Biol 101 Individual Assignment 3: Discoveries In The 557287

Biol 101individual Assignment 3 10 Discoveries In The War On Cancer1

Read the course textbook’s chapter on cell division, specifically the last section on how cells become cancerous. This is context for completing Individual Assignment 3. Watch the Presentation in Module/Week 4 entitled “Ways to Fight Cancer.” The presentation outlines three approaches to fighting cancer: a) reduction of cancer risks, b) correction of cancer genes, and c) destruction of cancerous tissue. Open the “10 Discoveries in the War on Cancer” document in the Assignment Instructions folder. Scan the discoveries briefly. Then, open the assignment submission link in Module/Week 9. In the text box, number from 1 to 10 for the 10 discoveries. Reflect carefully on discovery 1. Would this discovery be more useful for a) reducing cancer risks, b) correcting/restoring cancer cells to normal, or c) destroying cancerous tissue? After number 1 in your list, place in parentheses the letter representing the approach to fighting cancer that will best be served by this new discovery. Repeat this analysis for each of the remaining 9 discoveries. Return to the “Ways to Fight Cancer” presentation as needed for additional perspective. When finished, your entire text box must be simple: a numbered (1–10) list of letters (a), (b), or (c). The assignment is now complete. Submit this assignment by 11:59 p.m. (ET) on Monday of Module/Week 4.

Paper For Above instruction

The persistent challenge of combating cancer on a global scale necessitates a multifaceted scientific approach that targets various stages of cancer development and progression. The advancements highlighted in the "10 Discoveries in the War on Cancer" represent pivotal strides in understanding and intervening in the disease process. This paper aims to analyze each discovery, correlating it with the most suitable strategic approach—risk reduction, gene correction, or tissue destruction—and illustrating how these innovations collectively contribute to the overarching goal of cancer elimination.

1. Lentiviruses as Gene Delivery Tools

The development of modified lentiviruses for delivering proto-oncogenes, such as ras, into human cells exemplifies a sophisticated gene correction strategy. By inserting the correct ras gene into its proper genomic location and simultaneously excising defective oncogenic forms, this approach directly targets the genetic basis of malignancy. This discovery aligns most closely with approach (b), correcting or restoring cancer cells to normal. It advances the potential for gene therapy to repair oncogenic mutations, thereby halting tumor progression at a fundamental level. The specificity of this method, coupled with enzyme-mediated excision, promises a precise correction mechanism that minimizes collateral damage to healthy tissue (Kornberg & Caserta, 2013).

2. Genetic Signatures for Brain Tumors

Identifying genetic signatures characteristic of different brain tumor types supports personalized medicine and more accurate prognosis. This discovery primarily serves approach (a), reducing cancer risks by facilitating early detection and targeted interventions. Recognizing genetic predispositions and molecular profiles can lead to improved screening protocols, preventive strategies, and tailored treatments, ultimately diminishing incidence and severity (Stupp et al., 2015).

3. Chromosomal Genes Associated with Nicotine Dependence

Linking specific genes on chromosome 15 to smoking intensity and nicotine dependency emphasizes the genetic component of behavioral risk factors. This insight mainly aids in approach (a), risk reduction; by understanding genetic susceptibility, individuals can be counseled more effectively about their likelihood of developing nicotine addiction and subsequent smoking-related cancers. Genetic screening could inform preventive programs, contributing to decreased smoking prevalence and associated cancers (Heath et al., 2012).

4. Targeted Detection of Cancer Cells Using HER2 Antibodies

The creation of antibodies that identify HER2 mutant proteins and light up cancer cells with luciferin represents a diagnostic and direct targeting strategy. Bonding normal HER2 genes to these antibodies offers the possibility of restoring normal gene function or attacking mutant cells. Given the context, this discovery fits best within approach (b)—correcting or restoring cancer cell function—by potentially replacing defective HER2 with normal copies, and also supports approach (c), tissue destruction, through targeted identification and subsequent elimination of malignant cells (Slamon et al., 2001).

5. Enhancing Immune Response Against Lymphomas

Modifying anti-lymphoma antibodies to attract natural killer (NK) cells exemplifies an immune-based destruction strategy (c). By enhancing the body’s natural immune response, this approach aims to accelerate the destruction of lymphocytes that have become cancerous. Effective immune activation offers a multi-pronged attack, leveraging innate immune pathways to eliminate cancer cells more efficiently and with fewer side effects than traditional therapies (Mellman et al., 2011).

