Sex chromosome abnormalities in lung cancer patients

Davé, Bhavana J.; Hopwood, Vicki L.; Spitz, Margaret R.; Pathak, Sen

doi:10.1016/0165-4608(95)00245-6

Cited by 8 publications

(8 citation statements)

References 19 publications

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“…Our rate also is greater than the rate of 8–17% observed in other endocrine tumors such as parathyroid tumors and sporadic pheochromocytomas 29, 34. In comparison with the results of studies of nonendocrine tumors, our result is similar to the 44–60% rate of X‐chromosome LOH reported in cholangiocarcinomas,23 melanomas,24 and carcinomas of the breast,27, 51 ovary,26 and kidney;35 and greater than the 5–36% rate observed in carcinomas of the prostate,20 stomach,22 and lung 21. The elevated frequency of X‐chromosome LOH in gastrinomas in the current study (compared with most other studies of PETs or gastrointestinal carcinoids) could be a characteristic feature of gastrinomas.…”

Section: Discussionsupporting

confidence: 87%

“…Recently, studies of nonendocrine20–28, 48 and endocrine tumors19, 29–34 reported that LOH on the X chromosome may occur. This type of LOH may be associated with malignancy or growth,17, 27, 30 metastatic disease, or large tumors 27.…”

Section: Discussionmentioning

confidence: 99%

“…Assessment of genetic and molecular alterations in various neoplasms has provided a number of important insights that have proven to be clinically useful in determining prognosis or predicting growth behavior 12–19. A number of studies have shown that X‐chromosome loss of heterozygosity (LOH) occurs in some nonendocrine19–28 and endocrine tumors29–34 and can be associated with malignant tumor behavior17, 27, 30 and a shorter survival period 19, 35. However, the results of studies of patients with PETs and carcinoids are unclear, the conclusions of growth correlations with X‐chromosome LOH are conflicting, and only a small sample of patients with gastrinomas have been studied 30, 33, 36.…”

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confidence: 99%

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X‐chromosome loss of heterozygosity frequently occurs in gastrinomas and is correlated with aggressive tumor growth

Chen¹,

Vortmeyer²,

Zhuang³

et al. 2004

Cancer

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BACKGROUND Recent studies have shown that tumor growth, rather than hormone overproduction, is the leading cause of death among patients with gastrinomas and other malignant gastrointestinal endocrine tumors. No patient/laboratory characteristics accurately predict which tumors will exhibit aggressive growth. Furthermore, little is known regarding the molecular pathogenesis of these tumors. X‐chromosome loss of heterozygosity (LOH) occurs in some nonendocrine tumors, and its presence can be associated with aggressive growth/decreased survival. Data on X‐chromosome LOH in gastrointestinal endocrine tumors are conflicting. Therefore, the purpose of the current study was to determine whether X‐chromosome LOH occurred in gastrinomas and, if so, whether it was correlated with tumor growth, tumor behavior, and/or prognosis. METHODS X chromosome allelotyping was performed using 12 microsatallite markers spaced throughout the chromosome using DNA from leukocytes and microdissected gastrinoma specimens from 16 female patients. The presence of X‐chromosome LOH was analyzed for correlations with clinical and laboratory tumor characteristics as well as tumor growth characteristics. RESULTS Nine gastrinoma specimens (56%) had X‐chromosome LOH, ranging from 6% to 23% at the 12 different loci studied. X‐chromosome LOH was significantly associated with aggressive postoperative tumor growth, increased primary tumor size, and pancreatic primaries. In 6 tumor specimens, LOH occurred on Xp22.1–22.3 over a 28.4‐centimorgan region. CONCLUSIONS X‐chromosome LOH was common in gastrinoma specimens from female patients, and its presence was found to be a potentially useful molecular/genetic prognostic factor for aggressive growth. Cancer 2004;100:1379–87. Published 2004 American Cancer Society.

