Wednesday, 21 October 2015

Answers to Questions based on Chemotherapy lecture: 30th Sep. 2015

  1. Which was the first anti-metabolite used for the treatment of ALL? Name the scientist.
Anti folate, Subba Rao
  1. Chemotherapy will not affect the cancer cells which are ________ [Slow growing, fast growing].
Slow Growing
  1. Minimal residual disease in cancer can be detected with PCR with sensitivity of __________ as compared to microscopy with sensitivity of ____________ [1 in 500 cells,  1 in 104 to 106  cells]. 
1 in 104 to 106  cells
  1. The chemotherapy is aimed at getting _________ cell killing [99.9%, 50%, 100%]
99.9%
  1. The anticancer drug dose is decided as per the     [mg/ml/day, Gm/Kg of body weight X age/day, mg/meter square/week]
mg/meter square/week
  1. Which are the various modes in which resistance to cancer therapy is achieved? Give examples.
  • Reduced cellular uptake [Methotrexate]
  • Reduced drug activation [Cytarabine]
  • Increased catabolism [6-Mercaptopurine, increased activity of Thiopurine Methyltransferase]
  • Increased detoxification [Alkylating agents, Platinum analogs, due to increased Glutathione production]
  • Increased efflux and multidrug resistance [Vinca group of compounds, Anthracycline, Paclitaxel]
  • Increased DNA repair [Procarbazine, Nitrosourea]
  • Altered Target [Topoisomerase, Anthracyclin, Epipodophyllotoxins]
  1. To increase the efficacy and decrease the induction of resistance the strategy of _____________ is used in chemotherapy.
Combination Chemotherapy
  1. If decrease in number of cancer cells by at least _______ is not achieved, dose is increased [1 log, 1 million, 40%]
1 log
  1. What is major molecular response? 
Reduction in cancer cell number up to less than 10 [3] 
  1. A cancer patient taking Amethopterin is monitored for ejection fraction by echocardiogram to avoid ____________ [immune suppression, alkemia, cardiotoxicity]
Cardiotoxicity

Tuesday, 13 October 2015

Cancer Therapy Lecture: Answer the question


  1. Which was the first anti-metabolite used for the treatment of ALL? Name the scientist.
  2. Chemotherapy will not affect the cancer cells which are ________ [Slow growing, fast growing].
  3. Minimal residual disease in cancer can be detected with PCR with sensitivity of __________ as compared to microscopy with sensitivity of ____________ [1 in 500 cells,  1 in 104 to 106  cells]. 
  4. The chemotherapy is aimed at getting _________ cell killing [99.9%, 50%, 100%]
  5. The anticancer drug dose is decided as per the     [mg/ml/day, Gm/Kg of body weight X age/day, mg/meter square/week]
  6. Which are the various modes in which resistance to cancer therapy is achieved? Give examples.
  7. To increase the efficacy and decrease the induction of resistance the strategy of _____________ is used in chemotherapy.
  8. If decrease in number of cancer cells by at least _______ is not achieved, dose is increased [1 log, 1 million, 40%]
  9. What is major molecular response?
  10. A cancer patient taking Amethopterin is monitored for ejection fraction by echocardiogram to avoid ____________ [immune suppression, alkemia, cardiotoxicity]

Tuesday, 21 July 2015

Special issue of journal Human Mutation on P53!

http://onlinelibrary.wiley.com/doi/10.1002/humu.10191/abstract

There have been very pertinent questions from you all, I have yet to find the answer!

Cancer and mitochondria

http://medicalxpress.com/news/2015-07-mitochondria-oncogenesis-metabolic-reprogramming.html

Monday, 11 August 2014

Sunday, 21 July 2013

Objective and Scope

Objective

The Cancer Biology course includes understanding of cellular mechanisms and players contributing to successful cancer onset, progression, and metastasis. Molecular cell biology of cancer will be studied to know the roles of various gene pathways in initiation, promotion, and progression of cancer that are required to be switched On or Off for turning a normal cell into a cancerous one. The cancer onset is not entirely dependent on a start button from outside, but there are several external agents that 'hit' the button. The cascade that follows a hit is explained in principles of carcinogenesis that is driven by chemical, radiation, virus, or even nothing. Cancer spread requires orchestration of various molecules that dictate site and extent of secondary cancers in the body, is not a natural and predictable fate of the deadly disease, rather cancer has to fight the host barriers at every single stage of its survival and sustenance. Identification of mechanisms and molecules of cancer has enabled the onco-clinicians with tools of detection; preferably early, and treatment. This background is intended to better equip the learners not only for research but also laboratory management, pre-clinical and clinical trials and related areas. These areas require man power capable of  bridging the bench with bed-side. It is this basic research over the years that has changed the norm that was 'cancer means cancel' to 'cancer is a chronic manageable disease' today.