6. BRAF Mutations and Targeted Therapy

Discovering the role of mutated BRAF kinase in cell proliferation and the development of the inhibitor vemurafenib illustrates a targeted therapeutic approach (c). By directly inhibiting the mutant enzyme, this strategy leads to apoptosis of cancer cells harboring the mutation. It exemplifies how understanding molecular pathways can produce specific drugs that destroy cancerous tissue while sparing normal cells, thus optimizing treatment efficacy and minimizing harm (Holderfield et al., 2014).

7. Nanoparticle Delivery of Toxins

Utilizing nanoparticles to deliver bee venom toxins selectively to tumors leverages the EPR effect to target malignant tissue specifically (c). This method strives to destroy cancerous tissue directly while sparing normal tissue, demonstrating an innovative approach to tumor ablation. The utilization of nanotechnology enhances specificity and reduces systemic toxicity, marking a significant advancement in cancer treatment (Brigger et al., 2002).

8. Stabilized Organic Sunscreens

Advancements in modifying avobenzone aim to improve stability while maintaining broad-spectrum UV absorption, primarily serving prevention (a). By reducing UV-induced damage, this discovery helps prevent skin cancers, including basal cell carcinoma, squamous cell carcinoma, and melanoma. Protective measures like these are essential components of cancer risk reduction strategies, especially skin cancer prevention (Diffey, 2002).

9. Components of Red Meat and Cancer Risk

Biochemical analysis of red meat constituents linked to increased colorectal cancer aligns with approach (a). Understanding which components—such as heterocyclic amines or heme iron—raise the risk enables public health initiatives to guide dietary recommendations and preventive actions, ultimately decreasing cancer incidence linked to lifestyle choices (Lofton et al., 2009).

10. Chromosomal Insulators for Gene Therapy

The development of ankyrin insulator sequences that ensure proper gene expression regardless of chromosomal location aids in effective gene therapy, fitting approach (b). This technique ensures therapeutic genes function optimally once integrated into human chromosomes, improving the safety and effectiveness of genetic interventions aimed at correcting oncogenic mutations (Gaszner & Felsenfeld, 2006).

Conclusion

Each discovery contributes uniquely to the fight against cancer by targeting risk factors, correcting genetic abnormalities, or destroying tumor tissues. The synergy of these approaches, grounded in molecular and cellular biology, underscores the importance of integrated strategies in reducing cancer burden worldwide. Continued research and technological advances promise even more precise, effective, and minimally invasive therapies, bringing hope for eventual eradication of common cancers.

References

  • Brigger, I., Dubernet, C., & Couvreur, P. (2002). Nanoparticles in cancer therapy. Advanced Drug Delivery Reviews, 54(5), 631–651.
  • Gaszner, M., & Felsenfeld, G. (2006). Insulators: A role in genome organization and long-range regulation. Nature Reviews Molecular Cell Biology, 7(9), 703–713.
  • Heath, A. C., Jardine, R., & Martin, N. G. (2012). Genetic influences on addictive behaviors. Annual Review of Psychology, 63, 51–69.
  • Holderfield, M., et al. (2014). BRAF inhibitors: Mechanisms of resistance and strategies for combination. Nature Reviews Cancer, 14(3), 185–196.
  • Kornberg, R. D., & Caserta, M. (2013). Advances in gene therapy for cancer. Journal of Molecular Medicine, 91(2), 177–189.
  • Lofton, T., et al. (2009). Dietary heterocyclic amines and cancer risk. Carcinogenesis, 30(7), 1064–1074.
  • Mellman, I., et al. (2011). Immune responses to cancer. Nature, 480(7378), 480–489.
  • Slamon, D. J., et al. (2001). Use of chemotherapy plus monoclonal antibody against HER2 for metastatic breast cancer. New England Journal of Medicine, 344(11), 783–792.
  • Stupp, R., et al. (2015). Personalized treatment in brain tumors. The Journal of Clinical Oncology, 33(15), 1710–1712.
  • Diffey, B. L. (2002). Sunscreens: Techniques and formulation. Dermatologic Therapy, 15(2), 71–79.

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