Natural history of pulmonary scar cancers clinical and pathologic implications

Pt, Cagle; Sd, Cohle; Sd, Greenberg

doi:10.1002/1097-0142(19851015)56:8<2031::aid-cncr2820560824>3.0.co;2-k

Cited by 30 publications

(10 citation statements)

References 15 publications

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“…On the one hand, chronic inflammatory reaction associated with latent TB infection may serve as a cause of malignancy. This possibility is indirectly supported by observations of the so-called 'scar carcinomas' (Cagle et al, 1985). Ardies postulated that in many cases lung scarring occurred as a result of spontaneous healing after recurrent TB infection, and by triggering cycles of inflammatory and tissue repair processes generated a favorable environment for tumorigenesis (Ardies, 2003).…”

Section: Introductionmentioning

confidence: 90%

Lung carcinogenesis induced by chronic tuberculosis infection: the experimental model and genetic control

et al. 2009

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Coexistence of pulmonary tuberculosis (TB) and lung cancer in clinic poses significant challenges for the diagnostic and treatment of both diseases. Although association of chronic inflammation and cancer is welldocumented, causal relationship between TB infection and lung cancer are not understood. We present experimental evidence that chronic TB infection induces cell dysplasia and squamous cell carcinoma (SCC) in a lung-specific manner. First, squamous cell aggregates consistently appeared within the lung tissue associated with chronic TB lesions, and in some cases resembled SCCs. A transplantable tumor was established after the transfer of cells isolated from TB lung lesions into syngeneic recipients. Second, the (Mycobacterium tuberculosis) MTB-infected macrophages play a pivotal role in TBinduced carcinogenesis by inducing DNA damage in their vicinity and by the production of a potent epidermal growth factor epiregulin, which may serve as a paracrine survival and growth factor responsible for squamous metaplasia and tumorigenesis. Third, lung carcinogenesis during the course of chronic TB infection was more pronounced in animals with severe lung tissue damage mediated by TB-susceptibility locus sst1. Together, our experimental findings showed a causal link between pulmonary TB and lung tumorigenesis and established a genetic model for further analysis of carcinogenic mechanisms activated by TB infection.

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Section: Introductionmentioning

confidence: 90%

Lung carcinogenesis induced by chronic tuberculosis infection: the experimental model and genetic control

et al. 2009

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“…In spite of these limitations, in some reports there is evidence that the scar (and scarring process) predates the tumor, [6][7][8][9][10][11] in others it is impossible to tell, 12,13 and in others there is evidence that there was an active scarring process as a result of the tumor. 2,3,5,[14][15][16] The basic assumption behind any conclusions of no association between a pulmonary scar and its "associated" tumor [1][2][3][4][5] is that the scar itself cannot have directly caused the tumor. In one article, 4 the authors even ruled out tuberculosis as a contributing cause even though 10 of 49 cancer patients had tuberculosis that predated the cancer.…”

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confidence: 99%

Inflammation as Cause for Scar Cancers of the Lung

Ardies

2003

Integr Cancer Ther

112

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The molecular and cellular basis of inflammation has become a topic of great interest of late because of the association between mechanisms of inflammation and risk for cancer. Inflammatory-mediated events, such as the production of reactive oxygen species (ROS), the activation of growth factors (for wound repair), and the altering of signaltransduction processes to activate cell-proliferation (to replace necrotic/apoptotic tissue cells), events that also can occur independently of inflammation, are all considered to be components of risk for a variety of cancers. Using scar cancer of the lung as an example, mechanisms of inflammation associated with recurring infections with Mycobacterium tuberculosis are discussed in the context that they may, in fact, be the major or sole cause of a cancer. Production of ROS, prostaglandins, leukotrienes, and cytokines in pulmonary tissues is greatly enhanced due to a cell-mediated immune response against macrophages infected with M. tuberculosis. These responses lead to the extensive fibrosis associated with recurring infections, possibly leading to decreased clearance of lymph and lymph-associated particles from the infected region. They also will enhance rates of cell division by inhibiting synthesis of P21, leading to enhanced progression from G0 arrest to G1 phase, from G1 to S phase, and from G2 to M phase of the cell cycle. By increasing rates of oxidative DNA damage and inhibiting apoptosis by enhancing synthesis of BCL-2, mutagenesis of progeny cells is enhanced, and these effects coupled with enhanced angiogenesis stimulated by COX-2 products lead to an environment that is highly conducive to tumorigenesis. Based on the evidence, it appears that but for an inflammatory response to recurring infections, some cases of scar cancer would not exist. By making appropriate lifestyle and dietary changes, a variety of anti-inflammatory effects can be produced, which should attenuate inflammation-induced risk for cancer.

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“…Thus in these old fibrotic areas, presumptively produced by a previous bout of inflammation, the epithelia of small airways enclosed within the scar were considered to be particularly susceptible to malignant transformation. However, Shimosato et al (15) have proposed an alternative explanation that the central fibrotic focus with anthracosis is formed after the development of carcinoma, probably as a result of alveolar wall collapse brought about by degeneration, and death of tumor cells lining along the alveoli in the early stage adenocarcinoma (16). Subsequently, fibroblastic cell proliferation and collagenization follow.…”

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confidence: 99%

Atypical Adenomatous Hyperplasia of the Lung: A Probable Forerunner in the Development of Adenocarcinoma of the Lung

et al. 2001

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An increasingly large body of work suggests that atypical adenomatous hyperplasia (AAH) of the lung may be a forerunner of pulmonary adenocarcinoma. Recognizing this fact, the World Health Organization now acknowledges the existence of AAH while noting difficulties that may be encountered in distinguishing AAH from the nonmucinous variant of bronchioloalveolar carcinoma. Regrettably, a universally acceptable definition of morphologic criteria for the diagnosis of AAH has not been achieved. This review of the literature examines the epidemiology, gross appearance, light microscopic findings, morphometry, immunohistochemistry, and molecular features of AAH and suggests a set of histopathologic features that may help the practicing pathologist identify this intriguing lesion. These features include the following: irregularly bordered focal proliferations of atypical cells spreading along the preexisting alveolar framework; prominent cuboidal to low columnar alveolar epithelial cells with variable degree of atypia but less than that seen in adenocarcinoma; increased cell size and nuclearcytoplasmic ratio with hyperchromasia and prominent nucleoli, generally intact intercellular attachment of atypical cells with occasional empty-looking spaces between them without high cellularity and without tufting or papillary structures; and slight thickening of the alveolar walls on which the AAH cells have spread, with some fibrosis but without scar formation or significant chronic inflammation of the surrounding lung tissue. Several lines of evidence indicate that AAH is a lesion closely associated with adenocarcinoma of the lung, suggesting AAH may be involved in the early stage of a complex multistep carcinogenesis of pulmonary adenocarcinoma.

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Natural history of pulmonary scar cancers clinical and pathologic implications

Cited by 30 publications

References 15 publications

Lung carcinogenesis induced by chronic tuberculosis infection: the experimental model and genetic control

Lung carcinogenesis induced by chronic tuberculosis infection: the experimental model and genetic control

Inflammation as Cause for Scar Cancers of the Lung

Atypical Adenomatous Hyperplasia of the Lung: A Probable Forerunner in the Development of Adenocarcinoma of the Lung

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