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A.K. Ganti



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    MO22 - Advanced Disease and Outcomes (ID 103)

    • Event: WCLC 2013
    • Type: Mini Oral Abstract Session
    • Track: Surgery
    • Presentations: 1
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      MO22.05 - Surgery in octogenarians with early stage non-small cell lung cancer: A SEER database analysis (ID 2923)

      10:30 - 12:00  |  Author(s): A.K. Ganti

      • Abstract
      • Presentation
      • Slides

      Background
      Surgical resection is the standard of care for patients with early stage non-small cell lung cancer (NSCLC). However outcomes in older patients, especially octogenarians, following resection have not been studied in detail. This analysis was undertaken to evaluate the variations in patterns of care over time and outcomes following resection in octogenarians with early stage NSCLC.

      Methods
      Patients 80 years of age and older diagnosed with clinical stages I and II NSCLC, between 1988 and 2007, were identified from the SEER database. Data abstracted included age at diagnosis, stage, gender, race, histology, year of diagnosis and cause of death. The type of surgical resection was not available for a majority of patients and hence was not considered. Overall survival was estimated as the time from the date of diagnosis to death, or date of last contact (if censored). Factors associated with survival were assessed using regression analysis based on the Cox proportional hazards model. Temporal trends in survival were compared using log-rank test. Lung cancer specific survival (LCSS) was also estimated in these patients and temporal trends were compared using log-rank tests.

      Results
      Six hundred and forty-nine patients ≥80 years of age, who underwent surgical resection for stages I and II NSCLC, were identified. The majority of these patients had stage I disease (n=549), were white (n=586) and had an adenocarcinoma (n=325). Females comprised 50.6% of stage I, but only 37% of stage II patients. Factors associated with worse overall survival on multivariate analysis in this cohort were: increasing age [Hazard ratio (HR) - 1.08; 95% CI - 1.03, 1.12], male gender (HR - 1.33; 95% CI - 1.07, 1.65), stage II (HR - 2.21; 95% CI - 1.71, 2.87) and squamous histology (HR - 1.36; 95% CI - 1.07, 1.74). The percentage of patients undergoing surgery increased over time. Of the patients who underwent surgery 8.6% were diagnosed between 1988-1992, 16% between 1993-1997, 24.2% between 1998-2002 and 51.2% between 2002-2007. Despite this the median survival was not significantly different over these time periods. Median survivals for the four different time periods were as follows: 1988-1992 – 3.9 years; 1993-1997 – 3.2 years; 1998-2002 – 3.8 years; 2002-2007 – 3.3 years (p = 0.09). These are comparable to those reported previously in younger patients (ages 65-75 years) (5.92 years - stage I, 2.6 years - stage II). Similarly lung cancer specific survival was not significantly different between the different time points. Median LCSS for the four time periods were 9.2 years, 6.8 years, 7.9 years, and not reached, respectively (p = 0.51).

      Conclusion
      Among octogenarians who had surgical resection for lung cancer, increasing age, male gender, higher stage and squamous histology were associated with worse survival. Despite an increased incidence of surgical resection for octogenarians, outcomes remained unchanged between 1988 and 2007. Octogenarians, when carefully selected, are capable of experiencing a similar advantage provided by surgical resection of early stage non small cell lung cancer as younger patients.

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    P3.02 - Poster Session 3 - Novel Cancer Genes and Pathways (ID 149)

    • Event: WCLC 2013
    • Type: Poster Session
    • Track: Biology
    • Presentations: 1
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      P3.02-021 - Interdependent role of MUC16/TSPYL5 in lung cancer cell proliferation (ID 3434)

      09:30 - 16:30  |  Author(s): A.K. Ganti

      • Abstract

      Background
      Lung cancer is the leading cause of cancer-related mortality in the world. These patients usually present at an advanced stage where treatment is mostly palliative. Hence, there is an urgent need to investigate the various pre-neoplastic pathways to identify suitable therapeutic targets to decrease lung cancer mortality. The expression patterns of mucins are drastically altered during lung cancer development, and these alterations facilitate lung cancer cell proliferation and metastasis. MUC16 mucin and Testis specific Y-like protein TSPYL5 are two proteins that are overexpressed in lung cancer and appear to promote growth of lung cancer cells. In addition overexpression of TSPYL5 facilitates chemoresistance and regulates aromatase (CYP19A1) enzyme expression. This study was conducted to assess the interplay between these two markers and evaluate their effect of cisplatin induced cytotoxicity in lung cancer cells.

      Methods
      Expression of MUC16 in normal lung as well as lung carcinoma tissues in a commercially available tissue array was assessed by immunohistochemical (IHC) analysis using MUC16 antibody (DAKO Company-M11 clone). MUC16 levels were semi-quantified using a composite score based on the intensity and extent of staining. Endogenously expressed MUC16 and TSPYL5 were stably knocked down using a MUC16 shRNA construct (pSUPER-Retro-MUC16-sh) and TSPYL5 ShRNA construct in H292 and H827 lung cancer cells by stable transfection method for investigating the oncogenic functions. Lung cancer cells were treated with cisplatin to examine the role of MUC16 and TSPYL5 on chemoresistance and survival in lung cancer cells.

      Results
      MUC16 is highly expressed in lung carcinoma and is not expressed in non-neoplastic lung tissues. MUC16 composite IHC scores increased progressively from stage I to stage III NSCLC. Knockdown of MUC16 led to decreased proliferation (due to G1 accumulation), invasion and motility in H292 lung cancer cells. TSPYL5 was significantly downregulated in MUC16 knockdown cells. TSYPL5 knockdown in H292 lung cancer cells resulted in decreased expression of MUC16 as well as aromatase. The knockdown studies suggested that silencing of MUC16 and TSPYL5 affected each other. These results indicate that there may be a feedback regulation between these two molecules during lung cancer cell proliferation. Furthermore, cisplatin treatment of these cells significantly abrogated MUC16 and TSPYL5 expression.

      Conclusion
      MUC16 is overexpressed in non small cell lung cancer. MUC16 plays an important role in lung cancer proliferation, through rapid G1/S transition in the cell cycle. MUC16 and TSPYL5 regulate each other during lung cancer cell proliferation, possibly through the aromatase pathway. One of the possible mechanisms through which cisplatin may decrease lung cancer proliferation is by downregulation of MUC16 and TSPYL5.