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Article ; Online: Mismatch repair deficiencies transforming stem cells into cancer stem cells and therapeutic implications.

Vaish, Minal

Molecular cancer

2007 Volume 6, Page(s) 26

Abstract: For the exceptional self-renewal capacity, regulated cell proliferation and differential potential to a wide variety of cell types, the stem cells must maintain the intact genome. The cells under continuous exogenous and endogenous genotoxic stress ... ...

Abstract	For the exceptional self-renewal capacity, regulated cell proliferation and differential potential to a wide variety of cell types, the stem cells must maintain the intact genome. The cells under continuous exogenous and endogenous genotoxic stress accumulate DNA errors, drive proliferative expansion and transform into cancer stem cells with a heterogeneous population of tumor cells. These cells are a common phenomenon for the hematological malignancies and solid tumors. In response to DNA damage, the complex cellular mechanisms including cell cycle arrest, transcription induction and DNA repair are activated. The cells when exposed to cytotoxic agents, the apoptosis lead to cell death. However, the absence of repair machinery makes the cells resistant to tumor sensitizing agents and result in malignant transformation. Mismatch repair gene defects are recently identified in hematopoietic malignancies, leukemia and lymphoma cell lines. This review emphasizes the importance of MMR systems in maintaining the stem cell functioning and its therapeutic implications in the eradication of cancer stem cells and differentiated tumor cells as well. The understanding of the biological functions of mismatch repair in the stem cells and its malignant counterparts could help in developing an effective novel therapies leaving residual non-tumorigenic population of cells resulting in potential cancer cures.
MeSH term(s)	Animals ; Biomarkers, Tumor/metabolism ; Cell Transformation, Neoplastic/drug effects ; DNA Mismatch Repair ; Humans ; Neoplasms/therapy ; Neoplastic Stem Cells/drug effects ; Neoplastic Stem Cells/metabolism ; Neoplastic Stem Cells/pathology
Chemical Substances	Biomarkers, Tumor
Language	English
Publishing date	2007-04-02
Publishing country	England
Document type	Journal Article ; Review
ISSN	1476-4598
ISSN (online)	1476-4598
DOI	10.1186/1476-4598-6-26
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Article ; Online: Mismatch repair deficiencies transforming stem cells into cancer stem cells and therapeutic implications

Vaish Minal

Molecular Cancer, Vol 6, Iss 1, p

2007 Volume 26

Abstract: Abstract For the exceptional self-renewal capacity, regulated cell proliferation and differential potential to a wide variety of cell types, the stem cells must maintain the intact genome. The cells under continuous exogenous and endogenous genotoxic ... ...

Abstract	Abstract For the exceptional self-renewal capacity, regulated cell proliferation and differential potential to a wide variety of cell types, the stem cells must maintain the intact genome. The cells under continuous exogenous and endogenous genotoxic stress accumulate DNA errors, drive proliferative expansion and transform into cancer stem cells with a heterogeneous population of tumor cells. These cells are a common phenomenon for the hematological malignancies and solid tumors. In response to DNA damage, the complex cellular mechanisms including cell cycle arrest, transcription induction and DNA repair are activated. The cells when exposed to cytotoxic agents, the apoptosis lead to cell death. However, the absence of repair machinery makes the cells resistant to tumor sensitizing agents and result in malignant transformation. Mismatch repair gene defects are recently identified in hematopoietic malignancies, leukemia and lymphoma cell lines. This review emphasizes the importance of MMR systems in maintaining the stem cell functioning and its therapeutic implications in the eradication of cancer stem cells and differentiated tumor cells as well. The understanding of the biological functions of mismatch repair in the stem cells and its malignant counterparts could help in developing an effective novel therapies leaving residual non-tumorigenic population of cells resulting in potential cancer cures.
Keywords	Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; RC254-282 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Oncology ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
Subject code	610
Language	English
Publishing date	2007-04-01T00:00:00Z
Publisher	BioMed Central
Document type	Article ; Online
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Article: Evaluation of microsatellite instability in tumors of central nervous system: A pilot study.

