Clinicopathological significance of mitochondrial D-Loop mutations in head and neck carcinoma. Select your operating system and version ,. Interestingly, associations have been made between D mutations and poor disease-free survival, a late onset age, and estrogen and progesterone-negative breast cancers Tseng et al , We compared the distributions of D sequences extracted from tumour tissues to sequences extracted from normal tissue controls. Please verify your product is powered on and connected, then try again in a few minutes. Solution and Diagnostic Data Collection.

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Mitochondria-to-nucleus stress signaling induces phenotypic changes, tumor progression and cell invasion. Previous studies have found telomere DNA alterations and allelic imbalance in histologically normal ductal epithelial tissues.

Int J Gynecol Cancer. As it has been suggested that local normal remnants of a field may develop into cancer after removal of the primary tumour site, further investigation is warranted to examine whether D mutations in adjacent normal tissue is associated with tumour recurrence. The multistep development model of breast cancer involves the progression from premalignant hyperplastic lesions, to pre-invasive carcinoma ductal carcinoma in situ DCISto invasive ductal carcinoma IDC.

Mitochondrial D310 mutations in the early development of breast cancer

Direct sequencing of the D region A bp fragment of the D-loop including the D sequence was amplified and sequenced as described previously Legras et al Many mtDNA mutations have been described in various forms of cancer, most of them in the regulatory region or D-loop, the replication origin for the heavy strand of mtDNA. Mutations affecting all copies of the mtDNA were defined as homoplasmic, whereas those which were present only in a proportion of copies of mtDNA were defined as heteroplasmic.


In the first five samples, our results were suggestive of a field cancerisation effect: The natural history of ductal carcinoma in situ of the breast: A bp fragment of the D-loop including the D sequence was amplified and sequenced as described previously Legras et al These alterations decreased as a function of distance from tumour Heaphy et al A mutation was scored when the D allele in tumour differed from the allele found in its matched normal sample.

Material and methods Patient selection Breast tumour and normal tissues were collected from 78 breast cancer patients selected from the files of the Department of Pathology at the University Health Network Toronto, Canada between and In this study, we investigated the frequency and pattern of mutations in a regulatory region of the mtDNA referred to as the D-loop.

Field cancerisation has been implicated in the lung, colon, cervix, bladder, skin, and breast cancers Heaphy et al Javascript is disabled in this browser.

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Acknowledgments We thank N Kanwar for providing assistance in sequencing and optimising PCR conditions and T Cawthorn for help in statistical analysis. Or, view all available drivers for your product below.

Select all Deselect all. Field cancerization in oral stratified squamous epithelium; clinical implications of multicentric origin.

Mitochondrial D mutations in the early development of breast cancer

Supplementary Table 2 lists the samples scored as somatic mutation. No software or drivers are available for this product entwork the selected operating system. Let HP networ any out-of-date or missing drivers and software How does HP use product data collected with this service?


Europe, Middle East, Africa. Genotype similarities found in both normal and tumour tissues mtDNA could be due to germ-line polymorphism, field cancerisation genetic alterations in histologically normal cells due to the clonal expansion of cancer progenitor cellsor contamination from tumour cells during microdissection.

It has been proposed as a marker for early tumour progression in head and neck cancer Ha et al The results of D genotyping were analysed using the Fragment Analysis v.

As D mutations occur at high frequency in pre-malignant lesions, it is important to consider whether they have a causative role in breast carcinogenesis. Thus, the timing of events explains the lack of association between D mutations and DCIS progression. It is postulated to have a central role in the maintenance of netowrk copy number.

To confirm the sequences from these samples, two independent microdissection and amplification experiments were performed. Tumour samples were also found to be more heteroplasmic than normal samples Table 2.

In the other five cases, both normal tissue adjacent and further away from the tumour shared the same alleles. Loss of heterozygosity in normal tissue adjacent to breast carcinomas.