Cancer statistics, 1997

Parker, Sheryl L.; Tong, Tony; Bolden, Sherry; Wingo, Phyllis A.

doi:10.3322/canjclin.47.1.5

Cited by 1,917 publications

(888 citation statements)

References 3 publications

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“…Lung cancer is the most frequent cause of cancer deaths in both men and women in the USA (Parker et al, 1997) and tobacco smoking is accepted as the major cause of this neoplasm (Parkin et al, 1994). Lung cancer is classi®ed into two major groups, small cell lung carcinoma (SCLC) and non small cell lung carcinoma (NSCLC) .…”

Section: Introductionmentioning

confidence: 99%

Sequential molecular abnormalities are involved in the multistage development of squamous cell lung carcinoma

et al. 1999

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To understand the molecular pathways involved in the pathogenesis of squamous cell lung carcinoma, we obtained DNA from 94 microdissected foci from 12 archival surgically resected tumors including histologically normal epithelium (n=13), preneoplastic lesions (n=54), carcinoma is situ (CIS) (n=15) and invasive tumors (n=12). We determined loss of heterozygosity (LOH) at 10 chromosomal regions (3p12, 3p14.2, 3p14.1-21.3, 3p21, 3p22-24, 3p25, 5q22, 9p21, 13q14 RB, and 17p13 TP53) frequently deleted in lung cancer, using 31 polymorphic microsatellite markers, including 24 that spanned the entire 3p arm. Our major ®ndings are as follows: (1) Thirty one percent of histologically normal epithelium and 42% of mildly abnormal (hyperplasia/metaplasia) specimens had clones of cells with allelic loss at one or more regions; (2) There was a progressive increase of the overall LOH frequency within clones with increasing severity of histopathological changes; (3) The earliest and most frequent regions of allelic loss occurred at 3p21, 3p22-24, 3p25 and 9p21; (4) The size of the 3p deletions increased with progressive histologic changes; (5) TP53 allelic loss was present in many histologically advanced lesions (dysplasia and CIS); (6) Analyses of 58 normal and non-invasive foci having any molecular abnormality, indicated that 30 probably arose as independent clonal events, while 28 were potentially of the same clonal origin as the corresponding tumor; (7) Nevertheless, when the allelic losses in the 30 clonally independent lesions and their clonally unrelated tumors were compared the same parental allele was lost in 113 of 125 (90%) of comparisons. The mechanism by which this phenomenon (known as allele speci®c mutations) occurs is unknown; (8) Four patterns of allelic loss in clones were found. Histologically normal or mildly abnormal foci had a negative pattern (no allelic loss) or early pattern of loss while all foci of CIS and invasive tumor had an advanced pattern. However dysplasias demonstrated the entire spectrum of allelic loss patterns, and were the only histologic category having the intermediate pattern. Our ®ndings indicate that multiple, sequentially occurring allele speci®c molecular changes commence in widely dispersed, apparently clonally independent foci, early in the multistage pathogenesis of squamous cell carcinomas of the lung.

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Section: Introductionmentioning

confidence: 99%

Sequential molecular abnormalities are involved in the multistage development of squamous cell lung carcinoma

et al. 1999

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“…1 The standard therapies for localized disease, including surgical resection and radiotherapy, may be effective in specific cases, but can produce serious side-effects and a low level of mortality. 2,3 Patients with occult or clinical metastatic disease are managed with palliative hormone therapy, as there are no documented curative therapies.…”

Section: Introductionmentioning

confidence: 99%

Adenovirus-mediated interleukin-12 gene therapy for prostate cancer: suppression of orthotopic tumor growth and pre-established lung metastases in an orthotopic model

et al. 1999

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Interleukin-12 (IL-12) can elicit potent antitumoral effects CD4 + and CD8 + T cells 7 days after virus injection. Howthat involve the recruitment of specific immune effector ever, splenocyte-derived cytotoxic T lymphocytes were not cells. We investigated the efficacy of a single injection of detected during the 14 days following treatment. Increased a recombinant adenovirus expressing murine IL-12 numbers of nitric oxide synthase-positive macrophages (AdmIL-12) directly into orthotopic mouse prostate carciwere seen in the AdmIL-12 treated group 7 days following nomas generated from a poorly immunogenic cell line (RMinjection. Systemic inhibition of natural killer cells with anti-9) derived from the mouse prostate reconstitution system. asialo-GM1 serum led to increased numbers of lung metSignificant growth suppression (Ͼ50% reduction of tumor astases in AdmIL-12-treated orthotopic tumors but did not weight) and increased mean survival time (23.4 to 28.9 affect local tumor growth. In this model system the antidays) were observed compared with controls. Suppression tumor effects of a single injection of adenovirus-mediated of pre-established lung metastases was also observed fol-IL-12 appears to be based to a large extent on the actilowing the injection of AdmIL-12 into the orthotopic tumor.vation of nitric oxide synthase in macrophages and possCytolytic natural killer cell activity was markedly enhanced ibly T cell activities, whereas the relatively early cytolytic 1-2 days after virus injection. Immunohistochemical analyactivity of natural killer cells are largely but not exclusively sis showed significantly elevated intratumoral infiltration of responsible for the antimetastatic effects.

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“…Prostate cancer is the most commonly diagnosed nonskin carcinoma, and is the second leading cause of cancer death in American men (Parker et al, 1997). Genetic analysis has identi®ed several chromosomal regions such as 8p12 ± 21, 10q22 ± 24, 16q22 ± 24, and 7q31 whose deletions appear to be involved in prostatic carcinogenesis (Dong et al, 1997b).…”

Section: Introductionmentioning

confidence: 99%

PTEN/MMAC1 is infrequently mutated in pT2 and pT3 carcinomas of the prostate

et al. 1998

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Deletion of the q23-24 region of human chromosome 10 is one of the most frequent genetic alterations in prostate cancer, suggesting that inactivation of a tumor suppressor gene in this region is involved in the development or progression of this carcinoma. A candidate gene, PTEN/ MMAC1, has been identi®ed from this chromosomal region; mutations of this gene have been found in various advanced tumors and cell lines including those of prostate cancer. To further de®ne the role of PTEN/ MMAC1 in the development of prostate cancer and its spectrum of genetic alterations, we analysed 40 pT2 or pT3 prostate tumors for allelic loss, mutations, and homozygous deletions using PCR-based methods. Six tumors showed loss of heterozygosity for one of the ten markers analysed, while one tumor showed loss of two markers. None of the markers within PTEN/MMAC1 was lost. Direct sequencing of PCR ampli®ed exons and intron/exon junctions of all 40 tumors revealed three sequence variants, one of which was a point mutation in exon 9, while the other two were polymorphisms. Using multiplex PCR, no homozygous deletions were detected in any of the neoplasms. Our results showing a low frequency of alterations of PTEN/MMAC1 in pT2 and pT3 prostate cancers suggest that this gene plays an insigni®cant role in the development of most low stage carcinomas of the prostate.

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Cancer statistics, 1997

Cited by 1,917 publications

References 3 publications

Sequential molecular abnormalities are involved in the multistage development of squamous cell lung carcinoma

Sequential molecular abnormalities are involved in the multistage development of squamous cell lung carcinoma

Adenovirus-mediated interleukin-12 gene therapy for prostate cancer: suppression of orthotopic tumor growth and pre-established lung metastases in an orthotopic model

PTEN/MMAC1 is infrequently mutated in pT2 and pT3 carcinomas of the prostate

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