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Question #46497
The Question
A patient with a history of chronic, untreated Plasmodium falciparum infection is diagnosed with a highly metastatic malignancy. Researchers hypothesize that the recurrent release of the parasite's metabolic byproduct, haemozoin, facilitated this oncogenic progression. Based on the principles of cellular health and disease pathogenesis, which of the following mechanisms best explains how chronic haemozoin exposure promotes metastasis?
Options
- A.
It acts as a viral oncogene (v-onc) that directly integrates into the host genome, triggering malignant transformation.
- B.
It induces chronic inflammation, causing phagocytes to persistently release reactive oxygen species (ROS) that mutate cellular oncogenes (c-onc).
- C.
It selectively depletes Helper T-cells, suppressing immune surveillance and allowing rapid proliferation of neoplastic cells.
- D.
It directly degrades the extracellular matrix and cadherins, physically abolishing contact inhibition between normal cells.
Check Your Answer
Correct Answer
Step-by-Step Solution
Explanation
How the Examiner Thinks
Regulatory_Failure
Understand how NOT, EXCEPT, and logical constraints are used to manipulate exam results.
Concepts Behind This Question
Haemozoin|Reactive Oxygen Species (ROS)|Cellular Senescence
Why This Question Is Tricky
Common Mistakes
Conceptual Pivot: Students typically memorize 'haemozoin = fever' and 'c-onc = cancer' in strict isolation.
This question requires synthesizing two distinct NCERT chapters (Human Health and Disease: Malaria & Cancer) to understand 'inflammation-associated carcinogenesis'.
The trap lies in confusing the indirect, ROS-mediated DNA damage caused by a pathogen's metabolic byproduct with the direct actions of oncogenic viruses (Option A) or metastatic enzymes (Option D).
Quick Facts About This Question
Question Information
| Subject | Biology |
| Chapter | Human Health and Disease - Class 12 |
| Concept | Haemozoin Release |
| Difficulty | 8 |
| Cognitive Load | 5 |
| Target Solve Time | 120 sec |
| Access | Free |