• Colon cancer
• Early CRC
• Histological risk factors
• Lymph node metastases

• Humans
• Female
• Male
• Colonic Neoplasms/pathology
• Colonic Neoplasms/surgery
• Colonic Neoplasms/epidemiology
• Lymphatic Metastasis
• Aged
• Middle Aged
• Risk Factors
• Follow-Up Studies
• Prognosis
• Neoplasm Invasiveness
• Aged, 80 and over
• Cohort Studies
• Lymph Nodes/pathology
• Lymph Nodes/surgery
• Machine Learning
• Adult
• Netherlands/epidemiology
• Neoplasm Staging

• chinese population
• clinicopathological feature
• colorectal cancer
• genetic mutation
• msi

• Humans
• Proto-Oncogene Proteins B-raf/genetics
• Microsatellite Instability
• Proto-Oncogene Proteins p21(ras)/genetics
• Retrospective Studies
• Colorectal Neoplasms/epidemiology
• Colorectal Neoplasms/genetics
• Colorectal Neoplasms/pathology
• Mutation
• Adenocarcinoma, Mucinous
• Membrane Proteins/genetics
• GTP Phosphohydrolases/genetics

• Female
• Humans
• Middle Aged
• Aged
• MutL Protein Homolog 1/genetics
• MutL Protein Homolog 1/metabolism
• Colorectal Neoplasms, Hereditary Nonpolyposis/diagnosis
• Colorectal Neoplasms, Hereditary Nonpolyposis/genetics
• Genetic Testing
• Promoter Regions, Genetic
• Endometrial Neoplasms/diagnosis
• Endometrial Neoplasms/genetics
• Endometrial Neoplasms/pathology
• DNA Mismatch Repair/genetics
• Mismatch Repair Endonuclease PMS2/genetics
• Mismatch Repair Endonuclease PMS2/metabolism
• Germ-Line Mutation

• APC mutations
• BRAF mutation V600E
• colorectal cancer
• late onset colorectal cancer
• mismatch repair (MMR) deficiency

• Swim Across America
• Bloomberg∼Kimmel Institute for Cancer Immunotherapy, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University

• Colon cancer
• Elderly
• Geriatric assessment
• Older patient
• Rectal cancer

• Humans
• Proto-Oncogene Proteins B-raf/genetics
• Colorectal Neoplasms/diagnosis
• Retrospective Studies
• Proto-Oncogene Proteins p21(ras)/genetics
• Mutation
• Microsatellite Instability
• Colonic Neoplasms
• Rectal Neoplasms
• Oncologists
• Biomarkers

• P30 CA006927 NCI NIH HHS
• 3 P30 CA006927 Fox Chase Cancer Center

Recent studies have reported that immune checkpoint inhibitors are effective against various defective mismatch repair (dMMR)/microsatellite instability-high (MSI-H) cancers. A limited number of reports are available on the frequency of dMMR/MSI-H carcinoma in biliary tract cancer (BTC), describing its clinicopathological characteristics and prognosis. The latter carcinoma is also associated with Lynch syndrome (LS). The present study was performed to investigate the frequency of patients with dMMR/MSI-H in BTC and the clinical characteristics of BTC with dMMR/MSI-H in a single institution in Japan. A total of 116 patients with BTC who underwent curative surgical resection at Kagawa University Hospital between January 2008 and December 2017 were included. The protein expression levels of the mismatch repair (MMR) genes [mutL homolog 1 (MLH1), mismatch repair endonuclease PMS2 (PMS2), MutS homolog (MSH)2 and MSH6] were assessed by immunohistochemistry (IHC) using formalin-fixed paraffin-embedded tissue specimens. Subsequently, MSI testing was performed on patients who exhibited loss of MMR protein expression. Loss of expression of one or more proteins was detected in five cases (4.3%). Loss of MLH1/PMS2 expression was observed in one case of intrahepatic cholangiocarcinoma, whereas loss of PMS2 expression was noted in one case of perihilar cholangiocarcinoma. Loss of MSH2/MSH6 and MSH6 expression was noted in two cases of distal cholangiocarcinoma and loss of PMS2 expression in one case of ampullary carcinoma. Out of the five patients, two demonstrated MSI-H. Microsatellite stability was observed in two cases and for one case, no data were available. Two MSI-H cases were patients with loss of expression of MLH1/PMS2 and MSH2/MSH6. None of the five patients exhibited a past medical history or family history of suspected LS. The frequency of dMMR in BTC was ~5%, which was similar to that reported by similar studies performed in other countries. In the present study, IHC appeared to be more useful than MSI testing for detecting MMR abnormalities with regards to the detection rate. Furthermore, there may only be a limited number of patients with BTCs who are likely to benefit from the therapeutic effects of treatment with immune checkpoint inhibitors.

