Indian Journal of Cancer
Home  ICS  Feedback Subscribe Top cited articles Login 
Users Online :2547
Small font sizeDefault font sizeIncrease font size
Navigate here
  Search
 
  
Resource links
   Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
   Article in PDF (180 KB)
   Citation Manager
   Access Statistics
   Reader Comments
   Email Alert *
   Add to My List *
* Registration required (free)  

 
  In this article

 Article Access Statistics
    Viewed199    
    Printed9    
    Emailed0    
    PDF Downloaded56    
    Comments [Add]    

Recommend this journal

 


 
  Table of Contents  
MCQS
Year : 2019  |  Volume : 56  |  Issue : 2  |  Page : 144-145
 

MCQs for “Analysis of clinicopathological and immunohistochemical parameters and correlation of outcomes in gastrointestinal stromal tumors”


1 Department of Radiation Oncology, Artemis Hospital, Gurugram, Haryana, India
2 Department of Surgical Oncology, Command Hospital, Bangalore, Karnataka, India

Date of Web Publication2-May-2019

Correspondence Address:
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijc.IJC_354_19

Rights and Permissions



How to cite this article:
Darling H S, Jayalakshmi S, Jaiswal P. MCQs for “Analysis of clinicopathological and immunohistochemical parameters and correlation of outcomes in gastrointestinal stromal tumors”. Indian J Cancer 2019;56:144-5

How to cite this URL:
Darling H S, Jayalakshmi S, Jaiswal P. MCQs for “Analysis of clinicopathological and immunohistochemical parameters and correlation of outcomes in gastrointestinal stromal tumors”. Indian J Cancer [serial online] 2019 [cited 2019 Jul 15];56:144-5. Available from: http://www.indianjcancer.com/text.asp?2019/56/2/144/257555




Q1. Which of the following mutations in GIST are mutually exclusive?

  1. c-kit and PDGFR-α
  2. c-kit and DOG-1
  3. DOG-1 and PDGFR-α
  4. None of the above


Q2. Common sites of GIST in descending order as per incidence are

  1. Ileum–duodenum–rectum–stomach
  2. Stomach–ileum–duodenum–rectum
  3. Rectum–ileum–duodenum–stomach
  4. Duodenum– stomach–ileum–rectum


Q3. In this study, the sole factor associated with poor recurrence-free survival in multivariate analysis is

  1. Site of disease
  2. Extent of resection


  3. Duration of adjuvant therapy
  4. Nuclear pleomorphism


Q4. Which of the following are driver mutations?

  1. c-kit and DOG-1
  2. PDGFR-α and DOG-1
  3. c-kit and PDGFR-α
  4. All of the above


Q5. Choose the false statement pertaining to GIST

  1. Wild-type GIST is c-kit and PDGFR-α negative
  2. GISTs are always of gastrointestinal origin
  3. Wild-type GIST can be DOG-1 positive
  4. Wild-type GIST can be c-kit driven


Q6. The most important prognostic factors in GIST are all, except

  1. Tumor size
  2. Site
  3. Mitotic index
  4. Lymph node involvement


Q7. Regarding surgery in GIST, true statement is

  1. Small tumors can be managed with maximal debulking
  2. Retroperitoneal GISTs are easier to resect
  3. Wide local excision is the standard of care
  4. R+ resection is acceptable to save adjacent organs


Q8. DOG-1 is a robust biomarker, it is

  1. A diagnostic IHC marker of GIST
  2. An activating mutation in the tyrosine kinase pathway
  3. The most sensitive marker of GIST
  4. May be positive in other soft tissue sarcomas


Q9. Adjuvant therapy in an R0 resected gastric GIST of 5 cm would be

  1. Cytotoxic chemotherapy
  2. None
  3. Local radiation therapy
  4. Tyrosine kinase inhibitor


Q10. The characteristics of PDGFR-α in GIST are all, except

  1. Is constitutively inactivated
  2. can be expressed in other soft tissue tumors
  3. can be detected by IHC
  4. can be positive along with DOG-1.


Answers and explanations:

  1. a) c-kit and PDGFR-α


  2. Approximately 17.6% of tumors lacking KIT mutations have activating mutations in a gene encoding a related receptor tyrosine kinase, the platelet-derived growth factor receptor-alpha (PDGFR-α). PDGFR-α mutation leads to the activation of downstream pathways identical to those in KIT-mutant GISTs. Although there is significant functional overlap, KIT and PDGFR-α mutations are mutually exclusive in GISTs.

  3. b) Stomach–ileum–duodenum–rectum


  4. The majority of cases were gastric in location (47.8%), followed by jejunoileal (18.5%) and duodenum (15.2%).

  5. d) Nuclear pleomorphism


  6. On multivariate analysis, only nuclearpleomorphism is significantly associated with recurrence.

  7. c) c-kit and PDGFR-α


  8. More than 90% of GISTs harbor activating KIT mutations. Approximately 17.6% of tumors lacking KIT mutations have activating mutations in a gene encoding a related receptor tyrosine kinase, the platelet-derived growth factor receptor-alpha (PDGFR-α).

  9. b) GISTs are always of gastrointestinal origin


  10. With the development of highly effective targeted therapies against GISTs, such as imatinib, the prognosis of these patients has significantly improved, which mandates a precise and accurate diagnosis of GISTs to be of utmost importance, especially for the wild-type (c-kit and PDGFR-α negative) GISTs. GIST arising from mesentery and retroperitoneum generally referred to as “extragastrointestinal stromal tumors” (EGISTs) constituted 10%–17.8% of cases in various studies.

  11. d) Lymph node involvement


  12. The proposed prognostic factor for survival includes tumor size, mitotic index, tumor location, tumor rupture, and kinase mutational status.

  13. c) Wide local excision is the standard of care


  14. Surgery with negative microscopic margins is the mainstay treatment for resectable nonmetastatic GISTs. Small tumors are usually managed by WLE. The most important factor to prevent recurrence is to prevent tumor rupture or hemorrhage intraoperatively. In half of the patients with retroperitoneal tumors, adjacent organ resection was required suggesting local infiltrating nature of the disease.

  15. a) A diagnostic IHC marker of GIST


  16. Since DOG1 is specifically expressed by GISTs as compared with ubiquitous positivity of c-kit in many normal cells and other tumors, it is a good supplementary marker.

  17. d) Tyrosine kinase inhibitor


  18. Imatinib therapy is recommended for tumor larger than 3 cm, especially the tumor adjacent to vital organs and at high risk of recurrence.

  19. a) Is constitutively inactivated


  20. PDGFR-α mutation leads to the activation of downstream pathways identical to those in KIT-mutant GISTs. Although there is significant functional overlap, KIT and PDGFR-α mutations are mutually exclusive in GISTs. However, PDGFR-α can be expressed in other soft tissue tumors such as synovial sarcoma and leiomyosarcoma and it has a variable expression among GISTs.







 

Top
Print this article  Email this article
 

    

  Site Map | What's new | Copyright and Disclaimer
  Online since 1st April '07
  2007 - Indian Journal of Cancer | Published by Wolters Kluwer - Medknow