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Biomedicines
Special Issues
Cancer Metastasis and Therapeutic Resistance 2.0
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Cancer Metastasis and Therapeutic Resistance 2.0

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cancer Biology and Oncology".

Deadline for manuscript submissions: closed (31 July 2023) | Viewed by 4443

Special Issue Editor

Dr. Elizabeth Shinmay Yeh

E-Mail Website
Guest Editor
Department of Pharmacology and Toxicology, Indiana University School of Medicine, Simon Comprehensive Cancer Center, Indianapolis, IN, USA
Interests: cancer; metastasis; kinases; cell signaling; therapeutic resistance; autophagy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Metastasis and resistance to cancer treatments often go hand in hand, relying on overlapping mechanisms that allow cancer to progress from its primary form to more severe disease states. These mechanisms include the activation of signaling pathways, evasion of immune surveillance, and alteration in cell surface receptors. While numerous targets and agents have been uncovered in recent years, cancer cells continue to evade these solutions. In this Special Issue, we aim to present high-quality research in these areas to share within the research community what we have learned, what is new, and what is on the cutting edge of mechanisms that cause metastasis and resistance. We welcome the submission of original research articles and review articles on signaling mechanisms, experimental therapeutics, and clinical observations.

Dr. Elizabeth Yeh
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • cancer
  • metastasis
  • resistance
  • signaling
  • receptors
  • biomarkers

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Published Papers (2 papers)

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Review

17 pages, 1922 KiB  
Review
Hyperactivation of p21-Activated Kinases in Human Cancer and Therapeutic Sensitivity
by Deivendran Sankaran, Revikumar Amjesh, Aswathy Mary Paul, Bijesh George, Rajat Kala, Sunil Saini and Rakesh Kumar
Biomedicines 2023, 11(2), 462; https://doi.org/10.3390/biomedicines11020462 - 5 Feb 2023
Cited by 2 | Viewed by 1947
Abstract
Over the last three decades, p21-activated kinases (PAKs) have emerged as prominent intracellular nodular signaling molecules in cancer cells with a spectrum of cancer-promoting functions ranging from cell survival to anchorage-independent growth to cellular invasiveness. As PAK family members are widely overexpressed and/or [...] Read more.
Over the last three decades, p21-activated kinases (PAKs) have emerged as prominent intracellular nodular signaling molecules in cancer cells with a spectrum of cancer-promoting functions ranging from cell survival to anchorage-independent growth to cellular invasiveness. As PAK family members are widely overexpressed and/or hyperactivated in a variety of human tumors, over the years PAKs have also emerged as therapeutic targets, resulting in the development of clinically relevant PAK inhibitors. Over the last two decades, this has been a promising area of active investigation for several academic and pharmaceutical groups. Similar to other kinases, blocking the activity of one PAK family member leads to compensatory activity on the part of other family members. Because PAKs are also activated by stress-causing anticancer drugs, PAKs are components in the rewiring of survival pathways in the action of several therapeutic agents; in turn, they contribute to the development of therapeutic resistance. This, in turn, creates an opportunity to co-target the PAKs to achieve a superior anticancer cellular effect. Here we discuss the role of PAKs and their effector pathways in the modulation of cellular susceptibility to cancer therapeutic agents and therapeutic resistance. Full article
(This article belongs to the Special Issue Cancer Metastasis and Therapeutic Resistance 2.0)
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10 pages, 1119 KiB  
Review
HUNK Gene Alterations in Breast Cancer
by Nicole Ramos-Solis, Tinslee Dilday, Alex E. Kritikos and Elizabeth S. Yeh
Biomedicines 2022, 10(12), 3072; https://doi.org/10.3390/biomedicines10123072 - 29 Nov 2022
Cited by 2 | Viewed by 2053
Abstract
Hormonally upregulated neu-associated kinase (HUNK) is a serine/threonine (S/T) protein kinase related to the adenosine monophosphate-activated protein kinase (AMPK) family of kinases. HUNK was originally discovered using a screen to identify kinases expressed in the mouse mammary gland. Therefore, the majority of studies [...] Read more.
Hormonally upregulated neu-associated kinase (HUNK) is a serine/threonine (S/T) protein kinase related to the adenosine monophosphate-activated protein kinase (AMPK) family of kinases. HUNK was originally discovered using a screen to identify kinases expressed in the mouse mammary gland. Therefore, the majority of studies to date have been carried out in models specific to this tissue, and the kinase was named to reflect its mammary gland-specific physiology and pathology. Prior studies show a clear pathogenic role for HUNK in breast cancer. HUNK is upregulated in response to oncogenic HER2/neu and Akt, and there is strong evidence that HUNK is critical for the survival of breast cancer cells. Further evidence shows that inhibiting HUNK using a variety of breast cancer models, including those that are resistant, inhibits tumorigenesis and metastasis. However, HUNK alterations are infrequent. Here, the incidence and consequence of HUNK alterations in breast cancer is reviewed using data mined from the online database cBioPortal and considered in relation to prior research studies. Full article
(This article belongs to the Special Issue Cancer Metastasis and Therapeutic Resistance 2.0)
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