• Lynch syndrome
• biliary tract cancer
• defective mismatch repair
• immunohistochemistry
• microsatellite instability-high

With the advent of next-generation sequencing (NGS), The Cancer Genome Atlas (TCGA) research network has given gynecologic cancers molecular classifications, which impacts clinical practice more and more. New cancer treatments that identify and target pathogenic abnormalities of genes have been in rapid development. The most prominent progress in gynecologic cancers is the clinical efficacy of poly(ADP-ribose) polymerase (PARP) inhibitors, which have shown breakthrough benefits in reducing hazard ratios (HRs) (HRs between 0.2 and 0.4) of progression or death from BRCA1/2 mutated ovarian cancer. Immune checkpoint inhibition is also promising in cancers that harbor mismatch repair deficiency (dMMR)/microsatellite instability (MSI). In this review, we focus on the druggable genetic alterations in gynecologic cancers by summarizing literature findings and completed and ongoing clinical trials.

• endometrial cancer
• gynecologic cancer
• homologous recombination repair
• mismatch repair
• ovarian cancer

Black patients are diagnosed and die earlier of endometrial cancer in comparison with their White counterparts. Factors that have been implicated in this racial disparity, such as socioeconomic status, increased frequencies of more aggressive tumor histology, and comorbid conditions, do not account for all of the disparity. Molecular defects in the endometrial tumors likely also contribute to the more aggressive tumor biology and the patient disparities. In this study, we reviewed the published data of molecular characteristics of endometrial cancer in different races. The majority of the publications compare Black and White patients, and identify molecules and pathways that can be targeted with existing drugs. These findings encourage molecular profile studies comparing additional races and ethnicities, and development of race-specific treatments.

In contrast to the decline in incidence and mortality of most other cancers, these rates are rising for endometrial cancer. Black women with endometrial cancer have earlier diagnosis, more aggressive histology, advanced stage and worse outcomes compared with their White counterparts. Socioeconomic status, a higher incidence of aggressive histology, and comorbid conditions are known factors leading to racial disparity in patients with endometrial cancer; nevertheless, they do not account for the entire racial disparity; which emphasizes the roles of molecular, histopathological and genetic factors. We performed a comprehensive review of all published scientific literature up to January 2021 reporting histopathologic, genetic and molecular factors associated with racial disparities in patients with endometrial cancer. The interactions and pathways of molecules reported to have significant differential expression in endometrial cancers from Black and White patients were identified with Ingenuity Pathway Analysis. The majority of studies compared Black and White patients; however, limited data are available for other racial and ethnic groups. Reported differences that could account for the worse survival of Black endometrial cancer patients include more aggressive histopathologies and molecular alterations, including upregulation of molecules driving cell cycle progression, and p53 and HER2/NEU signaling. Several of these molecules are targeted by existing pharmaceuticals. These findings encourage further study and the development of race-specific treatment strategies.

• endometrial cancer
• histopathology
• molecular profile
• racial disparity
• targeted agents

• deficient mismatch repair
• gynecological cancers
• microsatellite instability

For pathologists, how to precisely diagnose cancer from microscopy slides of tumor tissue samples so that each patient may receive the optimal treatment for his specific type of disease is a major task. Recent research based on digital pathology image analysis enables new approaches to assess tumor-host interaction at a microscopic level. The current study applies a novel spatial analysis method which computes Immunogradient indicators to estimate the migration of immune cells towards the tumor across the tumor/stroma interface. These indicators, computed for two types of immune cells (CD8 and CD20), proved to be independent prognostic factors in this study of 87 patients with colorectal cancer. The indicators were combined with infiltrative tumor growth pattern, assessed by a pathologist, into a new immuno-interface score which enabled prediction of the patient survival independent of other clinical, pathology and molecular characteristics of the tumor. The study demonstrates the value of computational pathology to advance the precision of clinical decision-making.

