Introduction: In this review, cases of herpes zoster (HZ) infection following receipt of COVID-19 vaccines will be analyzed. We also present two cases of oral HZ following the COVID-19 vaccine and discuss this clinical anatomy.Materials and Methods: A database search using PubMed was conducted in August 2021 and 20 articles were found to be eligible for review. Patient data and vaccine information were analyzed. In addition, two cases of oral HZ infection following the receipt of COVID-19 vaccines are presented.Results: A total of 399 cases were identified. The affected dermatomes mimicked the regular distribution of HZ. For the dermatomes of the face, the various reports used different ways to describe the areas involved; CNV, CNV1, CNV2, CNV3, lower jaw, forehead, and under the eyebrow (CNV, 2 cases; CNV1, 4 cases; CNV2, 3 cases; and CNV3, 3 cases). Some patients who had a history of varicella zoster virus vaccination had HZ following the COVID-19 vaccination. Two patients with oral HZ following vaccination were found to have involvement of the greater palatine nerve.Conclusions: Vaccine-related HZ cases have been reported worldwide. Although many studies with a larger number of cases are ongoing, detailed information can be obtained from case reviews as reported herein.

Phosphorylation of checkpoint kinase 2 (Chk2) at Thr68 (pChk2) induced by DNA double-strand breaks is required for inhibition of cell cycle progression in the G(2) phase. The purpose of the present paper was to investigate the expression of wild-type p53-induced phosphatase 1 (Wip1 or PPM1D), a negative regulator of Chk2, to better understand its role in human gastric cancer. In non-neoplastic gastric mucosa, most epithelial cells exhibited Wip1-positive and pChk2-negative immunoreactivity, whereas an inverse pattern of protein expression was detected at the surface of the foveolar epithelium. In tumor tissues, 74% of 53 gastric cancers had intense Wip1 immunoreactivity and close correlation with both tumor size (P = 0.0497) and Chk2 dephosphorylation (P = 0.0213). In MKN-74 gastric cancer cells, ionizing radiation (IR)-induced Wip1 upregulation was detected at protein levels, but the Chk2-mediated cell cycle regulatory mechanism was disrupted. In addition, protease inhibitor Z-Leu-Leu-Leu (ZLLL) effectively upregulated Wip1 levels in the presence or absence of IR, suggesting that Wip1 expression can be modulated post-transcriptionally. Understanding the Wip1-mediated signaling pathway in gastric cancer may provide useful information for the development of new chemo- and radiotherapies.

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Early in tumorigenesis, a DNA damage-response network is activated in preneoplastic cells that delays or prevents cancer. Activation of the Chk2 G 2 /M checkpoint kinase and loss of fragile histidine triad (Fhit) tumor suppressor expression increase cellular susceptibility to DNA-damaging 'oncogenic' stressors, particularly in precursor or precancerous lesions. To understand the mechanism of oral carcinogenesis, we assessed the association between phosphorylated Chk2 (pChk2) and Fhit expression in oral squamous cell carcinoma. Loss of Fhit expression was an early event during oral carcinogenesis, whereas a decrease in the number of pChk2-positive cells was associated with tumor progression. Although tyrosine 114 is known to be essential to Fhit's tumor-suppressing activity, both wild-type and tyrosine 114 mutant Fhit increased the population of subG 1 DNA-containing HSC-3 OSCC cells with elevated pChk2 levels. In particular, when cells were exposed to ionizing radiation, pChk2 levels were upregulated dramatically, as were those of its downstream target Cdc25C. (1) The incipient 'oncogenic' stress, involving hypoxia, nutrient starvation, UV, ionizing radiation (IR), and chemicals, causes DNA damage in cells in which the mechanism for elimination of such hazardous cells is already compromised in the initial step of human multistep carcinogenesis. (2)(3)(4) In normal cells, double-strand and single-strand DNA breaks lead to the activation of checkpoint responses and subsequent cell cycle arrest in the G 1 /S and G 2 /M phases, or to apoptosis. Two members of the phosphatidylinositol 3-kinase-related serine/ threonine protein kinase family, ataxia telangiectasia mutated (ATM) and ataxia telangiectasia and Rad3-related (ATR), are key molecules in controlling the DNA-damage checkpoint response.(5,6) ATM responds very rapidly to low levels of DNA damage, leading to a conformational change that stimulates autophosphorylation, (5) and ATR responds primarily to damage that causes bulky DNA adducts and stalled replication forks. (6) Of the many downstream targets of ATM and ATR, the tumor suppressors Chk1 and Chk2 have been suggested to play important roles in the regulation of the G 1 /S and G 2 /M checkpoint responses, respectively. Although cancer-associated CHK1 mutation is extremely rare, (10) CHK2 mutations occur in a number of sporadic cancers and in a subset of cases of Li-Fraumeni syndrome. (11,12) Chk2 is a serine/threonine protein kinase that phosphorylates a number of proteins involved in the DNA damage response, such as Cdc25C, Brca1, and p53, all of which can contribute to cell cycle arrest in the G 2 /M phase, apoptosis, and DNA repair. (13) New insights into the biological role of Chk2 in multistep carcinogenesis have been demonstrated using clinical specimens from different stages of human tumors: phosphorylated (p) Chk2 expression was upregulated in precursor or precancerous lesions, whereas defects in the ATM-Chk2 pathway might allow cell proliferation, survival, genomic instability, and tumor progressio...