Vaish, Minal / Kumar, Raj / Mittal, R D / Mittal, Balraj

Indian journal of clinical biochemistry : IJCB

2012 Volume 19, Issue 2, Page(s) 156–162

Abstract: Microsatellite instability (MSI) characterized by alterations at simple repetitive genomic sequences is a distinct mechanism in tumorogenesis. Central nervous system (CNS) tumors have been reported to exhibit MSI, indicator of defective mismatch repair ... ...

Abstract	Microsatellite instability (MSI) characterized by alterations at simple repetitive genomic sequences is a distinct mechanism in tumorogenesis. Central nervous system (CNS) tumors have been reported to exhibit MSI, indicator of defective mismatch repair system with controversies. The present study was undertaken to examine sixteen primary brain and two spinal tumors for MSI at six mono: BAT-26, BAT-40, BAX, TGFßRII, IGFIIR and hMSH3 and four dinucleotide loci: D2S123, D9S1851, D9S283 and D18S58. Polymerase chain reaction (PCR) was done to amplify tumour and blood DNA, analyzed on 8% denaturing Polyacrylamide gel followed by autoradiography. Out of 18 CNS tumors examined, 39% exhibited MSI at BAT-26, BAT-40, D9S1851, D9S283 and D18S58 in tumoral DNA. However, no alteration was observed at BAX, TGFßRII, IGFIIR, hMSH3 and D2S123 loci. Low incidence of MS1-high hypothesizes role of MSI in evolution of CNS tumors but not in cancer initiation or progression.
Language	English
Publishing date	2012-08-24
Publishing country	India
Document type	Journal Article
ZDB-ID	1033583-3
ISSN	0974-0422 ; 0970-1915
ISSN (online)	0974-0422
ISSN	0970-1915
DOI	10.1007/BF02894277
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Article: DNA mismatch repair, microsatellite instability and cancer.

Vaish, Minal / Mittal, B

Indian journal of experimental biology

2002 Volume 40, Issue 9, Page(s) 989–994

Abstract: Mismatch (MMR) repair system plays a significant role in restoration of stability in the genome. Mutations in mismatch repair genes hamper their activity thus bring about a defect in mismatch repair (MMR) mechanism thereby conferring instability in the ... ...

Abstract	Mismatch (MMR) repair system plays a significant role in restoration of stability in the genome. Mutations in mismatch repair genes hamper their activity thus bring about a defect in mismatch repair (MMR) mechanism thereby conferring instability in the microsatellite sequences of both the coding and non-coding regions of the genome. Mutated mismatch repair genes result in the expansion or contraction of microsatellite sequence and confer microsatellite unstable or replication error positive phenotype. Hypermethylation of promoter regions of some of the MMR genes also causes inactivation of these genes and thus contribute to MSI. Microsatellite instability is an indicator of MMR deficiency and is a prime cause of varied tumorogenesis.
MeSH term(s)	Animals ; Base Pair Mismatch/genetics ; DNA Damage ; DNA Methylation ; DNA Repair ; DNA Replication ; Humans ; Loss of Heterozygosity ; Microsatellite Repeats ; Mutation ; Neoplasms/diagnosis ; Neoplasms/genetics ; Neoplasms/therapy ; Phenotype
Language	English
Publishing date	2002-09
Publishing country	India
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	416061-7
ISSN	0975-1009 ; 0019-5189
ISSN (online)	0975-1009
ISSN	0019-5189
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Article ; Online: Microsatellite instability as prognostic marker in bladder tumors

Mittal RD / Mandhani Anil / Vaish Minal / Mittal Balraj

BMC Urology, Vol 5, Iss 1, p

a clinical significance

2005 Volume 2

Abstract: Abstract Background Carcinoma of urinary bladder is one of the leading causes of death in India. Successful treatment of bladder cancer depends on the early detection & specific diagnostic approaches. In the present study, microsatellite instability (MSI) ...