Tumor-associated immune cells have been shown to predict patient outcome in colorectal (CRC) and other cancers. Spatial digital image analysis-based cell quantification increases the informative power delivered by tumor microenvironment features and leads to new prognostic scoring systems. In this study we evaluated the intratumoral density of immunohistochemically stained CD8, CD20 and CD68 cells in 87 cases of CRC (48 were microsatellite stable, MSS, and 39 had microsatellite instability, MSI) in both the intratumoral tumor tissue and within the tumor-stroma interface zone (IZ) which was extracted by a previously developed unbiased hexagonal grid analytics method. Indicators of immune-cell gradients across the extracted IZ were computed and explored along with absolute cell densities, clinicopathological and molecular data, including gene mutation (BRAF, KRAS, PIK3CA) and MSI status. Multiple regression modeling identified (p < 0.0001) three independent prognostic factors: CD8+ and CD20+ Immunogradient indicators, that reflect cell migration towards the tumor, were associated with improved patient survival, while the infiltrative tumor growth pattern was linked to worse patient outcome. These features were combined into CD8-CD20 Immunogradient and immuno-interface scores which outperformed both tumor-node-metastasis (TNM) staging and molecular characteristics, and importantly, revealed high prognostic value both in MSS and MSI CRCs.

• CD20
• CD8
• Immunogradient
• colorectal cancer
• immuno-interface score
• tumor growth pattern
• tumor infiltrating lymphocytes
• tumor microenvironment

The value of adjuvant chemotherapy in elderly patients has been the subject of many overviews, with opinions varying from “not effective”, since randomized trials have not been performed, to “as effective as in young individuals”, based upon many retrospective analyses of randomized trials that have included patients of all ages. In the absence of randomized trials performed specifically with elderly patients, retrospective analyses demonstrate that the influence on the time to tumour recurrence (TTR) may be the same as in young individuals, but that endpoints that include death for any reason, such as recurrence-free survival (RFS), disease-free survival (DFS), and overall survival (OS), are poorer in the elderly. This is particularly true if oxaliplatin has been part of the treatment. The need for adjuvant chemotherapy after colorectal cancer surgery in elderly patients is basically the same as that in younger patients. The reduction in recurrence risks may be similar, provided the chosen treatment is tolerated but survival gains are less. Adding oxaliplatin to a fluoropyrimidine is probably not beneficial in individuals above a biological age of approximately 70 years. If an oxaliplatin combination is administered to elderly patients, three months of therapy is in all probability the most realistic goal.

• adjuvant chemotherapy
• colorectal cancer
• elderly

In light of recent Food and Drug Administration (FDA) approval of immune checkpoint inhibitors for mismatch repair deficient (dMMR) malignancies, identifying patients with dMMR malignancies has become increasingly important. Although screening for dMMR in colorectal cancer (CRC) is recommended, it is less common for extracolonic gastrointestinal (GI) malignancies. At Stanford Comprehensive Cancer Institute (SCCI), all GI malignancies have been screened for dMMR via immunohistochemistry since January 2016.

In this study, we conducted a retrospective review of all patients with GI malignancies screened for dMMR between January 2016 and December 2017. Tumor sequencing was performed on cases negative for germline pathogenic variants where tumor material was available.

A total of 1425 consecutive GI malignancies were screened for dMMR at SCCI during the study period, and 1374 were included for analysis. dMMR was detected in 7.2% of all GI malignancies. We detected the highest prevalence of dMMR in gastric (15 of 150, 10.0%) followed by colorectal (63 of 694, 9.1%), pancreatic (13 of 244, 5.3%), and gastroesophageal malignancy (6 of 132, 4.5%) patients. Lynch syndrome was the most common etiology for dMMR in colorectal cancer (41.5%), double somatic (confirmed or possible) pathogenic variants the most common etiology in pancreatic cancer (44.4%), and somatic MLH1 hypermethylation the most common etiology in gastric (73.3%) and gastroesophageal cancer (83.3%).

Given the relatively high incidence of dMMR in GI malignancies, we recommend screening all GI malignancies. Our results suggest that although a rare occurrence, double somatic pathogenic variants may be a biologically significant pathway causing dMMR in pancreatic cancer.

