Journal of Molecular Oncology Research

All submissions of the EM system will be redirected to Online Manuscript Submission System. Authors are requested to submit articles directly to Online Manuscript Submission System of respective journal.
Reach Us +1 (202) 780-3397

Short Communication - Journal of Molecular Oncology Research (2024) Volume 8, Issue 6

The role of genomic instability in oncology and molecular pathology.

Portik Steven *

Department of Radiotherapy, University Medical Center Rotterdam, Netherlands

*Corresponding Author:
Portik Steven
Department of Radiotherapy, University Medical Center Rotterdam, Netherlands
E-mail: Portik@steven.nl

Received: 01-Nov-2024, Manuscript No. AAMOR -24-155338 ; Editor assigned: 02-Nov-2024, PreQC No. AAMOR -24-155338 (PQ); Reviewed: 18-Nov-2024, QC No. AAMOR -24-155338 ; Revised: 22-Nov-2024, Manuscript No. AAMOR -24-155338 (R); Published: 29-Nov-2024, DOI: 10.35841/ aamor-8.6.270

Citation: : Steven P. The role of genomic instability in oncology and molecular pathology. J Mol Oncol Res. 2024;8(6):270.

Visit for more related articles at Journal of Molecular Oncology Research

Introduction

Melanoma, a type of skin cancer that originates in melanocytes, the pigment-producing cells of the skin, poses a significant threat to public health globally. Despite accounting for a small fraction of all skin cancer cases, melanoma is responsible for a disproportionate number of skin cancer-related deaths due to its aggressive nature and tendency to metastasize. This article aims to shed light on the causes, risk factors, symptoms, diagnosis, treatment, and prevention strategies associated with melanoma, emphasizing the importance of early detection and intervention in combating this potentially lethal disease [1, 2].

Melanoma arises when melanocytes, the cells responsible for producing melanin, the pigment that gives skin its color, undergo malignant transformation. While melanoma can develop anywhere on the body, it most commonly occurs on sun-exposed areas, such as the face, neck, chest, back, and legs. Melanoma can also develop in areas that are not typically exposed to sunlight, including the palms, soles, under the nails, and mucous membranes. Exposure to ultraviolet (UV) radiation from sunlight or artificial sources, such as tanning beds, is the primary environmental risk factor for melanoma. Other factors that increase the risk of melanoma include: Individuals with fair skin, light hair, and blue or green eyes are at higher risk due to reduced melanin production and less natural protection against UV radiation [3, 4].

History of Sunburns: Severe sunburns, especially during childhood or adolescence, increase the risk of developing melanoma later in life. Having a family member with melanoma increases the risk of developing the disease. Individuals with a history of melanoma or other skin cancers are at increased risk of developing subsequent melanomas. Conditions or medications that suppress the immune system can increase the risk of melanoma. Early detection of melanoma is critical for favorable outcomes. Common signs and symptoms of melanoma include: Moles with irregular shapes or uneven borders. Moles with blurred, jagged, or notched edges. Moles that exhibit multiple colors or shades of brown, black, blue, red, or white. Moles larger than the size of a pencil eraser (6 millimeters) or any new or changing mole should be evaluated [5, 6].

Skin Biopsy: Removal of a sample of suspicious tissue for examination under a microscope to confirm the presence of melanoma and determine its characteristics, such as thickness and subtype. A non-invasive technique that uses a specialized magnifying lens to evaluate skin lesions for features suggestive of melanoma. Treatment for melanoma depends on the stage of the disease, as well as factors such as tumor thickness, ulceration, and genetic mutations. Treatment modalities for melanoma may include: Surgical excision of the melanoma and a surrounding margin of normal tissue is the primary treatment for early-stage melanomas. Drugs that boost the body's immune response to target and destroy cancer cells, such as checkpoint inhibitors (e.g., pembrolizumab, nivolumab) and interleukin-2 (IL-2) [7, 8].

