scholarly journals Nestin-Expressing Cells in the Lung: The Bad and the Good Parts

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3413
Author(s):  
Gilberto Jaramillo-Rangel ◽  
María-de-Lourdes Chávez-Briones ◽  
Adriana Ancer-Arellano ◽  
Marta Ortega-Martínez

Nestin is a member of the intermediate filament family, which is expressed in a variety of stem or progenitor cells as well as in several types of malignancies. Nestin might be involved in tissue homeostasis or repair, but its expression has also been associated with processes that lead to a poor prognosis in various types of cancer. In this article, we review the literature related to the effect of nestin expression in the lung. According to most of the reports in the literature, nestin expression in lung cancer leads to an aggressive phenotype and resistance to chemotherapy as well as radiation treatments due to the upregulation of phenomena such as cell proliferation, angiogenesis, and metastasis. Furthermore, nestin may be involved in the pathogenesis of some non-cancer-related lung diseases. On the other hand, evidence also indicates that nestin-positive cells may have a role in lung homeostasis and be capable of generating various types of lung tissues. More research is necessary to establish the true value of nestin expression as a prognostic factor and therapeutic target in lung cancer in addition to its usefulness in therapeutic approaches for pulmonary diseases.

2014 ◽  
Vol 42 (6) ◽  
pp. 1519-1523 ◽  
Author(s):  
Udi Zurgil ◽  
Assaf Ben-Ari ◽  
Noa Rotem-Dai ◽  
Galia Karp ◽  
Ella Krasnitsky ◽  
...  

The successful treatment of cancer in a disseminated stage using chemotherapy is limited by the occurrence of drug resistance, often mediated by anti-apoptotic mechanisms. Thus the challenge is to pinpoint the underlying key factors and to develop therapies for their direct targeting. Protein kinase C (PKC) enzymes are promising candidates, as some PKCs were shown to be involved in regulation of apoptosis. Our studies and others have shown that PKCη is an anti-apoptotic kinase, able to confer protection on tumour cells against stress and chemotherapy. We have demonstrated that PKCη shuttles between the cytoplasm and the nucleus and that upon DNA damage is tethered at the nuclear membrane. The C1b domain mediates translocation of PKCη to the nuclear envelope and, similar to the full-length protein, could also confer protection against cell death. Furthermore, its localization in cell and nuclear membranes in breast cancer biopsies of neoadjuvant-treated breast cancer patients was an indicator for poor survival and a predictor for the effectiveness of treatment. PKCη is also a novel biomarker for poor prognosis in non-small-cell lung cancer (NSCLC). Thus PKCη presents a potential target for therapy where inhibition of its activity and/or translocation to membranes could interfere with the resistance to chemotherapy.


2018 ◽  
Vol 17 (5) ◽  
pp. 119-124
Author(s):  
Z. V. Grigorievskaya ◽  
V. L. Utkina ◽  
V. А. Byakhova ◽  
I. N. Petukhova ◽  
N. S. Bagirova ◽  
...  

The differential diagnosis of pulmonary diseases is extremely difficult and requires high qualifications of the radiologist and clinician. The differential diagnosis is used to distinguish different lung diseases: nonspecific inflammatory lung diseases (empyema, abscess, pneumonia), tuberculosis, sarcoidosis, benign tumors, lung cancer, lymphogranulomatosis, metastatic changes, and inflammatory changes in lung tissue. We present a clinical case, in which the differential diagnosis between tumor and inflammatory changes in lung tissue allowed the choice of optimal treatment tactics.


2020 ◽  
Vol 10 ◽  
Author(s):  
Kazuki Sone ◽  
Ken Maeno ◽  
Ayako Masaki ◽  
Eiji Kunii ◽  
Osamu Takakuwa ◽  
...  

2002 ◽  
Vol 29 (3 Suppl 12) ◽  
pp. 10-16 ◽  
Author(s):  
Angela Davies ◽  
David R. Gandara ◽  
Primo Lara ◽  
Zelanna Goldberg ◽  
Peter Roberts ◽  
...  

2018 ◽  
Vol 64 (4) ◽  
pp. 522-527
Author(s):  
Aleksey Shutko ◽  
Viktor Mus

Individual parameters of circulating hemopoietic stem cells (HSC) lymphoid origin were measured by cytofluorometry before treatment of patients with metastatic non-small cell lung cancer and were retrospectively compared with individual life span's (LS). The possibility of poor prognosis of treatment's results (LS


2006 ◽  
Author(s):  
Waun K. Hong ◽  
Reuben Lotan ◽  
David Stewart

2007 ◽  
Author(s):  
Waun K. Hong ◽  
Reuben Lotan ◽  
David Stewart

2018 ◽  
Vol 18 (8) ◽  
pp. 773-791
Author(s):  
Dhaval Sanchala ◽  
Lokesh K. Bhatt ◽  
Kedar S. Prabhavalkar

Lung cancer surfaces to be the predominant determinant of mortality worldwide constituting 13% and 19% of all new cancer cases and deaths related to cancer respectively. Molecular profiling has now become a regular trend in lung cancer to identify the driver mutations. Epidermal Growth Factor Receptor (EGFR) is the most regular driver mutation encountered in Non-Small Cell Lung Cancer (NSCLC). Targeted therapies are now available for the treatment of EGFR mutant NSCLC. EGFR mutation is more frequently expressed in adenocarcinoma than squamous cell carcinoma. This article presents a detailed molecular insight of the therapeutic approaches for the treatment of EGFR mutant lung cancer. The article delineates molecular mechanism of the drugs that are approved, the drugs that are in clinical trial and the drugs that have not entered a clinical trial but shows promising future in the treatment of EGFR mutant lung cancer. Furthermore, this article provides concise information on relevant combinational or monotherapy clinical trials that have been completed for various approaches.


2019 ◽  
Vol 19 (23) ◽  
pp. 2128-2142 ◽  
Author(s):  
Hao He ◽  
Chang Xu ◽  
Zhao Cheng ◽  
Xiaoying Qian ◽  
Lei Zheng

: KRAS is the most common oncogene to be mutated in lung cancer, and therapeutics directly targeting KRAS have proven to be challenging. The mutations of KRAS are associated with poor prognosis, and resistance to both adjuvant therapy and targeted EGFR TKI. EGFR TKIs provide significant clinical benefit for patients whose tumors bear EGFR mutations. However, tumors with KRAS mutations rarely respond to the EGFR TKI therapy. Thus, combination therapy is essential for the treatment of lung cancers with KRAS mutations. EGFR TKI combined with inhibitors of MAPKs, PI3K/mTOR, HDAC, Wee1, PARP, CDK and Hsp90, even miRNAs and immunotherapy, were reviewed. Although the effects of the combination vary, the combined therapeutics are one of the best options at present to treat KRAS mutant lung cancer.


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