Colorectal cancer (CRC) is increasingly appreciated as a heterogeneous disease, with factors such as microsatellite instability (MSI), cancer subsite within the colon versus rectum, and age of diagnosis associated with specific disease course and therapeutic response. Activating oncogenic mutations in KRAS and NRAS are common in CRC, driving tumor progression and influencing efficacy of both cytotoxic and targeted therapies. The RAS mutational spectrum differs substantially between tumors arising from distinct tissues. Structure-function analysis of relatively common somatic RAS mutations in G12, Q61, and other codons is characterized by differing potency and modes of action. Here we show the mutational profile of KRAS, NRAS, and the less common HRAS in 13,336 CRC tumors, comparing the frequency of specific mutations based on age of diagnosis, MSI status, and colon versus rectum subsite. We identify mutation hotspots, and unexpected differences in mutation spectrum, based on these clinical parameters.

Activating oncogenic mutations in KRAS and NRAS are common in colorectal cancer, which is a heterogenous disease. Here, the authors show that the RAS mutation spectrum is markedly different between colon and rectal cancer, and also different based on age of diagnosis and microsatellite instability.

• Endometrial cancer
• Genetics
• Obesity
• Targeted therapeutics

• Japan
• Korea
• T1 cancer
• colorectal cancer

• Age Factors
• Aged
• Aged, 80 and over
• Chemotherapy, Adjuvant/methods
• Colectomy
• Colorectal Neoplasms/epidemiology
• Colorectal Neoplasms/pathology
• Colorectal Neoplasms/therapy
• Female
• Humans
• Incidence
• Laparoscopy
• Male

• BRAF
• Biomarker stratification
• Colorectal cancer
• EGFR
• HER2
• Microsatellite instability
• Molecular subtypes
• Pathways
• Personalized medicine trials
• RAS
• Targeted therapy
• c-MET

• Cancer prevention
• Cancer therapy
• DNA damage
• Genomic instability
• Nutraceutical

• Centrosome/metabolism
• DNA Damage/genetics
• DNA Repair/genetics
• Diet
• Genomic Instability/drug effects
• Genomic Instability/genetics
• Humans
• Neoplasms/diet therapy
• Neoplasms/genetics
• Neoplasms/pathology
• Prognosis
• Telomerase/antagonists & inhibitors
• Telomerase/genetics

• R01CA172380 NCI NIH HHS
• R03 CA119310 NCI NIH HHS
• R13 CA119920 NCI NIH HHS
• R01 CA132996 NCI NIH HHS
• R01 CA166348 NCI NIH HHS
• RCIRFA0D09009 PHS HHS
• P01 AG024387 NIA NIH HHS
• P50 AT006268 NCCIH NIH HHS
• R21 CA188818 NCI NIH HHS
• 5R01 CA132996-03 NCI NIH HHS
• 1R01CA166348 NCI NIH HHS
• P30CA006973 NCI NIH HHS
• P30 CA006973 NCI NIH HHS
• R01 CA028704 NCI NIH HHS
• P30 DK079626 NIDDK NIH HHS
• P50 CA096784 NCI NIH HHS
• OBC 134038 CIHR
• R01 CA172380 NCI NIH HHS
• P50 DE019032 NIDCR NIH HHS
• R01 CA077355 NCI NIH HHS
• P01 CA077664 NCI NIH HHS

Classification of cancer patients using traditional methods is a challenging task in the medical practice. Owing to rapid advances in microarray technologies, currently expression levels of thousands of genes from individual cancer patients can be measured. The classification of cancer patients by supervised statistical learning algorithms using the gene expression datasets provides an alternative to the traditional methods. Here we present a new network-based supervised classification technique, namely the NBC method. We compare NBC to five traditional classification techniques (support vector machines (SVM), k-nearest neighbor (kNN), naïve Bayes (NB), C4.5, and random forest (RF)) using 50–300 genes selected by five feature selection methods. Our results on five large cancer datasets demonstrate that NBC method outperforms traditional classification techniques. Our analysis suggests that using symmetrical uncertainty (SU) feature selection method with NBC method provides the most accurate classification strategy. Finally, in-depth analysis of the correlation-based co-expression networks chosen by our network-based classifier in different cancer classes shows that there are drastic changes in the network models of different cancer types.

