Journals / Selçuk Tıp Dergisi / 2019 / Cilt: 35 - Sayı: 2

Evalution of The Puma and P53 Significance in Multiple Myelom

Multipl Miyelom Patogenezinde Puma ve P53'ün Öneminin Değerlendirilmesi

Pages
94–98
Publication Date
2022-10-17
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Conclusion: Our results showed that specially PUMA expression is significantly higher in bone marrow cells of MM patients compared to healthy controls.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Aim: Multipl myeloma is a disease of unknown pathogenesis.
📊
Key Findings & Data:PUMA may play a role in apoptosis, bound or unbound p53.
💡
Conclusion & Impact:Conclusion: Our results showed that specially PUMA expression is significantly higher in bone marrow cells of MM patients compared to healthy controls.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Aim: Multipl myeloma is a disease of unknown pathogenesis. Although there was a different hypotheses on the subject, recently mutations in the pathway of apoptosis come to the fore. PUMA may play a role in apoptosis, bound or unbound p53. The role is regulated by various signals of transcription factors. In this study; the expressions of p53 and PUMA in bone marrow hematopoetic cells of have been worked and the relationship between myeloma pathogenesis with p53- PUMA was searched. Patients and Methods: The expression of p53 and PUMA was evaluated using immunohistochemistry. The procedure was carried out using specific antibodies against p53 and PUMA. Bone marrow biopsies of MM patients at the time of diagnosis (n=31) were included in the study group. Bone marrow biopsies from individuals who had normal hematopoiesis (n=12) were included as control. After staining, strength was calculated of each positively staining cells. Results: The percentage of cells showing PUMA expression was significantly higher in bone marrows of MM patients as compared to normal bone marrow samples (p=0.000). We found a correlation between the percentage of plasma cells with staining prevalence of PUMA, but it was not statistically significant (p=0.385). There was no correlation between the stage of the disease with PUMA expression. Conclusion: Our results showed that specially PUMA expression is significantly higher in bone marrow cells of MM patients compared to healthy controls. Higher positivity of PUMA suggested that, PUMA induced nongenotoxic reasons at the time of diagnosis. The lack of p53 and PUMA positivite suggests that, apoptosis play a role in myeloma pathogenesis.

Özet

Amaç: Multipl miyelom (MM) patogenezi tam olarak bilinmeyen bir hastalıktır. Konuyla ilgili farklı hipotezlerde ileri sürülse de son zamanlarda apopitozis yolaklarındaki mutasyonlar ön plana çıkmaktadır. PUMA p53 ile ilişkili veya ilişkisiz olarak transkripsiyon faktörlerince düzenlenen çeşitli sinyallerle apopitozisde rol alabilir. Bu çalışmada; p53 ve PUMA ekspresyonlarını çalışılmış ve p53-PUMA ekspresyonu ile hastalık patogenezi arasında bir ilişki aranmıştır. Hastalar ve Yöntem: p53 ve PUMA ekspresyonları immünohistokimyasal yöntemle değerlendirildi. İşlem p53 ve PUMA’ya karşı spesifik antikor kullanılarak gerçekleştirildi. MM hastalarının tanı anındaki kemik iliği biyopsiler örnekleri (n=31) çalışma grubu olarak alındı. Normal hematopoez tespit edilen kemik iliği biyopsileri (n=12) kontrol grubu olarak alındı. Boyandıktan sonra pozitif boyanan her bir örneğin boyanma kuvveti hesaplandı. Bulgular: MM hastalarının kemik iliklerinde PUMA ekspresyonu gösteren hücrelerin yüzdesi, normal bireylerin kemik iliklerine göre önemli ölçüde yüksekti (p=0.000). Plazma hücre yüzdesi ile PUMA boyanma yaygınlığı arasında istatiksel olarak anlamlı olmasa da bir ilişki mevcuttu (p=0.385). PUMA ekspresyonları ile hastalığın evresi arasında bir ilişki yoktu. Sonuç: Sonuçlarımız, MM hastalarının kemik iliği örneklerinde özellikle PUMA ekspresyonunun, sağlıklı kontrollere göre önemli ölçüde daha yüksek olduğunu gösterdi. PUMA pozitifliğinin p53’ e oranla daha fazla olması tanı anında PUMA’ nın nongentoksik nedenlerle indüklendiğini düşündürdü. p53 ve PUMA pozitifliğinin kontrol grubuna göre yüksek olması miyelom patogenezinde apopitozisin rol oynadığını düşündürmektedir.

