Targeting nodal in conjunction with dacarbazine induces synergistic anticancer effects in metastatic melanoma.

Author: GuptaKanika, HardyKatharine M, HendrixMary J C, MargaryanNaira V, MurphyGeorge F, ScolyerRichard A, StrizziLuigi

Paper Details 
Original Abstract of the Article :
Metastatic melanoma is a highly aggressive skin cancer with a poor prognosis. Despite a complete response in fewer than 5% of patients, the chemotherapeutic agent dacarbazine (DTIC) remains the reference drug after almost 40 years. More recently, FDA-approved drugs have shown promise but patient out...See full text at original site
Dr.Camel IconDr.Camel's Paper Summary Blogラクダ博士について

ラクダ博士は、Health Journal が論文の内容を分かりやすく解説するために作成した架空のキャラクターです。
難解な医学論文を、専門知識のない方にも理解しやすいように、噛み砕いて説明することを目指しています。

* ラクダ博士による解説は、あくまで論文の要点をまとめたものであり、原論文の完全な代替となるものではありません。詳細な内容については、必ず原論文をご参照ください。
* ラクダ博士は架空のキャラクターであり、実際の医学研究者や医療従事者とは一切関係がありません。
* 解説の内容は Health Journal が独自に解釈・作成したものであり、原論文の著者または出版社の見解を反映するものではありません。


引用元:
https://pubmed.ncbi.nlm.nih.gov/25767211

データ提供:米国国立医学図書館(NLM)

Combating Melanoma: A Double-Edged Sword Approach

The fight against metastatic melanoma, a highly aggressive skin cancer, is a challenging endeavor. While dacarbazine (DTIC) has been the standard chemotherapeutic agent for nearly 40 years, it only achieves a complete response in a small percentage of patients. This research explores a promising new strategy: targeting the growth factor Nodal in combination with DTIC to overcome drug resistance and improve patient outcomes.

The authors investigate the effects of DTIC treatment on Nodal-positive human melanoma cells, finding that while DTIC inhibits cell growth, it does not induce apoptosis (programmed cell death). Interestingly, DTIC was found to actually increase the size of the Nodal-positive subpopulation, leading to increased cellular invasion. The study also examines clinical tissue specimens from patients with melanomas refractory to DTIC therapy, revealing that these tumors, both before and after DTIC treatment, stained positive for Nodal expression, emphasizing the potential value of targeting Nodal.

Synergy in the Desert of Cancer Treatment

In vitro studies demonstrate that while anti-Nodal antibodies alone have some adverse effects on melanoma cells, combining DTIC treatment with anti-Nodal antibodies synergistically decreases cell growth and increases apoptosis at concentrations that are ineffective as monotherapy. These findings suggest that targeting Nodal in conjunction with DTIC may be a more effective approach than either treatment alone.

A New Dawn for Melanoma Treatment

This research sheds light on a potential new avenue for melanoma treatment, offering hope for improved outcomes for patients with this aggressive disease. The findings suggest that targeting Nodal in combination with DTIC may provide a more effective and less toxic treatment strategy. Further research is needed to fully understand the potential of this combination therapy and to translate these promising results into clinical practice.

Dr.Camel's Conclusion

This research, like a desert oasis, offers a glimmer of hope in the fight against melanoma. The discovery of a synergistic approach to targeting Nodal and DTIC could revolutionize treatment strategies, offering a more effective and less toxic option for patients. This groundbreaking discovery represents a significant step forward in the fight against melanoma, paving the way for a brighter future for those affected by this challenging disease.

Date :
  1. Date Completed 2016-02-04
  2. Date Revised 2022-03-10
Further Info :

Pubmed ID

25767211

DOI: Digital Object Identifier

NIHMS657698

Related Literature

SNS
PICO Info
in preparation
Languages

English

Positive IndicatorAn AI analysis index that serves as a benchmark for how positive the results of the study are. Note that it is a benchmark and requires careful interpretation and consideration of different perspectives.

This site uses cookies. Visit our privacy policy page or click the link in any footer for more information and to change your preferences.