Inflammatory breast cancer (IBC) is an aggressive form of locally advanced breast cancer. Multimodality therapy, with neoadjuvant chemotherapy followed by locoregional therapy, has become the standard approach. Therefore, I will briefy review what is publicly and generally known about these and then address your question about inflammatory cells.

1. NEOADJUVANT CHEMOTHERAPY. Anthracycline- and taxane-based adjuvant chemotherapy regimens are widely used for neoadjuvant chemotherapy. Anthracyclines and especially taxanes are particularly effective in IBC and a regimen containing an anthracycline and a taxane was recommended by an international expert group on IBC. (Reference: Dawood S, Merajver SD, Viens P, et al. International expert panel on inflammatory breast cancer: consensus statement for standardized diagnosis and treatment. Ann Oncol 2011; 22:515). An example would be: Adriamycin/Doxorubicin + Taxol; (Doxorubicin + Taxotere)

Patients with IBC and HER2 overexpression should also receive HER2-directed therapy (e.g Herceptin) in conjunction with neoadjuvant chemotherapy. Generally known monitoring and precautions important regarding the timing of Herceptin and anthracyclins due to risk of cardiotoxicity.

2. SURGEY. Following neoadjuvant chemotherapy, standard locoregional treatment includes mastectomy (NOT BREAST CONSERVING SURGERY!!!) and radiation therapy (RT). Patients who do not achieve optimal tumor debulking or who remain inoperable should receive radiation therapy with subsequent surgery, if feasible.

However, generally, surgery generally precedes RT since higher doses of RT can be more safely delivered in the postoperative compared to the preoperative setting [16,33].

An international expert panel on IBC recommended that the only method of definitive surgery offered to women with IBC following preoperative systemic treatment should be a modified radical mastectomy. Skin-sparing mastectomy is contraindicated for women with IBC ((Reference: Dawood S, Merajver SD, Viens P, et al. International expert panel on inflammatory breast cancer: consensus statement for standardized diagnosis and treatment. Ann Oncol 2011; 22:515)

Standard fractionation RT with treatment fields giving broad coverage to the chest wall and axillary, infraclavicular, supraclavicular, and internal mammary lymph nodes remains the standard approach. Generally, patients receive 50 Gy in 1.8 or 2 Gy fractions to locoregional sites followed by a 10 Gy boost to the chest wall (total dose 60 Gy).

An expert consensus panel on IBC recommended escalating the dose to 66Gy in women who are

Inflammatory breast cancer is one category of cancers. But in general every cancer is preceded by chronic inflammation. The drug and the mode of treatment depends on the site and the stage of cancer. In general it is realized that even after chemo and radiotherapy inflammation still persists, and hence to achieve a better prognosis administration of anti-inflammatory drugs is advisable.

Dear Krishan,

The role of inflammatory cells, especially macrophages in the tumor microenvironment is a rather controversial matter. Some serve to "contain" cancer cells (Example: https://www.apollon.uio.no/english/articles/2011/lifescience-inflammation.html), while others may contribute to cancer pathogenesis (Example: sunburn and skin cancer; Barrett esophagitis and easophageal cancer; ulcerative colitis and colon cancer). There has been a lit of discussion - here is an old file: http://web.mit.edu/newsoffice/2006/cancer-links.html

I am not aware of evidence based recommendations regarding the use of anti-inflammatory drugs in any specific type of cancer and cancer in general. Indeed anti-inflammatory drugs targeting the TNF pathway (Example: Humira, Enbrel, Remicade) have been associated with increased cancer risk as well as increased risk of potentially fatal infections requiring TV ads to include public warnings.

1...Many standard cytotoxic cancer chemotherapeutic drugs have been shown to kill tumor cells without influencing "inflammatory cells".

2...The quotation marks above are important. The details of what inflammatory cells and what cancer are crucial in a discussion of inflammation and cancer.

3...The research literature is huge on both sides, inflammatory infiltrate helps the cancer grow, the inflammatory infiltrate inhibits cancer's growth. It doesn't help much to even speak of "macrophages" or T or B cell lymphocytes in a cancer. Which subtype, which sub-sub-type, etc. is essential.

4...."Anti-inflammatory drugs" don't exist if my statement that "inflammatory cells" don't exist as a physiologically meaningful category. The data on "non-steroidal anti-inflammatory drugs", NSAID's is puzzling. They aren't really anti-inflammatory. This is why they aren't DMARD's. Prednisone is clearly anti-inflammatory, does kill off many subclasses of lymphocytes, does not kill the usual non-hematopoetic cancer cell, is in fact commonly used in cancer treatment, and yet the effect on overall survival is surprisingly unclear, but doesn't seem to be huge. I just used the word "anti-inflammatory" in the clinical sense recognized by the early Greek physicians, Calor, Rubor, Dolor, Tumor. In that clinical meaning most cancer chemotherapeutic agents target the cancer cell, not inflammation.

Dear R Kast,

The fact that chemotherapy drugs have anti-inflammatory properties has been demonstrated. Methotrexate for example is a chemotherapy drug used against germ cell tumors, bone cancer, and leukemia. But it is also a "disease-modiying" standard drug against rheumatoid arthritis.

Cyclophosphamide is an anti-cancer drug used against a large spectrum of cancers; but it is also used against autoimmune diseases and inflammation such as very aggressive SLE

Mitoxantrone is a chemotherapy drug and used extensively in leukemias, but it is also an anti-inflammatory drug used for multiple sclerosis.

These are but a few examples.

In general, any cytotoxic agent can be used for treatment of cancers originating from cells that are sensitive to its cytotoxic actions and it can also be used for treatment of inflammation resulting from immune system elements that are sensitive to its cytotoxic effects.

agreed, methotrexate and azathioprene are commonly used to treat some cancers and some inflammation-related diseases. mitoxantrone use in MS is ill-advised i think, due to its carcinogenic potential. we probably agree that the two implications of the original question remain interesting and deeply unresolved- to what extent do inflammation related cells and stroma contribute to or inhibit a given cancer's growth? and the related question, once we determine this in a given cancer [or in a given cancer in a specific given patient] what can we do to kill off or enhance such cells respectively. agreed? these questions are upper most in many researcher's minds. also we consider it likly that BOTH cancer growth facilitating and growth inhibiting inflammation-related cells and interactions with stroma are common in cancers generally.

There is a difference between acute and chronic inflammation. Chronic inflammation is cancerogenic especially in people with damaged DNA repair mechanism. Acute inflammatory response, especially granulocytic component, has a important role in tumor regression (see on internet about Coley toxin and SR/CR mice)

http://www.ncbi.nlm.nih.gov/pubmed/22684101

http://www.ncbi.nlm.nih.gov/pubmed?term=granulocytes%20as%20effective%20Jaganjac

1...the relationship between "inflammatory cells" and cancer is interesting and important to understand but not as simple as stated by Saric. there is a large research base supporting the notion that neutrophils, and granulocytic related, bone marrow-derived cells contribute growth enhancing factors to a given human cancer.

2...in science generally and in this matter specifically [of bone marrow derived white cells' and lymphocytes'] presence within and around a human cancer when we have solid data supporting opposite conclusions [as we do in the matter of "inflammatory cells" in cancer] the resolution comes from looking with a finer eye- data not dogma.

3...so abandoning talk of "inflammatory cells" and collecting data on sub-types and sub-sub-types of macrophages, lymphocytes etc is required.

4...the same cell, the same drug or intervention can [and often is] both disease process facilitating and disease process inhibiting.