Increased c-Ki-ras expression in hamster lung exposed to N-nitrosodiethylamine and hyperoxia as detected by the polymerase chain reaction

Ning, Hansun; Oreffo, Victor; Gumerlock, Paul H.; Witschi, Hanspeter

doi:10.1016/0304-3835(91)90138-8

Cited by 8 publications

(5 citation statements)

References 9 publications

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“… 287 , 288 Conversely, different groups have observed that respiration hyperoxia can act as a promoting stimulus to induce lung tumorigenesis of neuroendocrine tumors. 289 , 290 , 291 , 292 , 293 , 294 Initially, the effect of hyperoxia on cancer cells was poorly characterized. With the deepening of hyperoxia research and the understanding of the hypoxic TME, respiration hyperoxia was not thought to promote tumor development.…”

Section: Antitumor Effects Of Hyperoxia Therapymentioning

confidence: 99%

“…demonstrated that sustained exposure to 70% oxygen in mice inhibited the development of lung tumors 287,288 . Conversely, different groups have observed that respiration hyperoxia can act as a promoting stimulus to induce lung tumorigenesis of neuroendocrine tumors 289–294 . Initially, the effect of hyperoxia on cancer cells was poorly characterized.…”

Section: Antitumor Effects Of Hyperoxia Therapymentioning

confidence: 99%

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Hypoxia signaling in cancer: Implications for therapeutic interventions

Zhuang

Liu

et al. 2023

MedComm

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Hypoxia is a persistent physiological feature of many different solid tumors and a key driver of malignancy, and in recent years, it has been recognized as an important target for cancer therapy. Hypoxia occurs in the majority of solid tumors due to a poor vascular oxygen supply that is not sufficient to meet the needs of rapidly proliferating cancer cells. A hypoxic tumor microenvironment (TME) can reduce the effectiveness of other tumor therapies, such as radiotherapy, chemotherapy, and immunotherapy. In this review, we discuss the critical role of hypoxia in tumor development, including tumor metabolism, tumor immunity, and tumor angiogenesis. The treatment methods for hypoxic TME are summarized, including hypoxia‐targeted therapy and improving oxygenation by alleviating tumor hypoxia itself. Hyperoxia therapy can be used to improve tissue oxygen partial pressure and relieve tumor hypoxia. We focus on the underlying mechanisms of hyperoxia and their impact on current cancer therapies and discuss the prospects of hyperoxia therapy in cancer treatment.

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Section: Antitumor Effects Of Hyperoxia Therapymentioning

confidence: 99%

Section: Antitumor Effects Of Hyperoxia Therapymentioning

confidence: 99%

Hypoxia signaling in cancer: Implications for therapeutic interventions

Zhuang

Liu

et al. 2023

MedComm

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“…␤-Actin is a well-known housekeeping gene and has been commonly used as an internal control for the RT-PCR studies. [25][26][27][28] As mRNA of ␤-actin exists in both the viable epithelial and dermal cells, in this series we just simply excised the epithelial part of the keloid for all the specimens used in RT-PCR studies. In this circumstance, identification of the ␤-actin fragments in the RT-PCR study mainly indicated the existence of viable dermal cells.…”

Section: Discussionmentioning

confidence: 99%

“…Analysis of ␤-actin cDNA was an internal control for the immersed skin organ culture model and PCR reactions. [25][26][27][28] Primers for ␤-actin cDNA were ␤A-1 (5'-CTCTTCCAGCCTTCCTTCC-3') and ␤A-2 (5'-GTCACCT-TCACCGTTCCAG-3'), which generated a 559-bp PCR product. The cycling parameters were 5 minutes at 94°C, followed by 35 cycles of 1 minute at 94°C, 1 minute at 60°C, and 1 minute at 72°C.…”

Section: Rt-pcr Amplification Of Aav Lacz and ␤-Actin Mrnamentioning

confidence: 99%

Gene Transfer into Human Keloid Tissue with Adeno-Associated Virus Vector

Cheng

et al. 2003

The Journal of Trauma: Injury, Infection, and Critical Care

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BACKGROUND Gene transfer is a new territory for clinicians. Intractable disorders might be approached in such a way. Adeno-associated virus (AAV) vector has been transfected successfully into a variety of tissues including skin. We evaluated the ability of this vector to transfer and cause expression of the reporter gene in human keloid tissue. METHODS Human keloid specimens were injected with an AAV vector encoding beta-galactosidase and incubated for 4 weeks after injection. The presence of mRNA and beta-galactosidase enzymatic activity were assayed by reverse-transcriptase polymerase chain reaction and the X-gal technique. RESULTS Gene expression shown by reverse-transcriptase polymerase chain reaction was observed in keloid tissue 4 weeks after injection, and so was the positive X-gal staining. CONCLUSION Our results showed that AAV vector could transduce human keloid tissue effectively. Replacement of the reporter gene with a functioning gene might be feasible for keloid treatment.

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“…T h e strategy for quantitative RT-PCR that we used here is a further extension of our previous reports (Ning et al, 1991;Fishman et al, 1994). Briefly, one microgram of extracted total cellular RNA was reverse transcribed to a pool of cDNA with random hexamer primers.…”

Section: Quantitative Rt-pcr Analysismentioning

confidence: 99%