Field cancerization: Why late “recurrent” ovarian cancer is not recurrent

Buller, Richard E.; Skilling, Jeffrey S.; Sood, Anil K.; Plaxe, Steve; Baergen, Rebecca N.; Lager, Donna J.

doi:10.1016/s0002-9378(98)70473-9

Cited by 48 publications

(21 citation statements)

References 16 publications

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“…On the basis of clinicopathological observations of oral squamous cell carcinomas, in 1953, Slaughter et al (1953) proposed the concept of ®eld cancerization to explain the development of SPTs. The hypothesis was supported by subsequent clinical and molecular studies (Chung et al 1993;Buller et al, 1998;Sozzi et al, 1995). The SPTs in patients with HNSCC have become an important clinical issue because of the increasing incidence of SPTs in head and neck cancer and the negative impact of such tumors on long-term survival of patients (Vokes et al, 1993;Jones et al, 1995;Schwartz et al, 1994).…”

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confidence: 83%

Multiple oral squamous epithelial lesions: are they genetically related?

et al. 2001

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The development of second primary tumors (SPTs) in patients with head and neck squamous cell carcinoma (HNSCC) has become an increasingly important factor in clinical treatment decison. Currently, clinical and histologic parameters are used to determine whether or not SPT is present. Recent studies suggest that many SPTs in the upper aerodigestive tract have a common clonal origin, challenging the longstanding multiclonal origin concept. To determine genetic relationships among multiple oral cancerous and precancerous lesions (MOCP), we analysed 100 lesions from 26 Japanese patients. Lesion development was synchronous and metachronous. We looked for patterns of microsatellite alterations (MA) using seven markers at chromosomes 3p14, 9p21, and 17p13, where MA occurs early in oral carcinogenesis. Loss of heterozygosity (LOH) was found in 52.6% (41/78), 62.5% (60/96), and 59.3% (32/54) of informative MOCP at 3p14, 9p21, and 17p13, respectively. Microsatellite instability (MI) was observed in 11, 26 and 13% of the samples at 3p14, 9p21, and 17p13 markers, respectively. Patterns of MA were concordant in only nine (14%) of 63 lesions from four (18%) of 22 patients who initially presented with noninvasive lesions. However, two of four patients with invasive cancer as indexed lesion showed 16 (43%) clonally related MOCP among 37 lesions (P=0.003). The results suggest that the majority of MOCP arise from clonally independent cells a ected by ®eld cancerization. However, the probability of mucosal spread of clonal malignant or premalignant cells may increase along with malignant progression. Oncogene (2001) 20, 2235 ± 2242.

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confidence: 83%

Multiple oral squamous epithelial lesions: are they genetically related?

et al. 2001

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“…This analysis has been successfully used to discriminate between multicentricity and multifocality in breast carcinoma (1), to distinguish between primary and secondary carcinoma in the breast (2), and to identify the origin of late recurrent ovary carcinoma (3). These studies have also helped to clarify the origin of macroscopically and microscopically heterogeneous nodules present in many multinodular goitres (4).…”

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confidence: 99%

Clonal origin of non-medullary thyroid tumours assessed by non-random X-chromosome inactivation

Moniz

Catarino²,

Marques

et al. 2002

European Journal of Endocrinology

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Objective: X-chromosome inactivation analysis was performed in order to assess the clonal origin of non-medullary thyroid tumours and to distinguish between multicentricity and multifocality in multiple papillary thyroid carcinoma (PTC). Methods: One hundred and thirteen tumour samples from 31 patients with isolated PTC, 16 patients with multinodular PTC, 14 patients with follicular thyroid adenoma (FTA) and 15 patients with follicular thyroid carcinoma (FTC) were collected. The corresponding normal thyroid tissues were analysed, and in 14 cases, tumour-surrounding tissue was also studied. Genomic DNA was digested with HpaII and HhaI previous to PCR amplification of the polymorphic CAG repeat, on exon 1 of the human androgen receptor gene (HUMARA). PCR products were analysed by denaturing gel electrophoresis, silver staining and densitometric analysis. PCR products were also used to determine the number of CAG repeats of patients with isolated PTC, FTA, FTC and of 41 healthy volunteers. Results: Heterozygosity for the HUMARA polymorphism was found in 64/76 (84%) cases. Lyonization of the thyroid was observed in 15/76 (20%) cases, which were excluded from clonal analysis. Except for two cases of isolated PTC, all tumour samples studied presented monoclonal X-inactivation patterns, while normal thyroid tissue was polyclonal. Monoclonal patterns were also found in 4/14 tumour-surrounding tissues. No difference was found in the length of CAG alleles between patients and controls. Of eight informative cases of multinodular PTC, three showed evidence of multicentricity and five revealed patterns consistent with multifocality. Conclusions: Both isolated and multinodular PTC as well as FTA and FTC are of monoclonal origin. Our results also suggest that approximately one-third of multiple PTC have an independent origin for the different nodules (multicentricity). Monoclonality was also found in tissues surrounding some PTC nodules. No association was found between the length of CAG alleles and thyroid malignancies.

