.033). MMR protein loss was seen in 11 (34%) out of 32 patients fulfilling the revised Bethesda criteria compared to 4 (20%) out of 20 patients who did not fulfil the criteria (p = 0.352). Conclusion: This study demonstrates high frequency of MMR protein loss in colorectal cancer in north Indian patients which was more common in right colon cancer. Many patients having MMR protein loss do not satisfy the revised Bethesda criteria and would have been missed if selective testing was done. Further research and larger studies are required to validate these findings and develop India specific clinical criteria.

show abstract

Section: Discussionmentioning

confidence: 96%

Pattern of mismatch repair protein loss and its clinicopathological correlation in colorectal cancer in North India

et al. 2018

View full text Add to dashboard Cite

show abstract

“…Total RNA isolation, RT-PCR and quantitative PCR were performed as previously described (52)(53)(54). Primer sequences used were as previously described (39,52).…”

Section: Reverse Transcription Polymerase Chain Reaction (Rt-pcr) and Pcr Primersmentioning

confidence: 99%

ARTEMIN Promotes Oncogenicity and Resistance to 5-Fluorouracil in Colorectal Carcinoma by p44/42 MAPK Dependent Expression of CDH2

et al. 2021

Self Cite

View full text Add to dashboard Cite

ARTEMIN (ARTN), one of the glial-cell derived neurotrophic factor family of ligands, has been reported to be associated with a number of human malignancies. In this study, the enhanced expression of ARTN in colorectal carcinoma (CRC) was observed; the expression of ARTN positively correlated with lymph node metastases and advanced tumor stages and predicted poor prognosis. Forced expression of ARTN in CRC cells enhanced oncogenic behavior, mesenchymal phenotype, stem cell-like properties and tumor growth and metastasis in a xenograft model. These functions were conversely inhibited by depletion of endogenous ARTN. Forced expression of ARTN reduced the sensitivity of CRC cells to 5-FU treatment; and 5-FU resistant CRC cells harbored enhanced expression of ARTN. The oncogenic functions of ARTN were demonstrated to be mediated by p44/42 MAP kinase dependent expression of CDH2 (CADHERIN 2, also known as N-CADHERIN). Inhibition of p44/42 MAP kinase activity or siRNA mediated depletion of endogenous CDH2 reduced the enhanced oncogenicity and chemoresistance consequent to forced expression of ARTN induced cell functions; and forced expression of CDH2 rescued the reduced mesenchymal properties and resistance to 5-FU after ARTN depletion. In conclusion, ARTN may be of prognostic and theranostic utility in CRC.

show abstract

“…Western blot analysis: Western blot analysis was performed as previously described [ 22 , 35 ], using a primary monoclonal antibody against CCND1 and β-ACTIN obtained from Cell Signalling, Danvers, Massachusetts, USA. Quantification of blot was performed by use of ImageJ software from NIH, USA ( ) as described previously [ 27 , 29 , 30 ].…”

Section: Methodsmentioning

confidence: 99%

“…The predicted sizes of detected protein bands in kDa are shown on the left side. The average of three independent densitometry analyses of CCND1 and β-ACTIN is shown above (right side) by use of Image J software from NIH, USA ( ) as described previously [ 27 , 29 , 30 ].…”

Section: Figures Scheme and Tablesmentioning

confidence: 99%

Novel Biphenyl Amines Inhibit Oestrogen Receptor (ER)-α in ER-Positive Mammary Carcinoma Cells

et al. 2021

Self Cite

View full text Add to dashboard Cite

Herein, the activity of adamantanyl-tethered-biphenyl amines (ATBAs) as oestrogen receptor alpha (ERα) modulating ligands is reported. Using an ERα competitor assay it was demonstrated that ATBA compound 3-(adamantan-1-yl)-4-methoxy-N-(4-(trifluoromethyl) phenyl) aniline (AMTA) exhibited an inhibitory concentration 50% (IC50) value of 62.84 nM and demonstrated better binding affinity compared to tamoxifen (IC50 = 79.48 nM). Treatment of ERα positive (ER+) mammary carcinoma (MC) cells (Michigan Cancer Foundation-7 (MCF7)) with AMTA significantly decreased cell viability at an IC50 value of 6.4 μM. AMTA treatment of MC cell-generated three-dimensional (3D) spheroids resulted in significantly decreased cell viability. AMTA demonstrated a superior inhibitory effect compared to tamoxifen-treated MC cell spheroids. Subsequently, by use of an oestrogen response element (ERE) luciferase reporter construct, it was demonstrated that AMTA treatment significantly deceased ERE transcriptional activity in MC cells. Concordantly, AMTA treatment of MC cells also significantly decreased protein levels of oestrogen-regulated CCND1 in a dose-dependent manner. In silico molecular docking analysis suggested that AMTA compounds interact with the ligand-binding domain of ERα compared to the co-crystal ligand, 5-(4-hydroxyphenoxy)-6-(3-hydroxyphenyl)-7- methylnaphthalen-2-ol. Therefore, an analogue of AMTA may provide a structural basis to develop a newer class of ERα partial agonists.

show abstract

Assessment of microsatellite instability in colorectal carcinoma at an Indian center

Abstract: Our study indicates a similar rate of incidence of MSI in colorectal cancers in the Indian cohort compared to the West (10-15%) despite lower incidence of colorectal cancers and predominance of rectosigmoid tumors in the Indian population.

Cited by 18 publications

References 17 publications

Pattern of mismatch repair protein loss and its clinicopathological correlation in colorectal cancer in North India

Pattern of mismatch repair protein loss and its clinicopathological correlation in colorectal cancer in North India

ARTEMIN Promotes Oncogenicity and Resistance to 5-Fluorouracil in Colorectal Carcinoma by p44/42 MAPK Dependent Expression of CDH2

Novel Biphenyl Amines Inhibit Oestrogen Receptor (ER)-α in ER-Positive Mammary Carcinoma Cells

Contact Info

Product

Resources

About