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This study suggests that the oncogene c-Myc can induce DNA damage by increasing reactive oxygen species, potentially overriding p53 and contributing to genetic instability in cancer cells.

This study found that rapamycin effectively inhibits TPA-induced keratinocyte proliferation and skin tumor promotion by targeting mTORC1 signaling in both wild-type and transgenic mice.

The study found that over-expressing ornithine decarboxylase in the outer root sheath of the hair follicle in mice increases UVB-induced tumor growth and invasive squamous cell carcinoma compared to inter-follicular epidermal keratinocytes.

New cancer treatments show promise in reducing tumor growth and improving skin regeneration in mice.

This review explores various theories of colorectal cancer stem cell biology and highlights the need for better identification and targeting of these cells to advance treatment strategies, but reports no new clinical findings.

This review discusses recent findings on molecular changes in cutaneous adnexal tumours and reports novel markers and pathways involved, highlighting the diverse oncogenic drivers and tumour suppressor alterations.

This study reported that overexpressing ornithine decarboxylase in C57Bl/6 mice increased their sensitivity to tumor promotion by TPA, a change reversible by doxycycline treatment.

In this study, researchers discovered that the HrasG12V oncogenic mutation in murine skin epithelial cells initially promotes progenitor cell renewal but later leads to a balanced differentiation, stabilizing clone growth.

This study found that mitochondrial fusion regulator Opa1 is crucial for maintaining melanocyte stem cells during the hair follicle cycle in mice, with Opa1 deficiency leading to impaired SCF-KIT signaling, reduced melanocyte populations, and early hair graying.

This case report describes a young woman with an adrenal oncocytic tumor of uncertain malignant potential, highlighting the need for ongoing surveillance due to possible malignancy.

In this study, PKCepsilon transgenic mice showed increased TNFalpha shedding during skin tumor promotion, which may contribute to the development of metastatic squamous cell carcinoma.

This study reports that VP-16-213 (etoposide) shows significant therapeutic activity in several cancers including small cell bronchogenic carcinoma and certain leukemias, with hematologic toxicity being the primary side effect.

In this study, researchers observed that oncogenic HrasG12V in single murine epidermal cells leads to an initial increase in progenitor cell renewal, but ultimately results in balanced cell fate choices that limit clone growth.

This study found that mutant cells in hair follicles can be tolerated or eliminated by surrounding normal tissue, suggesting the potential for wild-type cells to counteract oncogenic mutations.

This study found that in keratin 14-targeted transgenic mice, BMP antagonism via noggin led to the development of hair follicle tumors, mediated through alterations in Wnt and Shh signaling pathways.

This study found that overexpression of PKCepsilon in mouse epidermis was associated with increased susceptibility to metastatic squamous cell carcinoma, potentially through a mechanism involving tumor necrosis factor-alpha.

This study reviews prior research using transgenic K6/ODC mice and demonstrates that elevated polyamines in epithelial cells contribute significantly to skin tumor development and progression by stimulating proliferation, altering cell signaling and chromatin remodeling, and affecting immune functionality, amongst other mechanisms.

This study found that activating CXCR2 on ras-transformed keratinocytes promotes migration and tumor development in a mouse skin model.

In this study using genetic mouse models, researchers discovered that senescent melanocytes in nevi secrete osteopontin, which activates hair stem cells, enhancing hair growth; this process is mirrored in human hairy nevi, suggesting a potential therapeutic target for regenerative disorders.

This review reports that KRT80 is overexpressed in various cancers, enhancing cancer cell proliferation, invasiveness, and migration, suggesting it as a potential therapeutic target, though more clinical studies are needed to fully understand its role in cancer prognosis.

In this study, the authors found that targeting mTORC1 with rapamycin inhibited TPA-induced skin tumor promotion by affecting keratinocyte proliferation, including critical stem cell populations in the mouse epidermis.

In this study, activation of oncogenic K-ras in a mouse model caused the oral mucosa to rapidly progress from squamous hyperplasia to carcinoma within 14 days, demonstrating its acute sensitivity.

Noggin promotes skin tumors by activating certain cell signaling pathways.

The study observed that the tumor suppressor activity of bone morphogenetic proteins in mouse skin epithelium depends on Noggin levels, inhibiting Wnt and Shh signaling pathways to prevent tumor initiation and progression.

In this study, FOL-026, a peptide based on osteopontin, was shown to promote angiogenesis and stimulate vascular cell proliferation and migration through neuropilin-1, similar to VEGF, suggesting potential therapeutic applications in vascular repair and angiogenesis-related conditions.

This study found that inhibiting AP-1 transcription factors in mice causes squamous tumors to transform into sebaceous tumors and regulates tumor cell lineage.

This study proposes that mammalian target of rapamycin (mTOR) may connect various signaling pathways in hair follicle tumor formation, offering a potential unified model for understanding these tumors.