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Section: Discussionsupporting

confidence: 87%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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X‐chromosome loss of heterozygosity frequently occurs in gastrinomas and is correlated with aggressive tumor growth

Chen¹,

Vortmeyer²,

Zhuang³

et al. 2004

Cancer

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“…Age-related loss of the Y chromosome in both bone marrow and lymphocytes of phenotypically normal and abnormal subjects is well documented (Nowinski et al, 1990;Sandberg, 1990). Loss of the Y chromosome is also more frequently seen in cuhures of lymphocytes from patients with lung cancer than in those from the controls (Dave et al, 1996). This was also shown in the lung tumor cells by FISH analysis using the Y chromosome-specific DNA probe (Miyamoto et al, 1992).…”

Section: Discussionmentioning

confidence: 77%

Amplification of the Y chromosome in three murine tumor cell lines transformed in vivo by different human prostate cancers

Multani

Özen

Agrawal

et al. 1999

In Vitro Cell.Dev.Biol.-Animal

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Conventional and molecular cytogenetic analyses of three murine cancer cell lines that had been induced in male athymic mice by the injection of three different human prostate cancer cell lines revealed selective amplification of the Y chromosome. In particular, analysis of metaphase and interphase nuclei by fluorescence in situ hybridization (FISH) with the mouse Y chromosome-specific DNA painting probe revealed the presence of various numbers of Y chromosomes, ranging from one to eight, with a large majority of nuclei showing two copies (46.5-60.1%). In Interphase nuclei, the Y chromosomes showed distinct morphology, allowing identification irrespective of whether the preparations were treated for 15 min or for 5 h with Colcemid, a chemical known to cause chromosome condensation. However, FISH performed on human lymphocyte cultures with chromosome-specific DNA painting probes other than the Y chromosome did not reveal condensed chromosome morphology in interphase nuclei even after 12 h of Colcemid treatment. Our FISH results indicate that (1) the Y chromosome is selectively amplified in all three cell lines; (2) the mouse Y chromosome number is comparable in both interphase and metaphase cells: (3) the Y chromosome number varies between one and eight, with a large majority of cells showing two or three copies in most interphase nuclei; (4) the condensation of the Y chromosome is not affected by the duration of Colcemid treatment but by its inherent DNA constitution; and (5) the number of copies of the Y chromosome is increased and retained not only in human prostate tumor cell lines but also in murine tumors induced by these prostate tumor cell lines.

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“…From cytogenetic studies, deletions within the long arm of chromosome 7 have been found in breast cancer and other types of tumors, including myeloid leukemias (reviewed in Fischer et al, 1998), kidney carcinomas, colon carcinomas, ovarian carcinomas, lung carcinomas, head-and-neck carcinomas (Berkerkarauzum et al, 1998;Dave et al, 1995;Lundgren, 1991;Lundgren et al, 1992;Mertens et al, 1997;Solinas-Toldo et al, 1996;Storto et al, 1990) and uterine leiomyomas (Ozisik et al, 1993;Sargent et al, 1994;Xing et al, 1997). LOH analyses con®rmed that genetic material on 7q is frequently deleted in breast cancer, particularly in the 7q31 region (Bieche et al, 1997;Callahan et al, 1993;Champeme et al, 1995;Deng et al, 1994;Devilee et al, 1997;Kristjansson et al, 1997;Lin et al, 1996;Tougas et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

Refined mapping of the region of loss of heterozygosity on the long arm of chromosome 7 in human breast cancer defines the location of a second tumor suppressor gene at 7q22 in the region of the CUTL1 gene

et al. 1999

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In breast cancer, loss of heterozygosity (LOH) has been described on the long arm of chromosome 7, at band q31, suggesting the presence of a tumor suppressor gene in this region. In this study, we have identi®ed a second region of LOH on 7q, at band 7q22. Deletion of genetic material at 7q22 was found in all tumor types and grades and was associated with increased tumor size. The region of LOH at 7q22 in every case included one or more of three polymorphic markers that are located within the CUTL1 gene. LOH of 7q22 has also been documented in the case of human uterine leiomyomas (Zeng et al., 1997;Ishwad et al., 1997). Interestingly, in both leiomyomas and mammary tumors induced in transgenic mice expressing the Polyomavirus (PyV) large T (LT) antigen, immunocomplexes of CUTL1 and PyV LT antigen were detected (Webster et al., 1998). Altogether, genetic data in human breast cancer and biochemical analyses in breast tumors from transgenic mice suggest that CUTL1 is a candidate tumor suppressor gene.

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Sex chromosome abnormalities in lung cancer patients

Cited by 8 publications

References 19 publications

X‐chromosome loss of heterozygosity frequently occurs in gastrinomas and is correlated with aggressive tumor growth

X‐chromosome loss of heterozygosity frequently occurs in gastrinomas and is correlated with aggressive tumor growth

Amplification of the Y chromosome in three murine tumor cell lines transformed in vivo by different human prostate cancers

Refined mapping of the region of loss of heterozygosity on the long arm of chromosome 7 in human breast cancer defines the location of a second tumor suppressor gene at 7q22 in the region of the CUTL1 gene

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