Abstract	Abstract Background Carcinoma of urinary bladder is one of the leading causes of death in India. Successful treatment of bladder cancer depends on the early detection & specific diagnostic approaches. In the present study, microsatellite instability (MSI) has been evaluated as a prognostic marker in patients with superficial urinary bladder cancer in lower urinary tract for determining risk of recurrence. Methods A total of 44 patients with bladder tumors diagnosed with Transitional Cell Carcinomas [TCC] from lower urinary tract were selected for the study. Tumors were staged and graded according to AJCC-UICC (1997) classification and patients were followed with cystoscopy as per the protocol. Polymerase chain reaction (PCR) was done to amplify microsatellite sequences at mononucleotide BAT – 26, BAT – 40, TGFβ RII, IGFIIR, hMSH3, BAX and dinucleotide D2S123, D9S283, D9S1851 and D18S58 loci in blood (control) and tumor DNA. PCR products were separated on 8% denaturing polyacrylamide gel and visualized by autoradiography. Results MSI was observed in 72.7% of tumors at BAT – 26, BAT – 40, D2S123, D9S283, D9S1851 and D18S58 loci. Good association of MSI was seen with tumor stage and grade. MSI – High (instability at > 30% of loci) was frequently observed in high stage (40.6%) and high grade (59.4%) tumors. Of 24 tumors of Ta-T1 stage with different grades, 11 (9/18 high grade and 2/6 low grade tumors) recurred in the mean duration of 36 months. MSI positivity was significantly high in patients who had one or more recurrences (p = 0.02 for high grade and 0.04 for low grade tumors). Conclusions MSI may be an independent prognostic marker for assessing risk of recurrence in superficial tumors irrespective of the grade. Further studies on progression would help in stratifying the patients of T1G3 for early cystectomy vs bladder preservation protocol.
Keywords	Diseases of the genitourinary system. Urology ; RC870-923 ; Specialties of internal medicine ; RC581-951 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Urology ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
Subject code	616 ; 610
Language	English
Publishing date	2005-01-01T00:00:00Z
Publisher	BioMed Central
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Microsatellite instability as prognostic marker in bladder tumors: a clinical significance.

Vaish, Minal / Mandhani, Anil / Mittal, R D / Mittal, Balraj

BMC urology

2005 Volume 5, Page(s) 2

Abstract: Background: Carcinoma of urinary bladder is one of the leading causes of death in India. Successful treatment of bladder cancer depends on the early detection & specific diagnostic approaches. In the present study, microsatellite instability (MSI) has ... ...