• cancer classification
• comparison of classification techniques
• comparison of feature selection techniques
• feature selection
• network-based cancer prediction

• Adenoma
• Elderly
• Gender
• Proximal colon

• Colorectal Cancer
• Genetic
• Lynch-Like Syndrome
• Mismatch Repair Deficiency

The identification of mismatch-repair (MMR) defective colon cancer is clinically relevant for diagnostic, prognostic and potentially also for treatment predictive purposes. Preselection of tumors for MMR analysis can be obtained with predictive models, which need to demonstrate ease of application and favorable reproducibility.

We validated the MMR index for the identification of prognostically favorable MMR deficient colon cancers and compared performance to 5 other prediction models. In total, 474 colon cancers diagnosed ≥ age 50 were evaluated with correlation between clinicopathologic variables and immunohistochemical MMR protein expression.

Female sex, age ≥60 years, proximal tumor location, expanding growth pattern, lack of dirty necrosis, mucinous differentiation and presence of tumor-infiltrating lymphocytes significantly correlated with MMR deficiency. Presence of at least 4 of the MMR index factors identified MMR deficient tumors with 93% sensitivity and 76% specificity and showed favorable reproducibility with a kappa value of 0.88. The MMR index also performed favorably when compared to 5 other predictive models.

The MMR index is easy to apply and efficiently identifies MMR defective colon cancers with high sensitivity and specificity. The model shows stable performance with low inter-observer variability and favorable performance when compared to other MMR predictive models.

• Adenoma-carcinoma sequence
• Colorectal carcinoma
• Microsatellite instability
• Mismatch repair
• Mucin 2
• Mucin 5AC
• Pathogenesis
• Poorly differentiated adenocarcinoma
• Prognosis

• Adenocarcinoma/diagnosis
• Adenocarcinoma/metabolism
• Adenocarcinoma/pathology
• Adenocarcinoma, Mucinous/diagnosis
• Adenocarcinoma, Mucinous/metabolism
• Adenocarcinoma, Mucinous/pathology
• Adult
• Aged
• Aged, 80 and over
• Carcinoma, Signet Ring Cell/diagnosis
• Carcinoma, Signet Ring Cell/metabolism
• Carcinoma, Signet Ring Cell/pathology
• Colorectal Neoplasms/diagnosis
• Colorectal Neoplasms/metabolism
• Colorectal Neoplasms/pathology
• Diagnosis, Differential
• Female
• Humans
• Male
• Middle Aged
• Mucin 5AC/metabolism
• Mucin-2/metabolism
• Mucins/metabolism
• Phenotype
• Prognosis
• Retrospective Studies

• CHEK2
• EPCAM
• Lynch syndrome
• hereditary nonpolyposis colorectal cancer
• microsatellite instability
• mismatch repair

• Adult
• Aged
• Aged, 80 and over
• Biomarkers, Tumor/metabolism
• CDX2 Transcription Factor
• Colorectal Neoplasms/genetics
• Colorectal Neoplasms/immunology
• Colorectal Neoplasms/metabolism
• Colorectal Neoplasms/pathology
• CpG Islands/genetics
• DNA Methylation
• DNA, Neoplasm/genetics
• Female
• Homeodomain Proteins/metabolism
• Humans
• Lymphocytes, Tumor-Infiltrating/immunology
• Male
• Microsatellite Instability
• Middle Aged
• Mutation
• Neoplasm Proteins/metabolism
• Phenotype
• Proto-Oncogene Proteins/genetics
• Proto-Oncogene Proteins B-raf/genetics
• Proto-Oncogene Proteins p21(ras)
• Retrospective Studies
• ras Proteins/genetics

• Aged
• Aged, 80 and over
• Aging/physiology
• Female
• Humans
• Male
• Neoplasms/pathology

• lynch syndrome
• dna mismatch repair
• hereditary nonpolyposis colorectal cancer

To investigate the etiology of MLH1 promoter methylation in mismatch repair (MMR) mutation-negative early onset MSI-H colon cancer. As this type of colon cancer is associated with high ages, young patients bearing this type of malignancy are rare and could provide additional insight into the etiology of sporadic MSI-H colon cancer.