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“…All of these observations were potentially explained by a theory called field effect or field cancerization. 9,10 However, what is the field effect? Is there any molecular or structural basis that gives rise to multiclonal tumors?…”

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Quantitative analysis of follicle‐stimulating hormone receptor in ovarian epithelial tumors: A novel approach to explain the field effect of ovarian cancer development in secondary mullerian systems

Wang

Lin

Parkash

et al. 2002

Intl Journal of Cancer

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The role of FSHR expression in ovarian cancer development is not clear. We examined quantitative expression of FSHR in different types of OET, presumed precursor lesions and peritoneal implants and further discussed FSH as a key growth-promotion factor for the process of ovarian epithelial tumorigenesis. Thirty-five primary OET specimens, including 5 serous cystadenomas, 4 papillary serous cystadenomas, 9 SBTs and 17 serous carcinomas, were examined for quantitative FSHR expression. Ten paired samples (3 benign cystadenomas, 5 SBTs and 2 carcinomas) were obtained from several morphologically different areas, including benignlooking, borderline and cancerous areas in the same OETs, and from the remaining ovarian tissue and contralateral ovaries. Competitive RT-PCR was performed to measure the quantitative expression of FSHR in each tissue sample. FSHR expression levels were compared among nonpaired samples and within paired samples. We found that OSE had the lowest FSHR expression, whereas antral follicles had the highest level. Within benign OETs, papillary serous cystadenomas have 4.9-fold higher FSHR levels than nonpapillary serous cystadenomas. SBTs had the highest level of FSHR expression, which was 12.8-fold, 2.7-fold and 2.4-fold higher than that of serous cystadenomas, papillary serous cystadenomas and grade 1 carcinomas, respectively. A similarly high level of FSHR mRNA was found in peritoneal implants, which were associated with SBTs. FSHR levels among serous carcinomas decreased with an increase in carcinoma grade. Grade 3 carcinomas had the lowest FSHR level, which was similar to that of serous cystadenomas, while grade 1 carcinomas had 6.5-fold higher FSHR levels than those in serous cystadenomas. Our results suggest that not only serum FSH but also FSHR in ovarian epithelium may play important roles in ovarian OET development. Both the receptor and ligand may act in a synergistic way to promote tumor growth. The observation that high FSHR levels are present in peritoneal implants suggests that FSH may also play a similar role in the development of peritoneal serous tumors. From this perspective, circulating FSH may be considered a driving force in the field effect theory for the development of both ovarian neoplasms and their associated peritoneal implants. However, the exact role of FSH and/or FSHR in the development of epithelial tumors arising in both the ovary and peritoneum needs further investigation. © 2002 Wiley-Liss, Inc. Key words: gonadotropin; hormone receptor; ovarian cancer; field effectOETs are a heterogeneous group of tumors that include benign cystadenomas, borderline tumors and OECs. Although significant efforts have been made to understand the process of tumorigenesis, a full etiologic description has not been made.The understanding of tumor progression was first advanced by Foulds, 1 who proposed that tumors are in constant evolution based on the observation of tumor heterogeneity. Tumor heterogeneity is due to an intrinsic instability of the tumor genetic material, resulting in ...

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Field cancerization: Why late “recurrent” ovarian cancer is not recurrent

Cited by 48 publications

References 16 publications

Multiple oral squamous epithelial lesions: are they genetically related?

Multiple oral squamous epithelial lesions: are they genetically related?

Clonal origin of non-medullary thyroid tumours assessed by non-random X-chromosome inactivation

Quantitative analysis of follicle‐stimulating hormone receptor in ovarian epithelial tumors: A novel approach to explain the field effect of ovarian cancer development in secondary mullerian systems

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