Abstract	Background: Carcinoma of urinary bladder is one of the leading causes of death in India. Successful treatment of bladder cancer depends on the early detection & specific diagnostic approaches. In the present study, microsatellite instability (MSI) has been evaluated as a prognostic marker in patients with superficial urinary bladder cancer in lower urinary tract for determining risk of recurrence. Methods: A total of 44 patients with bladder tumors diagnosed with Transitional Cell Carcinomas [TCC] from lower urinary tract were selected for the study. Tumors were staged and graded according to AJCC-UICC (1997) classification and patients were followed with cystoscopy as per the protocol. Polymerase chain reaction (PCR) was done to amplify microsatellite sequences at mononucleotide BAT - 26, BAT - 40, TGFbeta RII, IGFIIR, hMSH3, BAX and dinucleotide D2S123, D9S283, D9S1851 and D18S58 loci in blood (control) and tumor DNA. PCR products were separated on 8% denaturing polyacrylamide gel and visualized by autoradiography. Results: MSI was observed in 72.7% of tumors at BAT - 26, BAT - 40, D2S123, D9S283, D9S1851 and D18S58 loci. Good association of MSI was seen with tumor stage and grade. MSI - High (instability at > 30% of loci) was frequently observed in high stage (40.6%) and high grade (59.4%) tumors. Of 24 tumors of Ta-T1 stage with different grades, 11 (9/18 high grade and 2/6 low grade tumors) recurred in the mean duration of 36 months. MSI positivity was significantly high in patients who had one or more recurrences (p = 0.02 for high grade and 0.04 for low grade tumors). Conclusions: MSI may be an independent prognostic marker for assessing risk of recurrence in superficial tumors irrespective of the grade. Further studies on progression would help in stratifying the patients of T1G3 for early cystectomy vs bladder preservation protocol.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Carcinoma, Transitional Cell/genetics ; Chromosomal Instability ; Female ; Humans ; Male ; Microsatellite Repeats ; Middle Aged ; Neoplasm Recurrence, Local/epidemiology ; Prognosis ; Urinary Bladder Neoplasms/genetics
Language	English
Publishing date	2005-01-12
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2059857-9
ISSN	1471-2490 ; 1471-2490
ISSN (online)	1471-2490
ISSN	1471-2490
DOI	10.1186/1471-2490-5-2
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Article: Allelic variation of BAT-26 and BAT-40 poly-adenine repeat loci in North Indians.

Mukherjee, Monisha / Minal, Vaish / Mittal, R D / Mittal, Balraj

International journal of molecular medicine

2002 Volume 9, Issue 1, Page(s) 91–94

Abstract: Analysis of mononucleotide repeats BAT-26 and BAT-40 in North Indians revealed that there were germline polymorphisms at both the loci. We evaluated BAT-26 and BAT-40 in 100 normal healthy individuals from North India. The DNA from normal blood was PCR ... ...

Abstract	Analysis of mononucleotide repeats BAT-26 and BAT-40 in North Indians revealed that there were germline polymorphisms at both the loci. We evaluated BAT-26 and BAT-40 in 100 normal healthy individuals from North India. The DNA from normal blood was PCR amplified using primers flanking the BAT-26 and BAT-40 loci. The allelic variation of BAT-26 and BAT-40 ranged between 117-130 and 94-112 bp respectively. The most frequent BAT-26 allele was 122 bp, which corresponded to 26 repeats and had a frequency of 32% while that of BAT-40 was 109 bp corresponding to 39 repeats with a frequency of 26%. These results suggest that polymorphisms in these poly-adenine repeat loci limit their applicability in studying the microsatellite instability in cancers.
MeSH term(s)	3-Hydroxysteroid Dehydrogenases/genetics ; Alleles ; DNA-Binding Proteins ; Ethnic Groups/genetics ; Gene Frequency ; Genetic Variation ; Heterozygote ; Humans ; India ; Microsatellite Repeats ; MutS Homolog 2 Protein ; Poly A/genetics ; Proto-Oncogene Proteins/genetics
Chemical Substances	DNA-Binding Proteins ; Proto-Oncogene Proteins ; Poly A (24937-83-5) ; 3-Hydroxysteroid Dehydrogenases (EC 1.1.-) ; MSH2 protein, human (EC 3.6.1.3) ; MutS Homolog 2 Protein (EC 3.6.1.3)
Language	English
Publishing date	2002-01
Publishing country	Greece
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1444428-8
ISSN	1107-3756
ISSN	1107-3756
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Zs.A 4942: Show issues

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Article: Microsatellite instability and its correlation with clinicopathological features in a series of thyroid tumors prevalent in iodine deficient areas.

Vaish, Minal / Mishra, Anjali / Kaushal, Manish / Mishra, Saroj K / Mittal, Balraj

Experimental & molecular medicine

2004 Volume 36, Issue 2, Page(s) 122–129

Abstract: Thyroid tumors display diverse spectrum of histopathological groups with geographic variation in its prevalence. Influence of iodine deficiency (a major causative factor) in its etiology, prevalence, or aggressiveness is debatable which reflects the ... ...

