Deletion of 6q is one of the most frequent chromosomal alterations in human malignant melanoma. Recently, we used chromosome painting probes of 6p and 6q to study 21 melanoma cell lines. A reciprocal translocation between chromosomes 6q and 17p was detected in one cell line (UACC-930). Upon further characterization of the translocation marker using the micro fluorescence in situ hybridization (FISH) technique, a complex rearrangement including an inversion of 6q and a translocation between the inverted 6q and 17p, [der(6)inv(6)(q16q27)t(6;17)(q26;p13)], was detected. A yeast artificial chromosome (YAC) clone spanning the breakpoint at 6q16 was isolated by the FISH screen. Loss of one or more copies of the YAC clone was also detected in 10 of 12 melanoma cell lines. This result implies that the YAC clone may contain a putative tumor suppressor gene related to the pathogenesis of malignant melanoma. Further characterizations of the breakpoint at 6q16 and molecular cloning breakpoints at 6q27 and 17p13 are in progress.
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http://dx.doi.org/10.1016/s0165-4608(01)00608-2 | DOI Listing |
BMJ Oncol
January 2025
Department of Medicine, UPMC Hillman Cancer Center, Pittsburgh, Pennsylvania, USA.
Objective: Cancer patients aged ≥80 years present unique characteristics affecting response to immune checkpoint inhibitors (ICIs), with unidentified molecular differences. This study aimed to explore potential biomarkers of response to ICI in patients ≥80 years.
Methods And Analysis: We analysed tumour samples (n=24 123) from patients ≥80 (versus<80) with non-small cell lung cancer (NSCLC), melanoma (MEL), and renal cell cancer (RCC).
Sci Rep
January 2025
Key Laboratory of Cancer Immunotherapy of Guangdong Tertiary Education, Guangdong CAR-T Treatment Related Adverse Reaction Key Laboratory, The First Affiliated Hospital/Clinical Medical School, Guangdong Pharmaceutical University, Guangzhou, 510080, China.
Previously, we demonstrated that natural host-defence peptide caerin 1.1/caerin 1.9 (F1/F3) increases the efficacy of anti-PD-1 and therapeutic vaccine, in a HPV16 + TC-1 tumour model, but the anti-tumor mechanism of F1/F3 is still unclear.
View Article and Find Full Text PDFCell Death Discov
January 2025
Department of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, China.
Besides the important pathogenic mechanisms of melanoma, including BRAF-driven and immunosuppressive microenvironment, genomic instability and abnormal DNA double-strand breaks (DSB) repair are significant driving forces for its occurrence and development. This suggests investigating novel therapeutic strategies from the synthetic lethality perspective. Poly (ADP-ribose) polymerase 4 (PARP4) is known to be a member of the PARP protein family.
View Article and Find Full Text PDFJ Invest Dermatol
January 2025
Mayo Clinic Arizona, Department of Dermatology, Scottsdale, AZ. Electronic address:
Cutaneous squamous cell carcinoma (cSCC) is one of the most common cancers in humans and kills as many people annually as melanoma. The understanding of the transcriptional changes with respect to high-risk clinical/histopathological features and outcome is poor. Here, we examine stage-matched, outcome-differentiated cSCC using whole exome and transcriptome sequencing.
View Article and Find Full Text PDFBiochem Biophys Res Commun
January 2025
Department of Anatomy, College of Medicine, King Khalid University, Abha, Saudi Arabia. Electronic address:
Background: Melanoma, a highly aggressive skin cancer is frequently driven by the BRAF mutation. Vemurafenib initially offers clinical benefits but often encounters resistance due to secondary mutations and compensatory signaling pathways. Targeting p300, a histone acetyltransferase involved in transcriptional regulation and resistance mechanisms, presents a potential strategy to overcome this therapeutic challenge.
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