Targeted Therapy: Drugs that specifically target genetic mutations in melanoma cells, such as BRAF inhibitors (e.g., vemurafenib, dabrafenib) and MEK inhibitors (e.g., trametinib, cobimetinib). Use of high-energy beams to target and destroy cancer cells, particularly in cases where surgery is not feasible or for palliative treatment of advanced disease. Systemic drugs that kill rapidly dividing cancer cells, although they are less commonly used in melanoma due to limited efficacy compared to other treatment options. Preventing melanoma involves adopting sun-safe behaviors and minimizing exposure to UV radiation. Use broad-spectrum sunscreen with SPF 30 or higher, wear protective clothing, seek shade during peak sun hours, and avoid indoor tanning beds. Regularly examine your skin for new or changing moles, and promptly report any concerning lesions to a healthcare provider. Undergo annual skin examinations by a dermatologist, especially if you have risk factors for melanoma [9, 10].

Conclusion

Melanoma is a formidable adversary, capable of metastasizing and threatening life if left untreated. However, with early detection, timely intervention, and advances in treatment modalities such as surgery, immunotherapy, and targeted therapy, the prognosis for patients with melanoma has improved significantly in recent years. By raising awareness of risk factors, promoting sun-safe behaviors, and advocating for regular skin examinations, we can work together to prevent melanoma, detects it at its earliest stages, and ultimately save lives.

References

  1. Schmitz M. Quantitative multiplex PCR assay for the detection of the seven clinically most relevant high-risk HPV types. J Clin Virol. 2009;44:302-07
  2. Indexed at, Google ScholarCross Ref

  3. Abidin AZ, Garassino MC, Raffaele C, et al. Targeted therapies in small cell lung cancer: A review. Ther Adv Med Oncol. 2010; 2:25-37.
  4. Indexed atGoogle ScholarCross Ref

  5. Frumovitz M. Sequencing of mutational hotspots in cancer-related genes in small cell neuroendocrine cervical cancer. Gynecol Oncol. 2016;141:588-91.
  6. Indexed atGoogle ScholarCross Ref

  7. Peeters M. Mutant KRAS codon 12 and 13 alleles in patients with metastatic colorectal cancer: assessment as prognostic and predictive biomarkers of response to panitumumab. J Clin Oncol. 2013; 31:759-65.
  8. Indexed atGoogle ScholarCross Ref

  9. Lyons YA, Frumovitz M, Soliman PT, et al. Response to MEK inhibitor in small cell neuroendocrine carcinoma of the cervix with a KRAS mutation. Gynecol Oncol Rep. 2014; 10:28-29.
  10. Indexed atGoogle ScholarCross Ref

  11. Wang Y, Wan YY. Golgi protein 73, hepatocellular carcinoma and other types of cancers. Liver Res. 2020; 4:161-67.
  12. Indexed at, Google ScholarCross Ref

  13. Shih TC, Wang L, Wang HC, et al. Glypican-3: a molecular marker for the detection and treatment of hepatocellular carcinoma. Liver Res. 2020; 4:168-72.
  14. Indexed atGoogle Scholar, Cross Ref

  15. Greuber EK, Smith-Pearson P, Wang J, et al. Role of ABL family kinases in cancer: from leukaemia to solid tumours. Nat Rev Cancer. 2013;13:559-71.
  16. Indexed atGoogle ScholarCross Ref

  17. Wang F, Hou W, Chitsike L, et al. ABL1, overexpressed in hepatocellular carcinomas, regulates expression of NOTCH1 and promotes development of liver tumors in mice. Gastroenterol. 2020; 159:289-05.
  18. Indexed atGoogle ScholarCross Ref

  19. Tong M, Che N, Zhou L, et al. Efficacy of annexin A3 blockade in sensitizing hepatocellular carcinoma to sorafenib and regorafenib. J Hepatol. 2018;69:826-39.
  20. Indexed at, Google ScholarCross Ref

Get the App