p53 mutation analysis for definite diagnosis of multiple primary lung carcinoma

The detection of a second tumor in patients with lung carcinoma raises the question whether this lesion is a metastasis or a second primary lung carcinoma. Patients cannot always be categorized satisfactorily according the criteria of multiple lung carcinoma proposed by Martini and Melamed. This may result in an inadequate treatment schedule in individual patients. Because p53 mutations can be used as clonal marker, the authors investigated whether p53 mutation analysis can differentiate between primary lung carcinomas and metastatic disease.

[1]  M. Rosenblum,et al.  p53 gene mutations in primary lung tumors are conserved in brain metastases , 1992, Journal of Neuro-Oncology.

[2]  P. Zanen,et al.  Survival in synchronous vs. single lung cancer: upstaging better reflects prognosis. , 2000, Chest.

[3]  Y. Yatabe,et al.  High frequency of clonally related tumors in cases of multiple synchronous lung cancers as revealed by molecular diagnosis. , 2000, Clinical cancer research : an official journal of the American Association for Cancer Research.

[4]  P. Slootweg,et al.  The origins of multiple squamous cell carcinomas in the aerodigestive tract , 2000, Cancer.

[5]  J. Minna,et al.  Multiple clonal abnormalities in the bronchial epithelium of patients with lung cancer. , 1999, Journal of the National Cancer Institute.

[6]  P. Slootweg,et al.  p53 tumor suppressor gene as a clonal marker in head and neck squamous cell carcinoma: p53 mutations in primary tumor and matched lymph node metastases. , 1999, Oral oncology.

[7]  A. Kropveld,et al.  Sequencing analysis of RNA and DNA of exons 1 through 11 shows p53 gene alterations to be present in almost 100% of head and neck squamous cell cancers. , 1999, Laboratory investigation; a journal of technical methods and pathology.

[8]  K. Ohshima,et al.  ©1999 Cancer Research Campaign Article no. bjoc.1998.0247 Discrimination of double primary lung cancer from intrapulmonary metastasis by p53 gene mutation , 2022 .

[9]  Y. Nishiwaki,et al.  Monoclonality of atypical adenomatous hyperplasia of the lung. , 1999, The American journal of pathology.

[10]  J. Jen,et al.  Distinguishing second primary tumors from lung metastases in patients with head and neck squamous cell carcinoma. , 1998, Journal of the National Cancer Institute.

[11]  Y. Miller,et al.  Widely dispersed p53 mutation in respiratory epithelium. A novel mechanism for field carcinogenesis. , 1997, The Journal of clinical investigation.

[12]  Y. Yatabe,et al.  Mutations of the P53 tumor suppressor gene as clonal marker for multiple primary lung cancers. , 1997, The Journal of thoracic and cardiovascular surgery.

[13]  S. Adebonojo,et al.  The results of modern surgical therapy for multiple primary lung cancers. , 1997, Chest.

[14]  C. Mountain,et al.  Revisions in the International System for Staging Lung Cancer. , 1997, Chest.

[15]  R. Iggo,et al.  Field cancerisation and polyclonal p53 mutation in the upper aero- digestive tract , 1997, Oncogene.

[16]  S. Piantadosi,et al.  Poster 7: A Genetic Progression Model for Head and Neck Cancer: Implications for Field Cancerization , 1996, Cancer research.

[17]  E. Gabrielson,et al.  Multiple head and neck tumors: evidence for a common clonal origin. , 1996, Cancer research.

[18]  G. Dekan,et al.  Molecular genetic differentiation between primary lung cancers and lung metastases of other tumors. , 1996, The Journal of thoracic and cardiovascular surgery.

[19]  R. Shorr,et al.  A food-borne outbreak of expensive antibiotic use in a community teaching hospital. , 1995, JAMA.

[20]  J. Minna,et al.  Allele-specific chromosome 3p deletions occur at an early stage in the pathogenesis of lung carcinoma. , 1995, JAMA.

[21]  C. Harris,et al.  Mutations in the p53 tumor suppressor gene: clues to cancer etiology and molecular pathogenesis. , 1994, Cancer research.

[22]  J. Izbicki,et al.  p53 in non-small-cell lung cancer. , 1994, Journal of the National Cancer Institute.

[23]  O. Parolini,et al.  Nonrandom X chromosome inactivation in natural killer cells from obligate carriers of X-linked severe combined immunodeficiency. , 1993, Journal of immunology.

[24]  B Palcic,et al.  Detection and localization of early lung cancer by imaging techniques. , 1993, Chest.

[25]  C. Harris,et al.  Chemical and physical carcinogenesis: advances and perspectives for the 1990s. , 1991, Cancer research.

[26]  J. Bishop.  Molecular themes in oncogenesis , 1991, Cell.

[27]  A. Cox,et al.  Surgical treatment of multiple primary lung cancers. , 1989, The Thoracic and cardiovascular surgeon.

[28]  J. Howard,et al.  Histological demonstration of mosaicism in a series of chimeric rats produced between congenic strains. , 1985, Science.

[29]  J. Deslauriers,et al.  Diagnosis and management of synchronous lung cancers. , 1985, The Journal of thoracic and cardiovascular surgery.

[30]  P. Pairolero,et al.  Roentgenographically occult lung cancer: pathologic findings and frequency of multicentricity during a 10-year period. , 1984, Mayo Clinic proceedings.

[31]  T. Fabian.  Multiple primary lung cancers. , 2018, Journal of thoracic disease.