Abstract	Thyroid tumors display diverse spectrum of histopathological groups with geographic variation in its prevalence. Influence of iodine deficiency (a major causative factor) in its etiology, prevalence, or aggressiveness is debatable which reflects the existence of various genetic events in pathogenesis. The present study was undertaken to study the role of Microsatellite instability (MSI) or LOH (loss of heterozygosity), an indicator of defective mismatch repair system as a genetic change and to explore it as a prognostic marker in thyroid tumors. Tumor tissues from total thyroidectomy surgical specimens and blood (matched control) of 36 patients from iodine deficient areas (10 benign; 26 malignant) were obtained after their consent. Urinary iodine analysis was done by alkali ash method for which 10 ml of urine was collected from 18 patients before surgery. Genomic DNA, isolated from tumor tissue and blood was amplified by polymerase chain reaction (PCR) using mono and dinucleotide markers - BAT-26, BAT-40, TGF(RII, IGFIIR, hMSH3, BAX, D2S123, D9S283, D9S851 and D18S58. PCR products were analysed on 8% denaturing polyacrylamide gel followed by autoradiography. Of total, 66.6% of tumors [70% (7/10) benign and 65.4% malignant cases (17/26)] showed MSI/LOH. Strong association of MSI/LOH with low iodine (P = 0.01) and with AMES risk groups i.e. age (P = 0.02), tumor size (P = 0.04) and metastases (P = 0.002) in thyroid tumors was observed. This may help in predicting the biological behaviour and strengthening the hypothesis that iodine deficiency has influence on MSI in thyroid tumors. Our results further substantiate the risk group classification and help in deciding the treatment modality in particular patient.
MeSH term(s)	Adult ; Aged ; Biomarkers, Tumor/genetics ; DNA, Neoplasm/genetics ; Female ; Genomic Instability/genetics ; Humans ; Iodine/deficiency ; Iodine/urine ; Loss of Heterozygosity/genetics ; Male ; Microsatellite Repeats/genetics ; Middle Aged ; Predictive Value of Tests ; Prevalence ; Risk Factors ; Thyroid Neoplasms/epidemiology ; Thyroid Neoplasms/etiology ; Thyroid Neoplasms/genetics ; Thyroid Neoplasms/pathology ; Thyroid Neoplasms/therapy ; Thyroid Neoplasms/urine ; Thyroidectomy
Chemical Substances	Biomarkers, Tumor ; DNA, Neoplasm ; Iodine (9679TC07X4)
Language	English
Publishing date	2004-04-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1328915-9
ISSN	1226-3613 ; 0378-8512
ISSN	1226-3613 ; 0378-8512
DOI	10.1038/emm.2004.18
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Zs.A 4775: Show issues

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Article: Assessment of microsatellite instability in bladder and thyroid malignancies.

Vaish, Minal / Mishra, S K / Mandhani, Anil / Mittal, R D / Mittal, Balraj

Teratogenesis, carcinogenesis, and mutagenesis

2003 Volume Suppl 1, Page(s) 255–265

Abstract: Microsatellite instability (MSI) is an indicator of a defective DNA mismatch repair system (MMR) that results from somatic mutations. The present work has been planned to investigate MSI and its clinical significance in human urinary bladder and thyroid ... ...