We studied a set of 46 MSI-H colon tumors cases with MLH1 promoter methylation which was enriched for patients with an age of onset below 50 years (n = 13). Tumors were tested for CIMP marker methylation and mutations linked to methylation: BRAF, KRAS, GADD45A and the MLH1 -93G>A polymorphism. When available, normal colon and leukocyte DNA was tested for GADD45A mutations and germline MLH1 methylation. SNP array analysis was performed on a subset of tumors.

We identified two cases (33 and 60 years) with MLH1 germline promoter methylation. BRAF mutations were less frequent in colon cancer patients below 50 years relative to patients above 50 years (p-value: 0.044). CIMP-high was infrequent and related to BRAF mutations in patients below 50 years. In comparison with published controls the G>A polymorphism was associated with our cohort. Although similar distribution of the pathogenic A allele was observed in the patients with an age of onset above and below 50 years, the significance for the association was lost for the group under 50 years. GADD45A sequencing yielded an unclassified variant. Tumors from both age groups showed infrequent copy number changes and loss-of-heterozygosity.

Somatic or germline GADD45A mutations did not explain sporadic MSI-H colon cancer. Although germline MLH1 methylation was found in two individuals, locus-specific somatic MLH1 hypermethylation explained the majority of sporadic early onset MSI-H colon cancer cases. Our data do not suggest an intrinsic tendency for CpG island hypermethylation in these early onset MSI-H tumors other than through somatic mutation of BRAF.

• protease inhibitor
• microsatellite instability
• dna mismatch repair
• smoking

• Adult
• Case-Control Studies
• Colonic Neoplasms/complications
• Colonic Neoplasms/genetics
• Colonic Neoplasms/pathology
• DNA Mismatch Repair
• Family
• Female
• Humans
• Immunohistochemistry
• Male
• Middle Aged
• Odds Ratio
• Registries
• Risk Factors
• Smoking/adverse effects
• alpha 1-Antitrypsin Deficiency/complications
• alpha 1-Antitrypsin Deficiency/pathology

• U01 CA074799 NCI NIH HHS
• UO1 CA074799 NCI NIH HHS
• U01 CA074800-03S1 NCI NIH HHS
• U01 CA074794 NCI NIH HHS
• #CA-95-011 NCI NIH HHS
• U01 CA097735 NCI NIH HHS
• U01 CA074800-08 NCI NIH HHS
• UO1 CA074794 NCI NIH HHS
• U01 CA074783 NCI NIH HHS
• U01 CA074806 NCI NIH HHS
• U01 CA074800 NCI NIH HHS
• UO1 CA074800 NCI NIH HHS
• U01 CA074800-09 NCI NIH HHS
• U01 CA074800-07 NCI NIH HHS
• CA074806 NCI NIH HHS
• UO1 CA097735 NCI NIH HHS
• UO1 CA074783 NCI NIH HHS

AIM: To investigate the role of mismatch repair genes human mutL homolog 1 (hMLH1) and human mutL homolog 2 (hMSH2) in the carcinogenesis of gastric cancer.

METHODS: A total of 40 gastric cancer patients who underwent surgical resection at our hospital were included in the study, of which 33 were pathologically diagnosed as adenocarcinoma, and 7 as mucinous adenocarcinoma. All the patients did not underwent preoperative chemotherapy or immunotherapy. The gastric cancer specimens, matched cancer-adjacent tissue specimens, and 20 chronic gastritis mucosa specimens (10 diagnosed as chronic superficial gastritis by gastroscopic biopsy, and 10 as chronic atrophic gastritis) were collected. The expression of hMLH1 and hMSH2 proteins in these specimens was detected by Western blot.

RESULTS: The positive rate of hMSH2 expression in cancer tissue was significantly higher than those in cancer-adjacent tissue and gastritis mucosa tissue (0.28 ± 0.10 vs 0.23 ± 0.07 and 0.11 ± 0.10, respectively; both P < 0.01). The positive rate of hMLH1 expression in cancer tissue was significantly lower than those in cancer-adjacent tissue and gastritis mucosa tissue (0.22 ± 0.06 vs 0.28 ± 0.07, 0.26 ± 0.06, both P < 0.01). The positive rates of hMLH1 and hMSH2 expression were not correlated with various clinicopathological parameters in gastric cancer.

CONCLUSION: High hMSH2 expression and low hMLH1 expression may be potential markers for prediction of the development of gastric cancer.

• Gastric cancer
• hMLH1
• hMSH2
• Western blot