PhD Public Seminar: SWATI MOHAPATRA, MS
When & Where
July 18
1:00 PM - 2:00 PM
Life Science Plaza, 9.4101-4104, 2130 W Holcombe Blvd, Houston 77030 and via Zoom (View in Google Map)
Contact
- Joy Lademora
- 713-500-9872
- [email protected]
Event Description
Swati Mohapatra, MS (Advisor: George Calin, MD, PhD)
The Role of an Ultraconserved Long Non-coding RNA in B-Cell Lymphomagenesis
Ultraconserved regions (UCRs) are genomic segments with perfect sequence conservation between the orthologous regions of human, rat, and mouse genomes. UCRs can be transcribed into mono-exonic long non-coding RNAs (lncRNAs) known as transcribed ultraconserved regions (T-UCRs). These regions, despite lacking protein-coding potential, are increasingly recognized for their regulatory roles in gene expression, including the modulation of non-coding RNA (ncRNA) transcripts. NcRNAs play crucial roles in cellular processes, including oncogenic transformation, with emerging evidence revealing their ability to encode small peptides known as ncRNA-encoded peptides that are functional (FuncPEPs). These peptides, originating from small open reading frames, contribute to diverse cellular functions and are implicated in disease pathogenesis.
Increasing evidence demonstrates the importance of UCRs and T-UCRs play an oncogenic role in human cancers. However, their role in Chronic Lymphocytic Leukemia (CLL) progression eliciting alterations to the host B cell immune landscape in lymphoid niches are still poorly understood. To elucidate novel regulators of Richter Transformation (RT), aggressive lymphoma transformed from CLL, a functional screen identified potential regulators of the p16INK4A pathway. Deletions of CDKN2A, the gene coding for p16INK4A, are seen in 30% of RT patients and is associated with poor overall survival. uc.206 transcribes into 599-base pair lncRNA called TRUC-16. TRUC-16 is overexpressed in 30-40% of CLL patients’ B cells as compared to normal B cells.
Forced B cell-specific overexpression of TRUC-16 in a murine model using CRISPR-Cas9, induced alterations in BCR signaling and aberrant B cell development providing an in vivo model of CLL progressing into RT in aged mice. Our data suggests that B cell-specific overexpression of TRUC-16 is sufficient to elicit lymphoma-like phenotypes in aged mice via the contribution of aberrant B cell development.
Advisory Committee:
- George Calin, MD, PhD, Chair
- Maria Teresa Bertilaccio, PhD
- Alessandra Ferrajoli, MD
- Yejing Ge, PhD
- Marina Konopleva, MD, PhD
- James You, MD, PhD
Join via Zoom
Meeting ID: 84435626665
Password: 249568
Swati Mohapatra, MS (Advisor: George Calin, MD, PhD)
The Role of an Ultraconserved Long Non-coding RNA in B-Cell Lymphomagenesis
Ultraconserved regions (UCRs) are genomic segments with perfect sequence conservation between the orthologous regions of human, rat, and mouse genomes. UCRs can be transcribed into mono-exonic long non-coding RNAs (lncRNAs) known as transcribed ultraconserved regions (T-UCRs). These regions, despite lacking protein-coding potential, are increasingly recognized for their regulatory roles in gene expression, including the modulation of non-coding RNA (ncRNA) transcripts. NcRNAs play crucial roles in cellular processes, including oncogenic transformation, with emerging evidence revealing their ability to encode small peptides known as ncRNA-encoded peptides that are functional (FuncPEPs). These peptides, originating from small open reading frames, contribute to diverse cellular functions and are implicated in disease pathogenesis.
Increasing evidence demonstrates the importance of UCRs and T-UCRs play an oncogenic role in human cancers. However, their role in Chronic Lymphocytic Leukemia (CLL) progression eliciting alterations to the host B cell immune landscape in lymphoid niches are still poorly understood. To elucidate novel regulators of Richter Transformation (RT), aggressive lymphoma transformed from CLL, a functional screen identified potential regulators of the p16INK4A pathway. Deletions of CDKN2A, the gene coding for p16INK4A, are seen in 30% of RT patients and is associated with poor overall survival. uc.206 transcribes into 599-base pair lncRNA called TRUC-16. TRUC-16 is overexpressed in 30-40% of CLL patients’ B cells as compared to normal B cells.
Forced B cell-specific overexpression of TRUC-16 in a murine model using CRISPR-Cas9, induced alterations in BCR signaling and aberrant B cell development providing an in vivo model of CLL progressing into RT in aged mice. Our data suggests that B cell-specific overexpression of TRUC-16 is sufficient to elicit lymphoma-like phenotypes in aged mice via the contribution of aberrant B cell development.
Advisory Committee:
- George Calin, MD, PhD, Chair
- Maria Teresa Bertilaccio, PhD
- Alessandra Ferrajoli, MD
- Yejing Ge, PhD
- Marina Konopleva, MD, PhD
- James You, MD, PhD
Join via Zoom
Meeting ID: 84435626665
Password: 249568
", "startDate":"2024-7-18", "endDate":"2024-7-18", "startTime":"13:00", "endTime":"14:00", "location":"Life Science Plaza, 9.4101-4104, 2130 W Holcombe Blvd, Houston 77030 and via Zoom", "label":"Add to Calendar", "options":[ "Apple", "Google", "iCal", "Microsoft365", "MicrosoftTeams", "Outlook.com", "Yahoo" ], "timeZone":"America/Chicago", "trigger":"click", "inline":true, "listStyle":"modal", "iCalFileName":"Reminder-Event" }