Treating neuroendocrine cancer/tumour


INCA: International Neuroendocrine Cancer Alliance

Living with NET

NET society of India

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This is a good summary:


Click to access Consensus_2.pdf


“this orphan group of tumors which does not hold much interest to the pharmaceutical companies.” [Source]


Depending on the type of NET, medications that may be used include:

  • Somatostatin analogs
  • Chemotherapy
  • Targeted therapy
  • Immunotherapy
  • Peptide receptor radionuclide therapy (PRRT)  [Source]

Octreotide LAR

This is a form of somatostatin treatment: From somatostatin to octreotide LAR: evolution of a somatostatin analogue

“Octreotide is a potent synthetic somatostatin analogue that has become the mainstay of medical therapy for tumor control in neuroendocrine disorders. The multiple effects of octreotide throughout the body, combined with its established safety profile, make it an appealing and reliable option for clinicians. ”

“the antiproliferative effect of octreotide LAR in patients with well-differentiated metastatic GEP-NETs of the midgut” – but this is POORLY differentiated.

“Octreotide was among the first biotherapeutic agents used in the management of GEP-NETs and continues to be a mainstay of therapy today, although it is rarely curative”

“In response to results from the PROMID study, guidelines from the National Comprehensive Cancer Network (NCCN) have been updated to recommend octreotide LAR 20–30 mg as a management option in patients with recurrent or unresectable metastatic carcinoid tumors originating from any primary site of disease (small bowel, colon, rectum, appendix, lung, thymus, stomach) irrespective of functional status, symptomatology and progression status” [While there might be an origin in the colon/rectum, there is also a possible link with the prostate]




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Chemotherapy for large cell neuroendocrine carcinoma

For NET: 

etoposide and cisplatin/ carboplatin (at 50% for 2 days at a time)


Comparing the adverse effects of platinum in combination with etoposide or irinotecan in previously untreated small-cell lung cancer patients with extensive disease: A network meta-analyses

See this PDF file (taken from here)

For lung

Chemotherapy medications commonly used to treat LCLC include Altima (pemetrexed) and Platinol (cisplatin) [Source]


Chemotherapy causes death in more than 25% of cancer patients

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Can Ivermectin help neuroendocrine cancer

Initial notes:


Ivermectin, a potential anticancer drug derived from an antiparasitic drug


“Ivermectin combined with other chemotherapy drugs or targeted drugs has powerful effects on cancer”.


“Various trials have been held over the course of a few years that have significant promise in ivermectin inhibiting the growth of cancer. The good news mainly has been the broad-spectrum working of Ivermectin. It has proven to be fairly effective against a large variety of cancers. The types of cancers it worked against included ovarian cancer, breast cancer, Oesophageal Squamous Cell Carcinoma, and many others.” [Source]

“ivermectin might be a new potential anticancer drug therapy for human colorectal cancer and other cancers. studies have shown that ivermectin has an inhibitory effect on various tumor cells and may be a potential broad-spectrum antitumor drug” [Source]

BUT “ivermectin is the most nonsensitive to the prostate cancer cell line DU145” [Source]


Ivermectin induces cell cycle arrest and apoptosis of HeLa cells via mitochondrial pathway

“IVM might be a new potential anticancer drug for therapy of human cancer”


Ivermectin reverses the drug resistance in cancer cells through EGFR/ERK/Akt/NF-?B pathway



Ivermectin is just one of many drugs that have surfaced in recent years that show promise against malignant tumors. There is a high possibility that ivermectin will be used in chemotherapy commonly in the near future, however, we must understand that tumor cells can easily develop drug resistance and render the effects of many drugs useless. Even so, the use of ivermectin with other drugs in conjunction with therapy can be highly effective for a vast number of malignant tumors. [Source]


ivermectin, at doses of 3–5 mg/kg, was able to suppress the growth of human melanoma and a number of other cancer xenografts in mice without adverse effects  [Source]


Ivermectin inhibits AR pathway in prostate cancer models. Resistance to AR pathway inhibitors in prostate cancer is associated with AR amplification, mutations, and expression of truncated AR variants, the latter characterized by loss of AR’s ligand-binding domain and constitutively active transcription (24). HSP27 has an established role in AR trafficking and stability, and its inhibition by either apatorsen or si-HSP27 reduces AR protein levels and activity, thereby delaying progression of castration-resistant prostate cancer (CRPC) (7825). Similarly to apatorsen (7), IVM significantly reduced AR and prostate-specific antigen (PSA) protein expression in castration-sensitive LNCaP cells and ARF876L protein expression in enzalutamide-resistant M49F cells, an effect that was enhanced in combination with androgen deprivation therapy (in LNCaP cells) or enzalutamide (in M49F cells) (Figure 4A). IVM increased sensitivity of LNCaP cells to androgen deprivation therapy and of enzalutamide-resistant ARF876L M49F cells to enzalutamide (Figure 4B). Interestingly, IVM also decreased AR variant 7 (AR-V7) protein levels in 22RV1 cells, similarly to either si-HSP27 or apatorsen (Figure 4C). The reduction of AR or AR-V7 protein expression was not related to modulation of mRNA levels (Supplemental Figure 4A). The functional effect of IVM on AR-V7 transcriptional activity was also assessed using a PC3V7_3TKNLuc system that incorporates a doxycycline-inducible AR-V7 and probasin-based ARR3tk-Nanoluciferase reporter construct. As shown in Figure 4D, IVM significantly inhibited AR-V7 transcriptional activity compared with PC3_3TKNLuc control. AR-V7 nuclear translocation in 22RV1 cells was also inhibited by IVM, decreasing nuclear AR-V7 levels, with a corresponding increase in the cytoplasmic fraction (Figure 4E).

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