🔖

Cite This Article

BİLGİN, A. U., BALOĞLU, İ. (2022). Evalution of The Puma and P53 Significance in Multiple Myelom. Selçuk Tıp Dergisi, Cilt: 35 - Sayı: 2, 94–98. https://ajindex.com/articles/591840

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (16)

  1. Kyle RA, Gertz MA, Witzig TE, et al. Review of 1027 patients with newly diagnosed multiple myeloma. Mayo Clin Proc 2003;78(1):21-33
  2. Yoshida Y. The role of apoptosis in MDS; in Steensma DP (ed): Myelodysplastic syndromes: Pathobiology and clinical management. Informa healthcare, 2009, pp 107-25
  3. Jabbour AM, Gordon L, Daunt CP, et al. p53-Dependent transcriptional responses to interleukin-3 signaling. Plos One 2012;7(2):e31428
  4. Gordon M. Stem cell and hematopoezis. In: Hoffbrand AV, Catovsky D, Tuddenham E (eds): Postgraduate Haematology. Blackwell publishing, 2005, pp 1-12
  5. Jabbour AM, Daunt CP, Green BD, et al. Myeloid progenitor cells lacking p53 exhibit delayed up-regulation of Puma and prolonged survival after cytokine deprivation. Blood 2010;115(2):344-52
  6. Yu J, Zhang L. No PUMA, no death: Implications for p53- dependent apoptosis. Cancer Cell 2003;4(4):248-9
  7. Loth TS, Perrotta AL, Lima J, et al. Genetic aspects of familial multiple myeloma. Mil Med 1991;156(8):430-3
  8. Isomaki HA, Hakulinen T, Joutsenlahti U. Excess risk of lymphomas, leukemia and myeloma in patients with rheumatoid arthritis. J Chronic Dis 1978;31(11):691-6
  9. Berenson JR, Vescio RA. HHV-8 is present in multiple myeloma patients. Blood 1999;93(10):3157-9; discussion 3164-56
  10. Hallek M, Bergsagel PL, Anderson KC. Multiple myeloma: Increasing evidence for a multistep transformation process. Blood 1998;91(1):3-21
  11. Taniwaki M, Nishida K, Ueda Y, et al. Non-random chromosal rearrangements and their implications in clinical features and outcome of multiple myeloma and plasma cell leukemia. Leuk Lymphoma 1996;21(1-2):25-30
  12. Feinman R, Sawyer J, Hardin J, et al. Cytogenetics and moleculer genetics in multiple myeloma. Hematol Oncol Clin North Am 1997;11(1):1-25
  13. Ryan KM. p53 and autophagy in cancer: Guardian of the genome meets guardian of the proteome. Eur J Cancer 2011;47(1):44-50
  14. Liu P, Leong T, Quam L, et al. Activating mutations of Nand Kras in multiple myeloma show different associations: Analysis of the Eastern Cooperative Oncology Group Phase III Trial. Blood 1996;88(7):2699-706
  15. Yu J, Zhang L. PUMA, potent killer with or without p53. Oncogene 2008;27 Suppl 1:S71-83 16. Qiu W, Wang X, Leibowitz B, et al. PUMA-mediated apoptosis drives chemical hepatocarcinogenesis in mice. Hepatology 2011;54(4):1249-58
  16. Raza A, Gezer S, Mundle S, et al. Apoptosis in bone marrow biopsy samples involving stromal and hematopoietic cells in 50 patients