Abstract	Microsatellite instability (MSI) is an indicator of a defective DNA mismatch repair system (MMR) that results from somatic mutations. The present work has been planned to investigate MSI and its clinical significance in human urinary bladder and thyroid cancers in Indian patients. Tumor tissues of histologically confirmed cases of urinary bladder and thyroid cancers, respectively, were obtained. Clinical data on tumor stage and histopathological grades were recorded. Corresponding matched peripheral blood was taken as a control. Genomic DNA was isolated from the tumor tissues and blood using a standard phenol-chloroform extraction method. Polymerase chain reaction was done to amplify mononucleotide microsatellite markers, BAT-26, BAT-40, TGFbetaRII, IGFIIR, hMSH3, and Bax by using specific primer sequences. For analysis of allelic patterns, the PCR products were run on 8% denaturing Polyacrylamide gel and sizing was done using a pUC18 sequencing ladder. The instability with BAT-26 and BAT-40 was found to be 20% and 45% in urinary bladder and 33% and 19% in thyroid cancers, respectively. However, no instability was observed with the other four-mononucleotide markers in either of the cancers studied. Eighty-three percent of the unstable urinary bladder cancers were found to have a high grade in a superficial group, whereas only 27% MSI+ve were muscle invasive cancers. Forty percent of unstable thyroid lesions were found to be at high risk of developing metastasis. Association of BAT-26 and BAT-40 instabilities with high grade tumors as well as risk tumors may help in choosing a more definite therapy at the outset.
MeSH term(s)	Base Pair Mismatch/genetics ; Carcinoma, Papillary/genetics ; Carcinoma, Papillary, Follicular/genetics ; Carcinoma, Transitional Cell/genetics ; DNA-Binding Proteins/genetics ; Goiter, Nodular/genetics ; Humans ; Hyperplasia ; Microsatellite Repeats/genetics ; MutS Homolog 3 Protein ; Phenotype ; Protein-Serine-Threonine Kinases ; Receptors, Transforming Growth Factor beta/genetics ; Thyroid Neoplasms/genetics ; Urinary Bladder Neoplasms/genetics
Chemical Substances	DNA-Binding Proteins ; MSH3 protein, human ; MutS Homolog 3 Protein ; Receptors, Transforming Growth Factor beta ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; transforming growth factor-beta type II receptor (EC 2.7.11.30)
Language	English
Publishing date	2003
Publishing country	United States
Document type	Journal Article
ZDB-ID	82089-1
ISSN	1520-6866 ; 0270-3211
ISSN (online)	1520-6866
ISSN	0270-3211
DOI	10.1002/tcm.10053
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Zs.A 1725: Show issues

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Article: Clinicopathological and genetic study in cerebral aspergillosis and leukemic infitration in ALL

Kumar, Raj / Singh, Vinita / Vaish, Minal / Pal, Lily / Mittal, Balraj

Journal of Pediatric Neurology

2004 Volume 02, Issue 01, Page(s) 39–43

Abstract: An 11-year-old neutropenic female child with acute lymphoblastic leukemia (ALL) developed a large right frontal mass a month following the induction of chemotherapy. A well encapsulated mass on surgical excision turned out to be aspergilloma with ... ...

Abstract	An 11-year-old neutropenic female child with acute lymphoblastic leukemia (ALL) developed a large right frontal mass a month following the induction of chemotherapy. A well encapsulated mass on surgical excision turned out to be aspergilloma with metastatic infiltration in frontal lobe. A genetic defect in form of microsatellite instability was also demonstrated in frontal mass. A possibility of fungal granuloma in a neutropenic child treated for ALL (on chemotherapy) remained strong on clinico-radiological evaluation. However, the cranial involvement in ALL also amounts to be 50 to 80% in untreated children. The child under discussion had a rare manifestation of both leukemic infiltration and fungal granuloma formation. Though the microsatellite instability was demonstrated in the mass, but further genetic studies would be required to establish the role of genetic defect in evolution of such cerebral masses/leukemic deposits. (J Pediatr Neurol 2004; 2(1): 39–43).
Keywords	central nervous system ; fungal infections ; fungal granuloma ; microsatellite instability ; leukemic brain infiltration
Language	English
Publishing date	2004-03-01
Publisher	Georg Thieme Verlag KG
Publishing place	Stuttgart ; New York
Document type	Article
ISSN	1875-9041 ; 1304-2580
ISSN (online)	1875-9041
ISSN	1304-2580
DOI	10.1055/s-0035-1557189
Database	Thieme publisher's database

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